subject:(tumor suppressor tumor gene)

University of Minnesota

1. Clark, Christopher. Characterization Of TM9SF2 And WAC As Novel Colorectal Cancer Driver Genes.

Degree: PhD, Microbiology, Immunology and Cancer Biology, 2018, University of Minnesota

URL: http://hdl.handle.net/11299/201708

► The studies performed in this dissertation focused on the characterization of two candidate cancer genes, TM9SF2 and WAC, and their role in colorectal cancer (CRC).… (more)

Subjects/Keywords: Cancer; Driver gene; Genetics; Oncogene; Tumor suppressor

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APA (6^th Edition):

Clark, C. (2018). Characterization Of TM9SF2 And WAC As Novel Colorectal Cancer Driver Genes. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/201708

Chicago Manual of Style (16^th Edition):

Clark, Christopher. “Characterization Of TM9SF2 And WAC As Novel Colorectal Cancer Driver Genes.” 2018. Doctoral Dissertation, University of Minnesota. Accessed March 08, 2021. http://hdl.handle.net/11299/201708.

MLA Handbook (7^th Edition):

Clark, Christopher. “Characterization Of TM9SF2 And WAC As Novel Colorectal Cancer Driver Genes.” 2018. Web. 08 Mar 2021.

Vancouver:

Clark C. Characterization Of TM9SF2 And WAC As Novel Colorectal Cancer Driver Genes. [Internet] [Doctoral dissertation]. University of Minnesota; 2018. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/11299/201708.

Council of Science Editors:

Clark C. Characterization Of TM9SF2 And WAC As Novel Colorectal Cancer Driver Genes. [Doctoral Dissertation]. University of Minnesota; 2018. Available from: http://hdl.handle.net/11299/201708

2. Mesrobian, Cristina M. The Cul3 E3 Ligase Acts as a Tumor Suppressor by Targeting Ubiquitin-Mediated Proteolysis of Distinct Cell Cycle Regulators.

Degree: PhD, Division of Biology and Medicine. Pathobiology, 2009, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:173/

► Maintenance of an intricate balance between positive and negative regulators of the cell cycle is vital, as altered cell cycle regulation results in the uncontrolled… (more)

▼ Maintenance of an intricate balance between positive and negative regulators of the cell cycle is vital, as altered cell cycle regulation results in the uncontrolled cell division that leads to cancer. Cul3 is a novel type of SCF-like ubiquitin ligase that targets proteins for degradation by the ubiquitin-mediated proteolysis system. Cul3 binds to BTB domain-containing proteins that serve as adaptor molecules, binding the substrate for degradation. A yeast two-hybrid screen for proteins that interact with mammalian Cul3 identified nine BTB domain-containing proteins, called Cullin three binding proteins (Ctbs). More in depth analysis of Ctb9/KLHDC5 has begun to elucidate a role for Cul3 in the regulation of cytoskeletal structure. The work described here shows targeting of the microtubule severing protein, p60/katanin by the Cul3 complex using Ctb9/KLHDC5 as a specific substrate adaptor. Cells that are deficient in Cul3 accumulate excess p60/katanin, and are unable to complete mitosis normally, resulting in the accumulation of binucleated cells. This work represents a novel way in which Cul3 activity regulates the cell cycle by controlling microtubule dynamics during mitosis. A major substrate of Cul3 is cyclin E. Elevated levels of cyclin E protein have been detected in breast cancers, and such increased expression is correlated with a poorer prognosis. However, cell lines derived from human breast tumors rarely show increased cyclin E mRNA levels, implying the changes are occurring posttranscriptionally. We hypothesized that altered Cul3 activity may be responsible for the accumulation of cyclin E. The work presented in this thesis describes the development of a model system to determine the role Cul3 plays in breast cancer. Targeted deletion of Cul3 from mouse mammary tissue results in hyperplasia of the mammary ducts and increased cyclin E protein levels in the tissue. These conditions are extremely likely to lead to a malignant state. Based on this work and the work of others, we propose that Cul3 acts as a tumor suppressor by targeting for degradation multiple proteins involved in cell cycle regulation. Advisors/Committee Members: Singer, Jeffrey (director), Chung, Maureen (reader), Moss, Steven (reader), Salazar-Mather, Thais (reader), Diehl, Alan (reader).

Subjects/Keywords: tumor suppressor

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APA (6^th Edition):

Mesrobian, C. M. (2009). The Cul3 E3 Ligase Acts as a Tumor Suppressor by Targeting Ubiquitin-Mediated Proteolysis of Distinct Cell Cycle Regulators. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:173/

Chicago Manual of Style (16^th Edition):

Mesrobian, Cristina M. “The Cul3 E3 Ligase Acts as a Tumor Suppressor by Targeting Ubiquitin-Mediated Proteolysis of Distinct Cell Cycle Regulators.” 2009. Doctoral Dissertation, Brown University. Accessed March 08, 2021. https://repository.library.brown.edu/studio/item/bdr:173/.

MLA Handbook (7^th Edition):

Mesrobian, Cristina M. “The Cul3 E3 Ligase Acts as a Tumor Suppressor by Targeting Ubiquitin-Mediated Proteolysis of Distinct Cell Cycle Regulators.” 2009. Web. 08 Mar 2021.

Vancouver:

Mesrobian CM. The Cul3 E3 Ligase Acts as a Tumor Suppressor by Targeting Ubiquitin-Mediated Proteolysis of Distinct Cell Cycle Regulators. [Internet] [Doctoral dissertation]. Brown University; 2009. [cited 2021 Mar 08]. Available from: https://repository.library.brown.edu/studio/item/bdr:173/.

Council of Science Editors:

Mesrobian CM. The Cul3 E3 Ligase Acts as a Tumor Suppressor by Targeting Ubiquitin-Mediated Proteolysis of Distinct Cell Cycle Regulators. [Doctoral Dissertation]. Brown University; 2009. Available from: https://repository.library.brown.edu/studio/item/bdr:173/

NSYSU

3. Lin, James. The Differential Expression of Bcl10 in the Tumor Cell Lines.

Degree: Master, Biological Sciences, 2004, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816104-155835

► Bcl10 is one of the apoptosis regulatory protein. It is located at 1p22,one site harbor tumor suppressor tumor gene. We screen Bcl10 expression in different… (more)

Subjects/Keywords: tumor suppressor tumor gene

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APA (6^th Edition):

Lin, J. (2004). The Differential Expression of Bcl10 in the Tumor Cell Lines. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816104-155835

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lin, James. “The Differential Expression of Bcl10 in the Tumor Cell Lines.” 2004. Thesis, NSYSU. Accessed March 08, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816104-155835.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lin, James. “The Differential Expression of Bcl10 in the Tumor Cell Lines.” 2004. Web. 08 Mar 2021.

Vancouver:

Lin J. The Differential Expression of Bcl10 in the Tumor Cell Lines. [Internet] [Thesis]. NSYSU; 2004. [cited 2021 Mar 08]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816104-155835.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lin J. The Differential Expression of Bcl10 in the Tumor Cell Lines. [Thesis]. NSYSU; 2004. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816104-155835

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Gothenburg / Göteborgs Universitet

4. Visuttijai, Kittichate. Cellular, Molecular and Functional Characterization of the Tumor Suppressor Candidate MYO1C.

Degree: 2016, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/41552

► Tumor suppressor genes play a role as a growth regulator and a gatekeeper of a cell. Their inactivation is often detected in malignant tumors. Identification… (more)

▼ Tumor suppressor genes play a role as a growth regulator and a gatekeeper of a cell. Their inactivation is often detected in malignant tumors. Identification of novel tumor suppressor gene candidates may help to further understand tumorigenesis and aid in the discovery of a new treatment leading toward cure of cancer. This PhD research project aimed to understand functional significance of a novel tumor suppressor gene candidate, myosin IC (MYO1C) and to identify potential interaction(s) of the MYO1C protein with key components of the signaling pathways involving in cancer development. In an experimental rat model for endometrial carcinoma (EC), detailed molecular genetic analysis of a candidate tumor suppressor region located distal to the tumor protein 53 (Tp53) suggested the myosin IC gene (Myo1c) as the best potential target for deletion of the genetic material. The question arising was whether and how MYO1C could function as a tumor suppressor gene. By using qPCR, Western blot or immunohistochemistry analyses, we examined MYO1C protein level in panels of well-stratified human colorectal cancer (CRC) and EC respectively. We found that MYO1C was significantly down-regulated in these cancer materials and that for the EC panel, the observed down-regulation of MYO1C correlated with tumor stage, where tumors at more advanced stages had less expression of MYO1C. In cell transfection experiments, we found that over-expression of MYO1C significantly decreased cell proliferation, and silencing MYO1C with siRNA increased cell viability. Additionally, knockdown of MYO1C impaired the ability of cells to migrate, spread and adhere to the surface. Recent published studies suggested a potential interplay between MYO1C and the phosphoinositide 3-kinase (PI3K)/AKT pathway. To examine this hypothesis, we analyzed the expression and/or activation of components of the PI3K/AKT and RAS/ERK signaling pathways in vivo in CRC samples, and in vitro in cells transfected with the MYO1C gene expression construct or MYO1C-targeted siRNA. To identify other potential pathways/ mechanisms through which MYO1C may exert its tumor suppressor activity, we additionally performed new sets of MYO1C-siRNA knockdown experiments. At different time points post transfection, we performed microarray global gene expression experiments followed by bioinformatics analysis of the data. Altogether, the results suggested an early PI3K/AKT response to altered MYO1C expression. We additionally identified several cancer-related genes/pathways with late response to MYO1C knockdown. All things considered, the identification of MYO1C-expression impact on cell proliferation, migration, and adhesion in combination with its interplay between several cancer-related genes and signaling pathways provide further evidence for the initial hypothesis of a tumor suppressor activity of MYO1C.

Subjects/Keywords: MYO1C; myosin IC; tumor suppressor gene; cancer; tumor; PI3K/AKT signaling

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APA (6^th Edition):

Visuttijai, K. (2016). Cellular, Molecular and Functional Characterization of the Tumor Suppressor Candidate MYO1C. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/41552

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Visuttijai, Kittichate. “Cellular, Molecular and Functional Characterization of the Tumor Suppressor Candidate MYO1C.” 2016. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed March 08, 2021. http://hdl.handle.net/2077/41552.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Visuttijai, Kittichate. “Cellular, Molecular and Functional Characterization of the Tumor Suppressor Candidate MYO1C.” 2016. Web. 08 Mar 2021.

Vancouver:

Visuttijai K. Cellular, Molecular and Functional Characterization of the Tumor Suppressor Candidate MYO1C. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2016. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/2077/41552.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Visuttijai K. Cellular, Molecular and Functional Characterization of the Tumor Suppressor Candidate MYO1C. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2016. Available from: http://hdl.handle.net/2077/41552

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

NSYSU

5. Shin, Yi-Li. Part Iï¼Analysis of the tumor suppressor gene p16ï¼p27 and Rb expression in nasopharyngeal carcinoma in Taiwan Part IIï¼Tumor characteristics of two newly established nasopharyngeal carcinoma cell lines.

Degree: Master, Biological Sciences, 2000, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0808100-123811

► ç¬¬ä¸é¨ä»½ Nasopharyngeal carcinomaï¼NPCï¼ is a malignant tumor which occurs at high incidence in southern China. Several risk factors have now been recognized, but the molecular… (more)

▼ ç¬¬ä¸é¨ä»½ Nasopharyngeal carcinomaï¼NPCï¼ is a malignant tumor which occurs at high incidence in southern China. Several risk factors have now been recognized, but the molecular mechanism of this disease is not well understood. To investigate the c-mycãcyclin D1ãp16ãp27 and Rb gene expression in NPC at protein level, 46 cases of nasopharyngeal carcinoma in southern Taiwan were detected by immunohistochemistry. There was no detectable p16 in 31/45 casesï¼69ï¹ªï¼ï¼ 34/46 casesï¼73.9ï¹ªï¼had intense staining for the Rb proteinï¼ 29ï¼70.7ï¹ªï¼of 41 cases had c-myc protein expressionï¼cyclin D1 was not overexpression in nasopharyngeal carcinomaï¼ 32ï¼69.6ï¹ªï¼of 46 cases had high level expression of p27, which was inverse correlation with other tumors. No expression of c-myc protein correlated with higher neck metastasisï¼Pï¼0.05ï¼. No correlation was found between other proteins and any of the clinicopathological parameters. ç¬¬äºé¨ä»½ To better understand nasopharyngeal carcinomaï¼NPCï¼, we have newly established two NPC cell lines. Biopsy specimens from NPC patients were collected, primary culture were set up. Two NPC cell lines were establishedï¼NPCGK 01 was derived from differentiated carcinoma and NPCGK 02 was derived from undifferentiated carcinoma. Two cell lines have been passaged for more than 25 times. Two cell lines had telomerase activityï¼strong expression of hTERT gene and keratin-19 gene were also observed. TGFÎ² RI protein expression of these NPC cell lines is higher than normal epithelial cell.The oncogenes, c-mycãc-fos and cyclin D1 were overexpressed. The Rb protein was expressed stronger than normal epithelial cells. NPCGK 01 that was derived from differentiated carcinoma had p16 down-regulation and p27 gene not expression, but p21 protein had excess expression. In short, two cell lines had cancer cell characteristics, oncoproteins were overexpression and tumor suppressor proteins were abnormal expression. This result may lead to tumorigenesis of nasopharyngeal carcinoma. Advisors/Committee Members: Jiin-Tsuey (chair), Yi-Ren Hong (chair), Chung-Lung Cho (committee member).

Subjects/Keywords: nasopharyngeal carcinoma; tumor suppressor gene

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APA (6^th Edition):

Shin, Y. (2000). Part Iï¼Analysis of the tumor suppressor gene p16ï¼p27 and Rb expression in nasopharyngeal carcinoma in Taiwan Part IIï¼Tumor characteristics of two newly established nasopharyngeal carcinoma cell lines. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0808100-123811

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Shin, Yi-Li. “Part Iï¼Analysis of the tumor suppressor gene p16ï¼p27 and Rb expression in nasopharyngeal carcinoma in Taiwan Part IIï¼Tumor characteristics of two newly established nasopharyngeal carcinoma cell lines.” 2000. Thesis, NSYSU. Accessed March 08, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0808100-123811.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Shin, Yi-Li. “Part Iï¼Analysis of the tumor suppressor gene p16ï¼p27 and Rb expression in nasopharyngeal carcinoma in Taiwan Part IIï¼Tumor characteristics of two newly established nasopharyngeal carcinoma cell lines.” 2000. Web. 08 Mar 2021.

Vancouver:

Shin Y. Part Iï¼Analysis of the tumor suppressor gene p16ï¼p27 and Rb expression in nasopharyngeal carcinoma in Taiwan Part IIï¼Tumor characteristics of two newly established nasopharyngeal carcinoma cell lines. [Internet] [Thesis]. NSYSU; 2000. [cited 2021 Mar 08]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0808100-123811.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Shin Y. Part Iï¼Analysis of the tumor suppressor gene p16ï¼p27 and Rb expression in nasopharyngeal carcinoma in Taiwan Part IIï¼Tumor characteristics of two newly established nasopharyngeal carcinoma cell lines. [Thesis]. NSYSU; 2000. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0808100-123811

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

6. Zhao, Weilin. RERG suppresses cell proliferation, migration and angiogenesis through ERK/NF-кB signaling pathway in nasopharyngeal carcinoma.

Degree: 博士(医学), 2017, Mie University / 三重大学

URL: http://hdl.handle.net/10076/00017324

►

Background: Nasopharyngeal carcinoma (NPC) is a malignancy of the head and neck that is prevalent in Southeast Asia and southern China. Recent studies in epigenetics… (more)

▼

Background: Nasopharyngeal carcinoma (NPC) is a malignancy of the head and neck that is prevalent in Southeast Asia and southern China. Recent studies in epigenetics suggest that DNA methylation plays a pivotal role in the onset and progression of cancer. Combining the methyl- DNA binding domain capture technique and cDNA microarray analysis, we identified a unique hypermethylated gene, RERG (Ras-like estrogen-regulated growth inhibitor), that was downregulated in NPC tissues. RERG is a tumor suppressor gene that was first reported in breast cancer. However, the functions of RERG are largely unknown in other tumor types. Methods: RERG expression was assessed in human subjects (NPC primary tissues and noncancer tissues) and cell lines (NPC cell lines and an immortalized epithelial cell line NP460). Further, we investigated the methylation rate of RERG in both human subject and cell lines. 5- Aza-2’-deoxycytidine (Aza) or combined with trichostatin A (TSA) were treated to three NPC cell lines (HK1, C666-1 and HK1_EBV). In addition, the role of RERG in NPC cells and its underlying mechanisms were explored by overexpression of RERG in NPC cell lines. Results: RERG was significantly down-regulated in NPC cancer nests compared to normal nasopharyngeal epithelium cells. Furthermore, the RERG promoter was frequently methylated in NPC tissues and cell lines. The RERGmethylation rate yielded an area under the curve (AUC) of receiver operating characteristic (ROC) curve was 0.897 (95%CI: 0.818–0.976). The downregulation of RERG was restored in NPC cells treated with Aza and TSA. In addition, ectopic expression of RERG in NPC cell lines resulted in a significant suppression of cell proliferation, clonogenicity,migration and invasion. RERG-overexpressing cells showed significantly slower growth and less angiogenesis in tumor xenografts in nude mice. RERG suppressed the ERK/NF-κB signaling pathway and inhibited tumor growth and angiogenesis with downregulation of MMPs and IL8 in tumors of nude mouse xenografts. Conclusions: Our results suggest that RERG is frequently silenced by promoter CpG methylation in NPC, and acts as a functional tumor suppressor by suppressing the ERK/NF- κB signaling pathway. These findings support the potential use of RERG as a novel molecular target in NPC therapy.

本文 / Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine; Department of Otorhinolaryngology - Head and Neck Surgery, Mie University Graduate School of Medicine; Department of Otolaryngology Head and Neck Surgery, First Affiliated Hospital of Guangxi Medical University

47p

Subjects/Keywords: RERG; Nasopharyngeal carcinoma; Tumor suppressor gene; DNA methylation; Angiogenesis

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APA (6^th Edition):

Zhao, W. (2017). RERG suppresses cell proliferation, migration and angiogenesis through ERK/NF-кB signaling pathway in nasopharyngeal carcinoma. (Thesis). Mie University / 三重大学. Retrieved from http://hdl.handle.net/10076/00017324

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zhao, Weilin. “RERG suppresses cell proliferation, migration and angiogenesis through ERK/NF-кB signaling pathway in nasopharyngeal carcinoma.” 2017. Thesis, Mie University / 三重大学. Accessed March 08, 2021. http://hdl.handle.net/10076/00017324.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zhao, Weilin. “RERG suppresses cell proliferation, migration and angiogenesis through ERK/NF-кB signaling pathway in nasopharyngeal carcinoma.” 2017. Web. 08 Mar 2021.

Vancouver:

Zhao W. RERG suppresses cell proliferation, migration and angiogenesis through ERK/NF-кB signaling pathway in nasopharyngeal carcinoma. [Internet] [Thesis]. Mie University / 三重大学; 2017. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/10076/00017324.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zhao W. RERG suppresses cell proliferation, migration and angiogenesis through ERK/NF-кB signaling pathway in nasopharyngeal carcinoma. [Thesis]. Mie University / 三重大学; 2017. Available from: http://hdl.handle.net/10076/00017324

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Texas Southwestern Medical Center

7. Lu, Wan-Jin. Illuminating the P53 Regulatory Network in Genetic Models.

Degree: 2011, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/857

►

The file named "thesis.pdf" is the primary dissertation file. Supplemental videos ("Movie1.avi", "Movie2.avi") are also provided (in Audio Video Interleaved format).

The tumor suppressor gene… (more)

Subjects/Keywords: Genes, P53; Drosophila melanogaster; Gene Regulatory Networks; Tumor Suppressor Proteins

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lu, W. (2011). Illuminating the P53 Regulatory Network in Genetic Models. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/857

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lu, Wan-Jin. “Illuminating the P53 Regulatory Network in Genetic Models.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed March 08, 2021. http://hdl.handle.net/2152.5/857.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lu, Wan-Jin. “Illuminating the P53 Regulatory Network in Genetic Models.” 2011. Web. 08 Mar 2021.

Vancouver:

Lu W. Illuminating the P53 Regulatory Network in Genetic Models. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/2152.5/857.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lu W. Illuminating the P53 Regulatory Network in Genetic Models. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/857

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Vermont

8. Weinheimer, Adam S. Investigating the Tumor Suppressor Role of RUNX1 in Human Breast Cancer.

Degree: Biochemistry, 2018, University of Vermont

URL: https://scholarworks.uvm.edu/hcoltheses/260

► Breast cancer (BrCa) remains the leading cause of cancer-related deaths in women worldwide. Current research suggests that the transcription factor RUNX1 functions as a… (more)

▼ Breast cancer (BrCa) remains the leading cause of cancer-related deaths in women worldwide. Current research suggests that the transcription factor RUNX1 functions as a regulator and potentially as a tumor suppressor in breast cancer progression. RUNX1 is the most dominant RUNX family member expressed in normal mammary epithelial cells and it has been demonstrated that RUNX1 activity decreases as breast cancer aggression increases. Yet, the mechanism of this regulation remains unclear. The significance of this project is to further the in-depth investigation of the relationship between RUNX1 and differentially expressed genes that influence human breast cancer progression. This study addresses the hypothesis that RUNX1 controls a myriad of genes that play roles in the suppression of the breast cancer stem cell (BCSC) population, a subpopulation of cancer cells that are capable of self-renewal and demonstrate an ability to resist common chemotherapies and treatments. BCSCs are therefore the most dangerous and most essential to eradicate if the cancer is to be cured. To test this hypothesis, RUNX1 was downregulated in the MCF10A breast cancer cell line using both the inducible CRISPRi and the shRNA-mediated gene knockdown approaches. Fluorescence-activated cell sorting (FACS) and quantitative polymerase chain reaction (qPCR) confirmed successful knockdown of RUNX1 and further genetic and proteomic expression analyses of known breast cancer driver genes was performed to determine how RUNX1 depletion exerts control over the progression of BrCa. It was found that RUNX1 may aid in maintaining the epithelial phenotype in BrCa while also suppressing the expression of key BrCa driver genes such as phosphatidylinositol-3-kinases (PI3K) PIK3CA and PIK3R1. Investigating the role of RUNX1 as a suppressor of the BCSC population adds a new level of knowledge to the field of breast cancer research, and may allow development of a safer, more targeted, and more effective plan of action to eradicate one of the deadliest diseases that exists today. Advisors/Committee Members: Janet Stein, Jay Silveira, Matthew Liptak.

Subjects/Keywords: Breast Cancer; RUNX1; Gene Knockdown; CRISPR; Biochemistry; Tumor Suppressor

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APA (6^th Edition):

Weinheimer, A. S. (2018). Investigating the Tumor Suppressor Role of RUNX1 in Human Breast Cancer. (Thesis). University of Vermont. Retrieved from https://scholarworks.uvm.edu/hcoltheses/260

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Weinheimer, Adam S. “Investigating the Tumor Suppressor Role of RUNX1 in Human Breast Cancer.” 2018. Thesis, University of Vermont. Accessed March 08, 2021. https://scholarworks.uvm.edu/hcoltheses/260.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Weinheimer, Adam S. “Investigating the Tumor Suppressor Role of RUNX1 in Human Breast Cancer.” 2018. Web. 08 Mar 2021.

Vancouver:

Weinheimer AS. Investigating the Tumor Suppressor Role of RUNX1 in Human Breast Cancer. [Internet] [Thesis]. University of Vermont; 2018. [cited 2021 Mar 08]. Available from: https://scholarworks.uvm.edu/hcoltheses/260.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Weinheimer AS. Investigating the Tumor Suppressor Role of RUNX1 in Human Breast Cancer. [Thesis]. University of Vermont; 2018. Available from: https://scholarworks.uvm.edu/hcoltheses/260

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Texas Southwestern Medical Center

9. Hooks, Jared Cole. Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells.

Degree: 2016, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/6143

► Since its discovery, p14ARF (p19Arf in mice) has been shown to be an important regulator of the cell cycle, carrying out this function through p53-dependent… (more)

Subjects/Keywords: Gene Expression Regulation; Transforming Growth Factor beta; Tumor Suppressor Protein p14ARF

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hooks, J. C. (2016). Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/6143

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hooks, Jared Cole. “Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed March 08, 2021. http://hdl.handle.net/2152.5/6143.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hooks, Jared Cole. “Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells.” 2016. Web. 08 Mar 2021.

Vancouver:

Hooks JC. Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/2152.5/6143.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hooks JC. Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/6143

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Baylor University

10. Yu, Eun-Jeong. The integrin interacts with cki-1/p27kip1, a tumor suppressor gene, of the nematode Caenorhabditis elegans.

Degree: PhD, Biology., 2014, Baylor University

URL: http://hdl.handle.net/2104/9200

► Integrin is a heterodimeric cell surface receptor for extracellular matrix (ECM) and plays essential roles in regulating cell behaviors such as cell migration, adhesion, growth… (more)

▼ Integrin is a heterodimeric cell surface receptor for extracellular matrix (ECM) and plays essential roles in regulating cell behaviors such as cell migration, adhesion, growth and death. The cell-ECM interaction is particularly important for progression and arrest of cell cycle. However, the mechanism by which the ECM influences the cell cycle in vivo is poorly understood. To study the role of integrin in cell cycle, we generated a pat-3, Caenorhabditis elegans β integrin, transgenic mutant. The pat-3 (sp) carrying a defective splicing of intron 7 displayed growth defective phenotypes such as coldsensitive larval arrest, shorter body length, reduced lifespan, and increased sterility. To study the role of integrin in cell growth, we assessed for the interaction of integrin signaling to CKI-1 that is a C. elegans homologue of the cyclin dependent kinase inhibitor p27kip1, a tumor suppressor. In wild type pat-3 (+), CKI-1::GFP is localized to nucleoli in hypodermis; whereas, CKI-1::GFP appeares clumped and scattered in the nucleoplasm of pat-3 (sp). In addition, the level of CKI-1::GFP protein was found elevated in pat-3 (sp). In an RNAi screen, we found that integrin signaling and SCF E3 ubiquitin ligase genes appeared to involve in the localization and expression of CKI-1. This result suggests that integrin signaling and SCF E3 ligase work together to regulate the cellular distribution of CKI-1. We continued to study the localization of CKI-1 and investigate suppressors of pat-3 (sp) defects. RNAi screen revealed that genes involved in ribosome biogenesis, unfolded protein response, chromatin modification, rRNA processing, and ubiquitin-mediated protein degradation are required for the up regulation of CKI-1::GFP, suggesting that integrin signaling links to the function of many genes acting in nucleus, nucleolus, and protein degradation. My study demonstrated that integrin plays robust roles in regulating the proper localization and level of CKI-1/p27kip1 in concert with integrin signaling, protein degradation, and many nucleus expressed genes including dnc-1, hda-1, mig-32, and lpd- 7. This provides insight into potential molecular mechanism of the mammalian β1 integrin splice variants, β1B and β1C, in regulating cell behavior. Advisors/Committee Members: Lee, Myeongwoo. (advisor).

Subjects/Keywords: Caenorhabditis elegans.; Integrin.; Cell cycle.; Nucleolus.; Tumor suppressor gene.

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Yu, E. (2014). The integrin interacts with cki-1/p27kip1, a tumor suppressor gene, of the nematode Caenorhabditis elegans. (Doctoral Dissertation). Baylor University. Retrieved from http://hdl.handle.net/2104/9200

Chicago Manual of Style (16^th Edition):

Yu, Eun-Jeong. “The integrin interacts with cki-1/p27kip1, a tumor suppressor gene, of the nematode Caenorhabditis elegans.” 2014. Doctoral Dissertation, Baylor University. Accessed March 08, 2021. http://hdl.handle.net/2104/9200.

MLA Handbook (7^th Edition):

Yu, Eun-Jeong. “The integrin interacts with cki-1/p27kip1, a tumor suppressor gene, of the nematode Caenorhabditis elegans.” 2014. Web. 08 Mar 2021.

Vancouver:

Yu E. The integrin interacts with cki-1/p27kip1, a tumor suppressor gene, of the nematode Caenorhabditis elegans. [Internet] [Doctoral dissertation]. Baylor University; 2014. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/2104/9200.

Council of Science Editors:

Yu E. The integrin interacts with cki-1/p27kip1, a tumor suppressor gene, of the nematode Caenorhabditis elegans. [Doctoral Dissertation]. Baylor University; 2014. Available from: http://hdl.handle.net/2104/9200

University of Texas Southwestern Medical Center

11. Sung, Caroline Yeh-Chien. Establishing a Dual-Reporter Mouse Model to Monitor INK4A/ARF Regulation in Vivo.

Degree: 2015, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/7068

►

The general metadata – e.g., title, author, abstract, subject headings, etc. – is publicly available, but access to the submitted files is restricted to UT… (more)

▼

The general metadata – e.g., title, author, abstract, subject headings, etc. – is publicly available, but access to the submitted files is restricted to UT Southwestern campus access and/or authorized UT Southwestern users.

The INK4B-ARF-INK4A locus on human chromosome 9p21 (and on mouse chromosome 4) encodes three linked, yet functionally distinctive, gene products that coordinate signaling events in both normal development and disease states. INK4 proteins exert their function as gate-keepers for cell cycle progression by inhibiting D-type cyclin-dependent kinases (CDKs), which are responsible for the phosphorylation of the retinoblastoma (RB) protein and consequent G1 exit. The structurally distinct ARF protein (p14ARF in human and p19Arf in mouse), however, activates another major tumor suppressor, TP53, via direct inhibition of its negative regulator, murine double minute 2 (MDM2). The identification of these separate but interacting effector pathways has highlighted the importance of this locus in the initiation and progression of tumorigenesis. Indeed, loss of expression of these gene products, either by deletion or gene silencing, has been linked to many forms of adult and pediatric cancer. To gain a better understanding of how the two gene products of the Cdkn2a locus, p16Ink4a and p19Arf, are regulated in vivo, I generated a BAC reporter mouse by replacing the coding sequence of each gene with a unique fluorescent reporter, allowing us to monitor the coordinate and independent regulation of the two genes at single-cell resolution. Here, I report the generation of the dual-reporter mouse model, functional validation in response to physiological processes previously associated with Cdkn2a expression as well as the novel discovery of Arf promoter activation in the central nervous system under normal conditions. The use of this transgenic reporter system will further allow for the identification of cues conferring Ink4a/Arf locus regulation during normal development as well as disease pathogenesis.

Advisors/Committee Members: Amatruda, James F., Skapek, Stephen X., Johnson, Jane E., Mendelson, Carole R..

Subjects/Keywords: Cyclin-Dependent Kinase Inhibitor p16; Gene Silencing; Tumor Suppressor Protein p14ARF

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sung, C. Y. (2015). Establishing a Dual-Reporter Mouse Model to Monitor INK4A/ARF Regulation in Vivo. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/7068

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sung, Caroline Yeh-Chien. “Establishing a Dual-Reporter Mouse Model to Monitor INK4A/ARF Regulation in Vivo.” 2015. Thesis, University of Texas Southwestern Medical Center. Accessed March 08, 2021. http://hdl.handle.net/2152.5/7068.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sung, Caroline Yeh-Chien. “Establishing a Dual-Reporter Mouse Model to Monitor INK4A/ARF Regulation in Vivo.” 2015. Web. 08 Mar 2021.

Vancouver:

Sung CY. Establishing a Dual-Reporter Mouse Model to Monitor INK4A/ARF Regulation in Vivo. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2015. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/2152.5/7068.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sung CY. Establishing a Dual-Reporter Mouse Model to Monitor INK4A/ARF Regulation in Vivo. [Thesis]. University of Texas Southwestern Medical Center; 2015. Available from: http://hdl.handle.net/2152.5/7068

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Queens University

12. Chen, Jiamin. MicroRNA-193B Functions as a Tumor Suppressor in Malignant Melanoma .

Degree: Pathology and Molecular Medicine, 2012, Queens University

URL: http://hdl.handle.net/1974/7224

► Cutaneous melanoma is an increasingly common skin cancer characterized by aggressive metastatic growth and poor prognosis. The mechanisms behind melanoma progression are not fully understood,… (more)

▼ Cutaneous melanoma is an increasingly common skin cancer characterized by aggressive metastatic growth and poor prognosis. The mechanisms behind melanoma progression are not fully understood, but emerging evidence suggests that a group of newly discovered small regulatory RNAs, named microRNAs (miRNAs), plays an important role. miRNAs are ~ 22 nucleotide single strand non-coding RNAs that post-transcriptionally regulate gene expression by binding to target messenger RNAs (mRNAs), leading to mRNA degradation and translation inhibition. Abnormal expression of miRNAs has been observed in human malignancies and is associated with tumorigenesis. The main goals of this thesis are to investigate miRNA dysregulation in melanoma and to identify potential miRNAs involved in melanoma pathogenesis. Initially, the expression of 470 miRNAs was profiled in 8 metastatic melanoma and 8 benign nevus tissue samples. We discovered unique miRNA expression profiles and identified differentially expressed miRNAs in melanomas as compared to nevi. miR-193b was one of the most significantly downregulated miRNAs in melanoma, and its function and regulatory targets were unknown. Subsequently, in vitro functional studies revealed that ectopic expression of miR-193b in melanoma cells drastically repressed cell proliferation and migration. Although it does not directly induce apoptosis in melanoma cells, miR-193b does sensitize these cells to ABT-737-mediated cell death. In concert with functional studies, gene expression analysis and in silico target prediction were performed to globally screen for mRNA targets of miR-193b. We identified eighteen genes as candidates in that they were downregulated by miR-193b and contained predicted miR-193b binding sites. Based on their known biological functions, three genes were particularly interesting: cyclin D1 (CCND1), myeloid cell leukemia sequence 1 (Mcl-1), and stathmin 1 (STMN1). CCND1 and Mcl-1 are two well-known melanoma oncogenes, and we validated their role in cell proliferation and apoptosis respectively. Furthermore, using similar approach, we were the first to identify STMN1 as a novel melanoma oncogene. We demonstrated that CCND1, Mcl-1, and STMN1 were directly regulated by miR-193b. During melanoma progression, reduced expression of miR-193b may promote cell proliferation, migration and survival. Taken together, this thesis describes the dysregulation of miRNAs in melanoma and demonstrates that miR-193b functions as a tumor suppressor.

Subjects/Keywords: Melanoma ; miR-193b ; Tumor Suppressor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chen, J. (2012). MicroRNA-193B Functions as a Tumor Suppressor in Malignant Melanoma . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/7224

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chen, Jiamin. “MicroRNA-193B Functions as a Tumor Suppressor in Malignant Melanoma .” 2012. Thesis, Queens University. Accessed March 08, 2021. http://hdl.handle.net/1974/7224.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chen, Jiamin. “MicroRNA-193B Functions as a Tumor Suppressor in Malignant Melanoma .” 2012. Web. 08 Mar 2021.

Vancouver:

Chen J. MicroRNA-193B Functions as a Tumor Suppressor in Malignant Melanoma . [Internet] [Thesis]. Queens University; 2012. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/1974/7224.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chen J. MicroRNA-193B Functions as a Tumor Suppressor in Malignant Melanoma . [Thesis]. Queens University; 2012. Available from: http://hdl.handle.net/1974/7224

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Louisville

13. Barnoud, Thibaut François. Regulation of the retinoblastoma tumor suppressor by the novel Ras effector NORE1A.

Degree: PhD, 2015, University of Louisville

URL: 10.18297/etd/2320 ; https://ir.library.louisville.edu/etd/2320

► Ras is the most frequently mutated oncogene in human cancers. It acts as a critical branch point in signal transduction, regulating numerous downstream effectors… (more)

Subjects/Keywords: Ras; NORE1A; retinoblastoma protein; phosphoprotein phosphatase 1; senescence; tumor suppressor gene; Cancer Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Barnoud, T. F. (2015). Regulation of the retinoblastoma tumor suppressor by the novel Ras effector NORE1A. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/2320 ; https://ir.library.louisville.edu/etd/2320

Chicago Manual of Style (16^th Edition):

Barnoud, Thibaut François. “Regulation of the retinoblastoma tumor suppressor by the novel Ras effector NORE1A.” 2015. Doctoral Dissertation, University of Louisville. Accessed March 08, 2021. 10.18297/etd/2320 ; https://ir.library.louisville.edu/etd/2320.

MLA Handbook (7^th Edition):

Barnoud, Thibaut François. “Regulation of the retinoblastoma tumor suppressor by the novel Ras effector NORE1A.” 2015. Web. 08 Mar 2021.

Vancouver:

Barnoud TF. Regulation of the retinoblastoma tumor suppressor by the novel Ras effector NORE1A. [Internet] [Doctoral dissertation]. University of Louisville; 2015. [cited 2021 Mar 08]. Available from: 10.18297/etd/2320 ; https://ir.library.louisville.edu/etd/2320.

Council of Science Editors:

Barnoud TF. Regulation of the retinoblastoma tumor suppressor by the novel Ras effector NORE1A. [Doctoral Dissertation]. University of Louisville; 2015. Available from: 10.18297/etd/2320 ; https://ir.library.louisville.edu/etd/2320

University of Texas Southwestern Medical Center

14. Kurtz, Paula S. In Vivo Genome-Wide Analyses of the Drosophila p53 Transcriptional Network.

Degree: 2017, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/7197

► p53 is the most commonly mutated gene in human cancers. Despite decades of p53 studies we do not fully understand how p53 suppresses tumors. Similar… (more)

▼ p53 is the most commonly mutated gene in human cancers. Despite decades of p53 studies we do not fully understand how p53 suppresses tumors. Similar to human p53, the Drosophila counterpart is a transcription factor that can respond to genotoxic stress and promote adaptive responses at the cellular level. Our lab has leveraged the powerful genetics of Drosophila to study p53 functions in vivo. In the context of the developing fly, p53 robustly activates important apoptotic genes in response to DNA damage to promote cell death. In the embryo model, we discovered an important p53 enhancer that forms chromatin contacts through long genomic distances and enables p53 to activate various genes. How p53 programs are adapted in different cellular contexts is poorly understood. In my dissertation work I examined two layers of p53 regulation, long-range enhancer looping and p53 DNA occupancy. To further examine enhancer looping, I exploited the established embryo model and the well characterized p53 reaper enhancer. At the single cell resolution, I demonstrated that the p53 enhancer can contact multiple targets simultaneously; however these multigenic complexes appear in low frequency. I also have preliminary genome-wide data suggesting in embryos this p53 enhancer contacts additional p53 targets. In addition, through genome-scale analyses I dissected novel p53 programs in a postmitotic model (the Drosophila head). Interestingly, postmitotic p53 programs are distinct from networks described in developing cells. I found that the canonical p53 apoptotic program is unresponsive in Drosophila heads, establishing this system as an ideal in vivo model to study alternate functions of p53. To determine how p53 differential programs are specified, I tested two distinct mechanisms for tissue specific target activation, p53 enhancer looping and DNA binding. Interestingly, I observed no change in enhancer looping to cell death targets in heads. However, I did detect loss of p53 enhancer binding. Lastly, I integrated genome-wide analyses of p53 DNA occupancy and transcriptional control in embryos and heads. Interestingly, I found that at the genome-scale p53 binding landscapes poorly correlate with nearby transcriptional effects, indicating that p53 enhancers could be generally acting through long distances. Advisors/Committee Members: Fontoura, Beatriz, Abrams, John M., Kraus, W. Lee, Krämer, Helmut.

Subjects/Keywords: Drosophila Proteins; Gene Expression Regulation; Genome-Wide Association Study; Tumor Suppressor Protein p53

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kurtz, P. S. (2017). In Vivo Genome-Wide Analyses of the Drosophila p53 Transcriptional Network. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/7197

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kurtz, Paula S. “In Vivo Genome-Wide Analyses of the Drosophila p53 Transcriptional Network.” 2017. Thesis, University of Texas Southwestern Medical Center. Accessed March 08, 2021. http://hdl.handle.net/2152.5/7197.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kurtz, Paula S. “In Vivo Genome-Wide Analyses of the Drosophila p53 Transcriptional Network.” 2017. Web. 08 Mar 2021.

Vancouver:

Kurtz PS. In Vivo Genome-Wide Analyses of the Drosophila p53 Transcriptional Network. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2017. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/2152.5/7197.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kurtz PS. In Vivo Genome-Wide Analyses of the Drosophila p53 Transcriptional Network. [Thesis]. University of Texas Southwestern Medical Center; 2017. Available from: http://hdl.handle.net/2152.5/7197

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

15. fragou, aikaterini. Μεθυλίωση της κυτοσίνης στην κωδική περιοχή και θέσεις ματίσματος του p53: συσχέτιση με μεταβολές του ματίσματος κατά την καρκινογένεση.

Degree: 2015, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

URL: http://hdl.handle.net/10442/hedi/36439

► The dynamic process of DNA methylation and its catalytic involvement in the development, differentiation and pathological situations such as carcinogenicity has now been established. In… (more)

▼ The dynamic process of DNA methylation and its catalytic involvement in the development, differentiation and pathological situations such as carcinogenicity has now been established. In contrast to promoters’ methylation, the role of methylation in the coding region of the genes, which is also a dynamic process, remains unclear. Most studies on the effect of intragenic methylation are mainly located in CpG islands. However, the existence of methylation in non-CpG sequences that are often targets of increased genetic instability has attracted the increasing interest during the past few years.Recently, evidence suggested that a key role in the selection of the areas to be expressed on a gene, therefore being spliced, plays the intragenic methylation of the cell. One possible cause for the disorder of splicing could be the disruption in the methylation pattern. P53 is the most important tumour suppressor gene, and its integrity and regulation have a catalytic effect on carcinogenesis. The discovery of the multiplicity of p53 isoforms has greatly contributed to the understanding of the mechanism of action of p53 and could be used in both diagnostically and therapeutically applications. For these reasons, the investigation of alternative splicing in p53 is particularly crucial. This study aims to determine the intragenic pattern of p53 methylation and its correlation with the alternative splicing as well as with any expression of various RNA isoforms in non-small cell lung cancer. For this purpose, we analyzed the methylation pattern at CpG sites (exon 10) and at positions outside CpG sequences (exon 5) and the expression of 3-11 exons of p53 in non-small cell lung cancer. Also, the presence of the complete protein p53, of isoforms Δ133p53, and of p53β and p53γ that derive from alternative splicing in exon 9, was investigated by immunoblotting. Finally, the expression of the two major known genes that act as modulators in the path of p53 in regulating the process of apoptosis and cell cycle, MDM2 and p21, respectively was recorded.The study of the distribution of the methylation and expression pattern of p53 gene in non-small cell lung carcinoma enabled us to collect information on the importance of essential mechanisms of intragenic methylation and alternative splicing, to identify the presence of non-CpG methylation near the activation site of the isoform expressed primarily in the tissue cancer (Δ133p53) and correlate its presence with the existence of informal RNA transcripts. On the contrary, the sites that were examined at the 3΄ end of the gene (exons 9 and 10) showed no variation in the expression between the cancerous and non-cancerous tissue and any differentiation in the methylation pattern. Any disturbance in p53 expression and the production of incomplete transcripts as a result of alternative splicing or internal promoter activation and possible correlation with the methylation stressed the importance of the p53 isoforms function and therefore their relationship with apoptosis and ability to enhance the…

Subjects/Keywords: Μεθυλίωση DNA; Εναλλακτικό μάτισμα; p53 Ογκογονίδιο; Methylation; Alternative splicing; p53 tumor suppressor gene

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

fragou, a. (2015). Μεθυλίωση της κυτοσίνης στην κωδική περιοχή και θέσεις ματίσματος του p53: συσχέτιση με μεταβολές του ματίσματος κατά την καρκινογένεση. (Thesis). Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Retrieved from http://hdl.handle.net/10442/hedi/36439

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

fragou, aikaterini. “Μεθυλίωση της κυτοσίνης στην κωδική περιοχή και θέσεις ματίσματος του p53: συσχέτιση με μεταβολές του ματίσματος κατά την καρκινογένεση.” 2015. Thesis, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Accessed March 08, 2021. http://hdl.handle.net/10442/hedi/36439.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

fragou, aikaterini. “Μεθυλίωση της κυτοσίνης στην κωδική περιοχή και θέσεις ματίσματος του p53: συσχέτιση με μεταβολές του ματίσματος κατά την καρκινογένεση.” 2015. Web. 08 Mar 2021.

Vancouver:

fragou a. Μεθυλίωση της κυτοσίνης στην κωδική περιοχή και θέσεις ματίσματος του p53: συσχέτιση με μεταβολές του ματίσματος κατά την καρκινογένεση. [Internet] [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2015. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/10442/hedi/36439.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

fragou a. Μεθυλίωση της κυτοσίνης στην κωδική περιοχή και θέσεις ματίσματος του p53: συσχέτιση με μεταβολές του ματίσματος κατά την καρκινογένεση. [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2015. Available from: http://hdl.handle.net/10442/hedi/36439

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Michigan State University

16. Wei, Yiliang. Transcriptional regulation in Drosophila – from genome to gene.

Degree: 2016, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:4288

►

Thesis Ph. D. Michigan State University. Biochemistry and Molecular Biology 2016

Transcriptional regulation plays a major role in gene expression, and is critical for development… (more)

Subjects/Keywords: Gene regulatory networks; Drosophila melanogaster – Molecular genetics; Tumor suppressor proteins – Genetic aspects; Molecular biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wei, Y. (2016). Transcriptional regulation in Drosophila – from genome to gene. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:4288

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wei, Yiliang. “Transcriptional regulation in Drosophila – from genome to gene.” 2016. Thesis, Michigan State University. Accessed March 08, 2021. http://etd.lib.msu.edu/islandora/object/etd:4288.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wei, Yiliang. “Transcriptional regulation in Drosophila – from genome to gene.” 2016. Web. 08 Mar 2021.

Vancouver:

Wei Y. Transcriptional regulation in Drosophila – from genome to gene. [Internet] [Thesis]. Michigan State University; 2016. [cited 2021 Mar 08]. Available from: http://etd.lib.msu.edu/islandora/object/etd:4288.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wei Y. Transcriptional regulation in Drosophila – from genome to gene. [Thesis]. Michigan State University; 2016. Available from: http://etd.lib.msu.edu/islandora/object/etd:4288

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

17. Costa, Alexandra Fontes da. Análise imunoistoquímica das proteínas maspin, p63 e bcl2 em tumor odontogênico queratocístico, cisto dentígero e ameloblastoma.

Degree: Mestrado, Patologia Bucal, 2007, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/23/23141/tde-13082007-162555/ ;

►

Os cistos e tumores odontogênicos sempre tiveram grande importância dentro da Odontologia, seja pela grande prevalência clínica seja pelo grande acometimento do indivíduo afetado pela… (more)

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Os cistos e tumores odontogênicos sempre tiveram grande importância dentro da Odontologia, seja pela grande prevalência clínica seja pelo grande acometimento do indivíduo afetado pela lesão. A nova classificação da Organização Mundial de Saúde trouxe a mudança de categoria do queratocisto, que recebe agora a nômina de tumor odontogênico queratocístico, e que figura não mais na categoria de cisto odontogênico de desenvolvimento, mas sim de tumor odontogênico. Certa precipitação nessa mudança levou alguns autores a sugerirem a necessidade de estudos que esclareçam as características clínicas e histopatológicas dessa lesão para que se tenha uma classificação realmente precisa. O grande paradigma dessa lesão é: ao mesmo tempo em que apresenta características histológicas de um cisto, possui um comportamento clínico agressivo mais comumente observado nos tumores. O que realmente difere esta lesão das outras lesões que se inseriam no mesmo grupo é o padrão de crescimento diferenciado do tumor odontogênico queratocístico em relação às outras lesões císticas. Sendo assim, poderia se suspeitar que essa lesão possua um potencial proliferativo maior do que as outras que anteriormente pertenciam ao mesmo grupo, denotando uma regulação diferenciada do mecanismo proliferação-apoptose. Este estudo teve como objetivo comparar o tumor odontogênico queratocístico com uma lesão cística - o cisto dentígero - e com uma lesão tumoral - o ameloblastoma ? por meio de marcadores imunoistoquímicos para supressão tumoral e anti-apoptose. Os resultados demostraram que a maior diferença entre essas lesões está principalmente na atividade apoptótica, já que somente o resultado de bcl2 foi estatisticamente significante entre essas lesões.

Odontogenic cysts and tumors have always had a great importance in Dentistry, for its high clinical prevail and for its noticeable invasive behavior. The new classification released by WHO rearranged keratocyst, that is named now odontogenic keratocystic tumor, classifying it no longer as a development cyst, but now as odontogenic tumor. Certain haste in this change brought some authors to suggest the necessity of more studies to clarify the feautures of such lesions to determine a more accurate classification. The greatest paradigm of this lesion is that it shows cyst-like histological characteristics and simultaneuosly it has an aggressive clinical behavior, which is more commonly observed in tumors. The main difference between this lesion and the others cystic lesions is the growth pattern, which suggests that the odontogenic keratocystic tumor has higher proliferative potential than other cystic lesions. The aim of this research was to compare odontogenic keratocystic tumor with a cystic lesion ? dentigerous cyst ? and with a tumoral lesion ? ameloblastoma ? using tumor suppressor and anti-apoptosis immunohistochemical expression. Results show that the more important difference among the analysed lesions is apoptosis activity, since only bcl2 staining was significantly different among them.

Advisors/Committee Members: Martins, Marília Trierveiler.

Subjects/Keywords: Apoptose; apoptosis; Cisto; Cyst; Odontogenic tumor; Supressão de tumor; Tumor odontogênico; Tumor suppressor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Costa, A. F. d. (2007). Análise imunoistoquímica das proteínas maspin, p63 e bcl2 em tumor odontogênico queratocístico, cisto dentígero e ameloblastoma. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/23/23141/tde-13082007-162555/ ;

Chicago Manual of Style (16^th Edition):

Costa, Alexandra Fontes da. “Análise imunoistoquímica das proteínas maspin, p63 e bcl2 em tumor odontogênico queratocístico, cisto dentígero e ameloblastoma.” 2007. Masters Thesis, University of São Paulo. Accessed March 08, 2021. http://www.teses.usp.br/teses/disponiveis/23/23141/tde-13082007-162555/ ;.

MLA Handbook (7^th Edition):

Costa, Alexandra Fontes da. “Análise imunoistoquímica das proteínas maspin, p63 e bcl2 em tumor odontogênico queratocístico, cisto dentígero e ameloblastoma.” 2007. Web. 08 Mar 2021.

Vancouver:

Costa AFd. Análise imunoistoquímica das proteínas maspin, p63 e bcl2 em tumor odontogênico queratocístico, cisto dentígero e ameloblastoma. [Internet] [Masters thesis]. University of São Paulo; 2007. [cited 2021 Mar 08]. Available from: http://www.teses.usp.br/teses/disponiveis/23/23141/tde-13082007-162555/ ;.

Council of Science Editors:

Costa AFd. Análise imunoistoquímica das proteínas maspin, p63 e bcl2 em tumor odontogênico queratocístico, cisto dentígero e ameloblastoma. [Masters Thesis]. University of São Paulo; 2007. Available from: http://www.teses.usp.br/teses/disponiveis/23/23141/tde-13082007-162555/ ;

18. Longuini, Viviane Cristina. Identificação de moduladores genéticos em uma grande família com neoplasia endócrina múltipla (NEM1).

Degree: Mestrado, Endocrinologia, 2011, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5135/tde-05052011-145430/ ;

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A Neoplasia endócrina múltipla tipo 1 (NEM1; OMIM 131100) é uma síndrome endócrina hereditária, que envolve tumores nas glândulas paratireóides, pâncreas endócrino/duodeno e hipófise. Mutações… (more)

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A Neoplasia endócrina múltipla tipo 1 (NEM1; OMIM 131100) é uma síndrome endócrina hereditária, que envolve tumores nas glândulas paratireóides, pâncreas endócrino/duodeno e hipófise. Mutações germinativas no gene supressor de tumor MEN1 são identificadas em aproximadamente 80% dos casos familiais. Os casos restantes podem apresentar grandes deleções no gene MEN1 (raras), não identificáveis ao seqüenciamento direto, ou mutações em outros genes, ainda pouco conhecidos. Recentemente, mutações germinativas em genes que codificam quinases dependentes de ciclinas, como o gene supressor de tumor p27Kip1, foram identificadas em cerca de 1-2% dos pacientes NEM1 sem mutação no gene MEN1. Esses pacientes apresentam uma clínica similar à NEM1, sendo chamada de NEM-like ou NEM4. Estudos in vitro mostraram que a proteína codificada pelo gene MEN1, MENIN, controla a expressão gênica de p27Kip1, indicando que ambos os genes fazem parte da mesma via celular supressora de tumor. Devido à correlação genótipo-fenótipo ser muito fraca nessa síndrome e à grande variabilidade fenotípica encontrada em pacientes com NEM1 (mesmo entre indivíduos/familiares que possuem mesma mutação no gene MEN1), no presente estudo investigamos a hipótese do envolvimento do gene p27Kip1, e de outro gene supressor de tumor recentemente associado com um fenótipo tumores hipofisários famílias, o gene AIP, como possíveis moduladores de fenótipo entre os pacientes com NEM1 de uma extensa família brasileira com a mutação germinativa MEN1 c.308delC e ampla variabilidade fenotípica. Dentre uma série de variáveis clínicas investigadas, observamos um possível papel modulador de fenótipo do gene p27Kip1 nesta família com NEM1. Foi encontrada associação significante entre o genótipo do polimorfismo p.V109G do gene p27Kip1, localizado em um domínio de ligação com a proteína p38 (que é um regulador negativo de p27 por levar à degradação dessa proteína), com os seguintes aspectos clínicos: maior agressividade do tumor hipofisário (macro vs. microadenomas), precocidade no desenvolvimento do tumor pancreático, e presença de carcinóides e metástases nos pacientes analisados (p< 0,05). Não foi observada nenhuma associação do gene AIP e o fenótipo dos pacientes com NEM1. O presente estudo investigou, pela primeira vez, o status germinativo do gene p27Kip1 em pacientes com mutação MEN1 e identificou uma associação significante em relação à susceptibilidade e agressividade dos tumores na coorte estudada

Multiple endocrine neoplasia type 1 (MEN1) is an inherited tumoral syndrome that involves tumors in the parathyroids, anterior pituitary and in the pancreatic islet(s) cells. Germline mutations in the tumor suppressor gene MEN1 are detectable through direct sequencing in the majority (80%) of the patients with familial MEN1. The remaining patients may present large MEN1 gene deletions, not detectable through direct sequencing, or mutations in other genes, so far largely unknown. Recently, rare mutations in genes that encode cyclin-dependent kinases, as p27Kip1, have been…

Advisors/Committee Members: Toledo, Rodrigo de Almeida.

Subjects/Keywords: Gene supressor de tumor p27Kip1; Genes neoplásicos; Genes supressores de tumor; Moduladores de fenótipo; Multiple endocrine neoplasia type 1; Neoplasia endócrina múltipla tipo 1; Neoplasic genes; Phenotypic modifiers; Tumor suppressor gene p27Kip1; Tumor suppressor genes

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Longuini, V. C. (2011). Identificação de moduladores genéticos em uma grande família com neoplasia endócrina múltipla (NEM1). (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5135/tde-05052011-145430/ ;

Chicago Manual of Style (16^th Edition):

Longuini, Viviane Cristina. “Identificação de moduladores genéticos em uma grande família com neoplasia endócrina múltipla (NEM1).” 2011. Masters Thesis, University of São Paulo. Accessed March 08, 2021. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-05052011-145430/ ;.

MLA Handbook (7^th Edition):

Longuini, Viviane Cristina. “Identificação de moduladores genéticos em uma grande família com neoplasia endócrina múltipla (NEM1).” 2011. Web. 08 Mar 2021.

Vancouver:

Longuini VC. Identificação de moduladores genéticos em uma grande família com neoplasia endócrina múltipla (NEM1). [Internet] [Masters thesis]. University of São Paulo; 2011. [cited 2021 Mar 08]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5135/tde-05052011-145430/ ;.

Council of Science Editors:

Longuini VC. Identificação de moduladores genéticos em uma grande família com neoplasia endócrina múltipla (NEM1). [Masters Thesis]. University of São Paulo; 2011. Available from: http://www.teses.usp.br/teses/disponiveis/5/5135/tde-05052011-145430/ ;

University of Gothenburg / Göteborgs Universitet

19. Fransson, Susanne. From 1p3 to PI3K - Studies of neuroblastoma.

Degree: 2011, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/23820

► Neuroblastoma (NB) is a tumor of the sympathetic nervous system and is the most common extra-cranial tumor of childhood, accounting for 7% of all pediatric… (more)

▼ Neuroblastoma (NB) is a tumor of the sympathetic nervous system and is the most common extra-cranial tumor of childhood, accounting for 7% of all pediatric malignancies. Despite recent advances in therapeutics, outcome is still fatal for patients with aggressive NB and side-effects of treatment are severe. These are important reasons to gain further knowledge of the biology behind NB. Aims: The objective of this thesis was to explore genes and gene products that might contribute to initiation and progression of NB and possibly also other malignancies. Main focus has been on the chromosomal region 1p36.2-3 and participants of the PI3K/Akt signaling pathway. Results: Real-time expression analysis of 30 genes at 1p36.2-3 showed that TNFRSF9 and PIK3CD were down regulated in 1p-deleted compared to non-deleted NB tumors. Studies of the same region showed four genes (ERRFI, CASZ1, RBP7 and PIK3CD) possibly regulated by epigenetically means. Bisulphite sequencing of these four genes in NB cell lines and primary tumors showed that methylation probably is not involved but that histone deacetylation could be implicated in their regulation. Some rare sequence variants were also identified in ERRFI and PIK3CD. PIK3CD encodes a catalytic subunit of the phosphatidylinositol 3-kinase (PI3K) that is involved in activation of Akt. Analysis of mRNA levels in a set of 88 genes associated to PI3K/Akt signaling showed that PDGFRA, PIK3R1, PIK3CD, PRKCBI, PRKCZ and EIF4EBP1 were differentially expressed comparing stage 1-2 to stage 4 NB. At the protein level a stage-dependent expression of the different catalytic isoforms were detected, where levels of p110α were higher in stage 4 tumors compared to stage 1-2, while the opposite was seen for p110δ. Stage 4 NB also had higher levels of phosphorylated Akt (T308 and S473) compared to low stage NB. Furthermore, levels of phosphorylated Akt T308 showed inverse correlation to protein levels of the tumor suppressor Pten. We have also identified a novel splice variant p37δ, encoded by PIK3CD. Usage of an alternative donor site leads to truncation in the RAS-binding domain and loss of the catalytic domain. Despite the truncation, p37δ interact with RAS and there is a strong correlation between protein levels of p37δ and RAS in primary cells. Expression of p37δ is increased in human cancers of the ovaries and colon and ubiquitous expression of the human p37δ in Drosophila increased the body size of the fly. Furthermore, over-expression of p37δ in HEK-293 and mouse embryonic fibroblasts increased proliferation and invasive properties compared to controls, indicating a role in tumorgenicity. Conclusion: Analysis of expression levels of genes and proteins could be used for pinpointing important genes and pathways. This thesis has added more knowledge about the genes at 1p36.2-3, a region commonly deleted in NB, as well as the PI3K/Akt signaling in NB. We have also described a new splice variant of p110δ that is expressed in human cancer and increases proliferation in vitro and in vivo.

Subjects/Keywords: cancer; neuroblastoma; PI3K; PIK3CD; 1p36; alternative splicing; tumor; neural crest; mucosa; premalignant; tumor suppressor gene; oncogene; gene expression; epigenetics; splicing; signaling; akt; western blot; TaqMan; PIK3R1; p110H; p37H; p85; RAS

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fransson, S. (2011). From 1p3 to PI3K - Studies of neuroblastoma. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/23820

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Fransson, Susanne. “From 1p3 to PI3K - Studies of neuroblastoma.” 2011. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed March 08, 2021. http://hdl.handle.net/2077/23820.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Fransson, Susanne. “From 1p3 to PI3K - Studies of neuroblastoma.” 2011. Web. 08 Mar 2021.

Vancouver:

Fransson S. From 1p3 to PI3K - Studies of neuroblastoma. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2011. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/2077/23820.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Fransson S. From 1p3 to PI3K - Studies of neuroblastoma. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2011. Available from: http://hdl.handle.net/2077/23820

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universiteit Utrecht

20. Vreede, G.A.M. de. Endocytic control of tumor suppression in Drosophila melanogaster.

Degree: 2011, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/218766

► Mutations in Drosophila melanogaster tumor suppressor genes are able to cause neoplastic overgrowth in various epithelial tissues. Screens in Drosophila showed that a multitude of… (more)

Subjects/Keywords: endocytosis; neoplastic; tumor; suppressor; genes; drosophila; tumorigenesis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Vreede, G. A. M. d. (2011). Endocytic control of tumor suppression in Drosophila melanogaster. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/218766

Chicago Manual of Style (16^th Edition):

Vreede, G A M de. “Endocytic control of tumor suppression in Drosophila melanogaster.” 2011. Masters Thesis, Universiteit Utrecht. Accessed March 08, 2021. http://dspace.library.uu.nl:8080/handle/1874/218766.

MLA Handbook (7^th Edition):

Vreede, G A M de. “Endocytic control of tumor suppression in Drosophila melanogaster.” 2011. Web. 08 Mar 2021.

Vancouver:

Vreede GAMd. Endocytic control of tumor suppression in Drosophila melanogaster. [Internet] [Masters thesis]. Universiteit Utrecht; 2011. [cited 2021 Mar 08]. Available from: http://dspace.library.uu.nl:8080/handle/1874/218766.

Council of Science Editors:

Vreede GAMd. Endocytic control of tumor suppression in Drosophila melanogaster. [Masters Thesis]. Universiteit Utrecht; 2011. Available from: http://dspace.library.uu.nl:8080/handle/1874/218766

University of Rochester

21. Gaur, Kriti; Li, Willis X. A Role for Tumor Suppressor Gene Birt-Hogg-Dubé in Regulating Ribosomal RNA (rRNA) Synthesis.

Degree: PhD, 2011, University of Rochester

URL: http://hdl.handle.net/1802/15808

► Birt-Hogg-Dubé syndrome (BHD) is a hereditary human cancer disorder characterized by renal carcinoma of diverse histology, benign skin lesions and pulmonary cysts, and is caused… (more)

Subjects/Keywords: Kidney Cancer; rRNA Synthesis; Tumor Suppressor

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APA (6^th Edition):

Gaur, Kriti; Li, W. X. (2011). A Role for Tumor Suppressor Gene Birt-Hogg-Dubé in Regulating Ribosomal RNA (rRNA) Synthesis. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/15808

Chicago Manual of Style (16^th Edition):

Gaur, Kriti; Li, Willis X. “A Role for Tumor Suppressor Gene Birt-Hogg-Dubé in Regulating Ribosomal RNA (rRNA) Synthesis.” 2011. Doctoral Dissertation, University of Rochester. Accessed March 08, 2021. http://hdl.handle.net/1802/15808.

MLA Handbook (7^th Edition):

Gaur, Kriti; Li, Willis X. “A Role for Tumor Suppressor Gene Birt-Hogg-Dubé in Regulating Ribosomal RNA (rRNA) Synthesis.” 2011. Web. 08 Mar 2021.

Vancouver:

Gaur, Kriti; Li WX. A Role for Tumor Suppressor Gene Birt-Hogg-Dubé in Regulating Ribosomal RNA (rRNA) Synthesis. [Internet] [Doctoral dissertation]. University of Rochester; 2011. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/1802/15808.

Council of Science Editors:

Gaur, Kriti; Li WX. A Role for Tumor Suppressor Gene Birt-Hogg-Dubé in Regulating Ribosomal RNA (rRNA) Synthesis. [Doctoral Dissertation]. University of Rochester; 2011. Available from: http://hdl.handle.net/1802/15808

University of Alberta

22. Law, Jennifer. MOAP-1: A Candidate Tumor Suppressor Protein.

Degree: MS, Department of Biochemistry, 2011, University of Alberta

URL: https://era.library.ualberta.ca/files/dj52w5366

► Modulator of apoptosis 1 (MOAP-1) is a BH3-like protein that plays a key role in death receptor-dependent apoptosis and cooperates with the tumor suppressor protein… (more)

Subjects/Keywords: MOAP-1; Tumor Suppressor; Apoptosis; RACK1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Law, J. (2011). MOAP-1: A Candidate Tumor Suppressor Protein. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/dj52w5366

Chicago Manual of Style (16^th Edition):

Law, Jennifer. “MOAP-1: A Candidate Tumor Suppressor Protein.” 2011. Masters Thesis, University of Alberta. Accessed March 08, 2021. https://era.library.ualberta.ca/files/dj52w5366.

MLA Handbook (7^th Edition):

Law, Jennifer. “MOAP-1: A Candidate Tumor Suppressor Protein.” 2011. Web. 08 Mar 2021.

Vancouver:

Law J. MOAP-1: A Candidate Tumor Suppressor Protein. [Internet] [Masters thesis]. University of Alberta; 2011. [cited 2021 Mar 08]. Available from: https://era.library.ualberta.ca/files/dj52w5366.

Council of Science Editors:

Law J. MOAP-1: A Candidate Tumor Suppressor Protein. [Masters Thesis]. University of Alberta; 2011. Available from: https://era.library.ualberta.ca/files/dj52w5366

Kyoto University / 京都大学

23. Sanada, Masashi. Gain-of-function of mutated C-CBL tumor suppressor in myeloid neoplasms : 骨髄系腫瘍における腫瘍抑制遺伝子C-CBLの機能獲得型変異.

Degree: 博士(医学), 2014, Kyoto University / 京都大学

URL: http://hdl.handle.net/2433/192124 ; http://dx.doi.org/10.14989/doctor.r12855

This paper was published in Nature 2009 Aug 13;460(7257):904-8. doi: 10.1038/nature08240. http://www.nature.com/nature/journal/v460/n7257/full/nature08240.html

新制・論文博士

乙第12855号

論医博第2085号

Subjects/Keywords: myelodysplasia; LOH; tumor suppressor; ubiquitination; cytokine sensitivity

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sanada, M. (2014). Gain-of-function of mutated C-CBL tumor suppressor in myeloid neoplasms : 骨髄系腫瘍における腫瘍抑制遺伝子C-CBLの機能獲得型変異. (Thesis). Kyoto University / 京都大学. Retrieved from http://hdl.handle.net/2433/192124 ; http://dx.doi.org/10.14989/doctor.r12855

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sanada, Masashi. “Gain-of-function of mutated C-CBL tumor suppressor in myeloid neoplasms : 骨髄系腫瘍における腫瘍抑制遺伝子C-CBLの機能獲得型変異.” 2014. Thesis, Kyoto University / 京都大学. Accessed March 08, 2021. http://hdl.handle.net/2433/192124 ; http://dx.doi.org/10.14989/doctor.r12855.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sanada, Masashi. “Gain-of-function of mutated C-CBL tumor suppressor in myeloid neoplasms : 骨髄系腫瘍における腫瘍抑制遺伝子C-CBLの機能獲得型変異.” 2014. Web. 08 Mar 2021.

Vancouver:

Sanada M. Gain-of-function of mutated C-CBL tumor suppressor in myeloid neoplasms : 骨髄系腫瘍における腫瘍抑制遺伝子C-CBLの機能獲得型変異. [Internet] [Thesis]. Kyoto University / 京都大学; 2014. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/2433/192124 ; http://dx.doi.org/10.14989/doctor.r12855.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sanada M. Gain-of-function of mutated C-CBL tumor suppressor in myeloid neoplasms : 骨髄系腫瘍における腫瘍抑制遺伝子C-CBLの機能獲得型変異. [Thesis]. Kyoto University / 京都大学; 2014. Available from: http://hdl.handle.net/2433/192124 ; http://dx.doi.org/10.14989/doctor.r12855

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

24. Mikse, Oliver. CHARACTERIZATION OF FOXO3A AS A SUPPRESSOR OF LUNG ADENOCARCINOMA .

Degree: 2011, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/11586

► Lung tumor development is believed to occur through a step-wise series of molecular changes that influence cell growth and survival. This process is facilitated by… (more)

▼ Lung tumor development is believed to occur through a step-wise series of molecular changes that influence cell growth and survival. This process is facilitated by tobacco smoke which contains numerous carcinogens known to induce gene mutation and chromosomal instability (CIN). However, we have a poor understanding of the genes involved in lung cancer development. The FOXO family of transcription factors has been shown to elicit cell cycle arrest, apoptosis, and resistance to various physiologic and pathologic stresses relevant to sporadic cancer, such as DNA damage and oxidative stress. Although implicated as tumor suppressors, FOXO genetic inactivation has not been observed in human cancer. In an investigation of the two major types of non-small cell lung cancer (NSCLC) we have identified the FOXO3a gene (FOXO3a) as a novel target of deletion in human lung adenocarcinoma (LAC). Bi-allelic or homozygous deletion (HD) of FOXO3a was detected in 8 out of 33 (24.2%) mostly early-stage LAC of smokers. Another 60.6% of these tumors had losses of FOXO3a not reaching the level of HD (hereafter referred to as sub-HD). In contrast, no HD of FOXO3a was observed in 19 lung squamous cell carcinoma (LSqCC), but sub-HDs were evident. Consistent with the deletion of FOXO3a were corresponding decreases in its mRNA and protein levels in LAC. FOXO3a’s ability to induce apoptosis or cell cycle arrest in response to carcinogens was also investigated in LAC cell lines. The carcinogen (+)-anti-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE) is strongly implicated as a cause of human lung cancer. Here we have demonstrated that FOXO3a is functionally activated and augments caspase-dependent apoptosis in cells exposed to this DNA-damaging carcinogen. Consistent with this result was the FOXO3a-dependent upregulation of pro-apoptotic effectors BIM, BNIP3 and FASL with treatment. These results implicate FOXO3a in the elimination of carcinogen-damaged cells, a role consistent with the suppression of LAC carcinogenesis, and one frequently lost through gene deletion in LAC development. Inefficient methods of treatment lie among the main causes for poor response rates among patients who undergo lung cancer therapy. Docetaxel and vinorelbine are common anti-mitotic drugs used in second line therapy of several cancer types, including lung adenocarcinoma. These drugs include taxanes and vinca alkaloids, which induce mitotic arrest by disrupting mitotic spindle function. Previous studies in breast cancer and colon cancer cells have shown that FOXO3a stimulates apoptosis, a pro-therapeutic effect, in cells exposed to taxanes. Consequently, we investigated the role of FOXO3a in the cellular response to anti-mitotic agents in LAC cells, as this function would be lost in LAC as a consequence of gene deletion. MTS assays revealed that FOXO3a transfection causes a significant decrease in the number of viable LAC cells (both A549 and H460 cell lines) upon treatment with two different anti-mitotics, docetaxel and vinorelbine. Unlike… Advisors/Committee Members: Chris Herzog, Dissertation Advisor/Co-Advisor, Chris Herzog, Committee Chair/Co-Chair, Tim Ritty, Committee Member, Vincent Chau, Committee Member, Leslie Joan Parent, Committee Member, Lisa M Shantz, Committee Member.

Subjects/Keywords: CDC14A; Lung Cancer; FOXO3A; Tumor Suppressor

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APA (6^th Edition):

Mikse, O. (2011). CHARACTERIZATION OF FOXO3A AS A SUPPRESSOR OF LUNG ADENOCARCINOMA . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/11586

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mikse, Oliver. “CHARACTERIZATION OF FOXO3A AS A SUPPRESSOR OF LUNG ADENOCARCINOMA .” 2011. Thesis, Penn State University. Accessed March 08, 2021. https://submit-etda.libraries.psu.edu/catalog/11586.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mikse, Oliver. “CHARACTERIZATION OF FOXO3A AS A SUPPRESSOR OF LUNG ADENOCARCINOMA .” 2011. Web. 08 Mar 2021.

Vancouver:

Mikse O. CHARACTERIZATION OF FOXO3A AS A SUPPRESSOR OF LUNG ADENOCARCINOMA . [Internet] [Thesis]. Penn State University; 2011. [cited 2021 Mar 08]. Available from: https://submit-etda.libraries.psu.edu/catalog/11586.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mikse O. CHARACTERIZATION OF FOXO3A AS A SUPPRESSOR OF LUNG ADENOCARCINOMA . [Thesis]. Penn State University; 2011. Available from: https://submit-etda.libraries.psu.edu/catalog/11586

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Wayne State University

25. Dean, Ivory. The Tumor-Suppressive Role Of Secreted Maspin Via The Exosomes.

Degree: PhD, Cancer Biology, 2014, Wayne State University

URL: https://digitalcommons.wayne.edu/oa_dissertations/1089

► This dissertation highlights several novel findings. Maspin has been consistently detected in the conditioned media of maspin-expressing cells of normal and tumor breast, prostate… (more)

Subjects/Keywords: Exosomes; Maspin; Microenvironment; Tumor Suppressor; Biology

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APA (6^th Edition):

Dean, I. (2014). The Tumor-Suppressive Role Of Secreted Maspin Via The Exosomes. (Doctoral Dissertation). Wayne State University. Retrieved from https://digitalcommons.wayne.edu/oa_dissertations/1089

Chicago Manual of Style (16^th Edition):

Dean, Ivory. “The Tumor-Suppressive Role Of Secreted Maspin Via The Exosomes.” 2014. Doctoral Dissertation, Wayne State University. Accessed March 08, 2021. https://digitalcommons.wayne.edu/oa_dissertations/1089.

MLA Handbook (7^th Edition):

Dean, Ivory. “The Tumor-Suppressive Role Of Secreted Maspin Via The Exosomes.” 2014. Web. 08 Mar 2021.

Vancouver:

Dean I. The Tumor-Suppressive Role Of Secreted Maspin Via The Exosomes. [Internet] [Doctoral dissertation]. Wayne State University; 2014. [cited 2021 Mar 08]. Available from: https://digitalcommons.wayne.edu/oa_dissertations/1089.

Council of Science Editors:

Dean I. The Tumor-Suppressive Role Of Secreted Maspin Via The Exosomes. [Doctoral Dissertation]. Wayne State University; 2014. Available from: https://digitalcommons.wayne.edu/oa_dissertations/1089

University of Texas Southwestern Medical Center

26. Wylie, Annika Dawn. P53 Genes Act to Restrain Mobile Elements.

Degree: 2015, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/4461

► Oncogenic stress provokes tumor suppression by p53 but the extent to which this regulatory axis is conserved remains unknown. Using a biosensor to visualize p53… (more)

▼ Oncogenic stress provokes tumor suppression by p53 but the extent to which this regulatory axis is conserved remains unknown. Using a biosensor to visualize p53 action, we find that Drosophila p53 is selectively active in gonadal stem cells after exposure to stressors that destabilize the genome. Similar p53 activity occurred in hyperplastic growths that were triggered either by the RasV12 oncoprotein or by failed differentiation programs. In a model of transient sterility, p53 was required for the recovery of fertility after stress, and entry into the cell cycle was delayed in p53- stem cells. Together, these observations establish that the stem cell compartment of the Drosophila germline is selectively licensed for stress-induced activation of the p53 regulatory network. Furthermore, the findings uncover ancestral links between p53 and aberrant proliferation that are independent of DNA breaks and predate evolution of the ARF/Mdm2 axis. While exploring the role of p53 in this context, we made a series of observations that justify a comprehensive examination of the relationship between p53 and transposon biology. Using Drosophila, zebrafish, and mouse models, we found that p53 functions to restrict the activity of retrotransposons. Furthermore, Drosophila p53 genetically interacted with components of the piRNA pathway and, in complementation studies, normal human p53 alleles restrained these mobile elements, but mutant p53 alleles from cancer patients could not. Consistent with these results, we also found patterns of unrestrained retrotransposons in p53-driven human cancers. Together, these observations indicate that ancestral functions of p53 operate through conserved mechanisms to suppress retrotransposons. Furthermore, since human p53 mutants are disabled for this activity, our findings raise the possibility that p53 mitigates oncogenic disease, in part, by restricting retrotransposon mobility. Advisors/Committee Members: Amatruda, James F., Abrams, John M., Hobbs, Helen H., Morrison, Sean J..

Subjects/Keywords: Genes, p53; Retroelements; Tumor Suppressor Protein p53

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APA (6^th Edition):

Wylie, A. D. (2015). P53 Genes Act to Restrain Mobile Elements. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/4461

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wylie, Annika Dawn. “P53 Genes Act to Restrain Mobile Elements.” 2015. Thesis, University of Texas Southwestern Medical Center. Accessed March 08, 2021. http://hdl.handle.net/2152.5/4461.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wylie, Annika Dawn. “P53 Genes Act to Restrain Mobile Elements.” 2015. Web. 08 Mar 2021.

Vancouver:

Wylie AD. P53 Genes Act to Restrain Mobile Elements. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2015. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/2152.5/4461.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wylie AD. P53 Genes Act to Restrain Mobile Elements. [Thesis]. University of Texas Southwestern Medical Center; 2015. Available from: http://hdl.handle.net/2152.5/4461

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Hong Kong University of Science and Technology

27. Zuo, Hao LIFS. Regulation of the tumor suppressor Fhit by activated Gα subunits.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-92340 ; https://doi.org/10.14711/thesis-b1254497 ; http://repository.ust.hk/ir/bitstream/1783.1-92340/1/th_redirect.html

► The FHIT tumor suppressor gene is arguably the most commonly altered gene in cancer since it is inactivated in about 60% of human tumors. Despite… (more)

▼ The FHIT tumor suppressor gene is arguably the most commonly altered gene in cancer since it is inactivated in about 60% of human tumors. Despite the fact that Fhit functions as a tumor suppressor, the pathway through which Fhit inhibits growth of cancer cells remains largely unknown. Phosphorylation by Src tyrosine kinases provides a linkage between Fhit and growth factor signaling. Since many G proteins can regulate cell proliferation through multiple signaling components including Src, I explored the relationship between Gα subunits and Fhit. Several members of the Gα_q subfamily (Gα₁₆, Gα₁₄, and Gα_q) have been found to co-immunoprecipitate with Fhit in their GTP-bound active state in HEK293 cells. The binding of activated Gα_q members to Fhit appeared to be direct. The use of Gα_16/z chimeras further enabled the mapping of the Fhit-interacting domain to the α2-β4 region of Gα₁₆. Meanwhile, Fhit was up-regulated specifically by activating Gα subunits of the G_q subfamily but not by those of the other G protein subfamilies. This up-regulation effect was mediated by a PKC/MEK pathway independent of Src-mediated Fhit Tyr¹¹⁴ phosphorylation. I further demonstrated that elevated Fhit expression was due to the specific regulation of Fhit protein synthesis in the ribosome by activated Gα_q, where the regulations of cap-dependent protein synthesis were apparently not required. Stimulation of G_q-coupled receptors in HEK293 and H1299 cells stably overexpressing Fhit led to reduced cell proliferation, as opposed to an enhanced cell proliferation typically seen with parental cells. Moreover, I showed that activated Gα_q could increase cell-cell adhesion through Fhit and this effect did not involve the regulations of the expressions of E-cadherin and MMP2/9, the localizations of adhesive proteins and the the binding of p63RhoGEF to activated Gα_q. These findings provide a possible handle to modulate the level of the Fhit tumor suppressor and tumor suppression by manipulating the activity of G_q-coupled receptors.

Subjects/Keywords: Antioncogenes ; Tumor suppressor proteins ; G proteins ; Receptors

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APA (6^th Edition):

Zuo, H. L. (2013). Regulation of the tumor suppressor Fhit by activated Gα subunits. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-92340 ; https://doi.org/10.14711/thesis-b1254497 ; http://repository.ust.hk/ir/bitstream/1783.1-92340/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zuo, Hao LIFS. “Regulation of the tumor suppressor Fhit by activated Gα subunits.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed March 08, 2021. http://repository.ust.hk/ir/Record/1783.1-92340 ; https://doi.org/10.14711/thesis-b1254497 ; http://repository.ust.hk/ir/bitstream/1783.1-92340/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zuo, Hao LIFS. “Regulation of the tumor suppressor Fhit by activated Gα subunits.” 2013. Web. 08 Mar 2021.

Vancouver:

Zuo HL. Regulation of the tumor suppressor Fhit by activated Gα subunits. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2021 Mar 08]. Available from: http://repository.ust.hk/ir/Record/1783.1-92340 ; https://doi.org/10.14711/thesis-b1254497 ; http://repository.ust.hk/ir/bitstream/1783.1-92340/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zuo HL. Regulation of the tumor suppressor Fhit by activated Gα subunits. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-92340 ; https://doi.org/10.14711/thesis-b1254497 ; http://repository.ust.hk/ir/bitstream/1783.1-92340/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

28. Bassi, Christian. Nuclear PTEN Controls DNA Repair and Sensitivity to Genotoxic Stress.

Degree: PhD, 2015, University of Toronto

URL: http://hdl.handle.net/1807/69214

► Loss of function of the phosphatase and tensin homolog (PTEN) tumor suppressor is frequently found in many human malignancies. PTEN antagonizes the Phosphatidylinositide 3-kinase (PI3K)… (more)

▼ Loss of function of the phosphatase and tensin homolog (PTEN) tumor suppressor is frequently found in many human malignancies. PTEN antagonizes the Phosphatidylinositide 3-kinase (PI3K) pathway by dephosphorylating the 3 position of phosphatidylinositol (3,4,5)-trisphosphate [PtdIns(3,4,5)P3] (PIP3). PIP3 serves as a second messenger whose levels in the plasma membrane are elevated following cell stimulation with growth factors, mediated by the activity of PI3Ks. Proteins containing pleckstrin homology (PH) domains physically interact with PIP3, bringing them into close proximity with other PH domain-containing proteins and facilitating further functional interactions that serve to propagate the membranous signal. Although the cytoplasmic role of PTEN in antagonizing PI3K signaling has been well studied, PTEN also resides in the nucleus, where its function remains poorly understood. Here, I demonstrate that SUMOylation (SUMO) of PTEN controls its nuclear localization. Consistent with its restricted cytoplasmic localization, a SUMO-deficient PTEN mutant is fully competent for regulating PI3K signaling. Upon exposure to genotoxic stress, SUMO-PTEN is rapidly excluded from the nucleus in an ATM-dependent manner, identifying a connection between these two major tumor suppressors. Further, ATM phosphorylated PTEN on threonine 398, and a PTEN mutant that cannot be phosphorylated at this position (PTEN T398A) resist nuclear exclusion following genotoxic stress. Judging by various readouts of the DNA damage response, cells lacking nuclear PTEN are hypersensitive to DNA damage and display impaired homologous recombination-mediated repair of double-strand DNA breaks. Moreover, unlike cells with Wt PTEN, PTEN-deficient cells are susceptible to killing by a combination of genotoxic stress and a small molecule inhibitor of PI3K both in vitro and in vivo. The synergistc effect of genotoxic stress and PI3K inhibition on PTEN-null cells is dependent on the simultaneous inhibition of both p110alpha and p110beta isoform. Further in vivo studies revealed that effective inhibition of PI3K pathway can be achieved with a discontinuous administration schedule in order to reduce the adverse effects associated with this treatment. My findings have considerable implications for individualizing therapy for patients with PTEN-deficient tumors. Advisors/Committee Members: Stambolic, Vuk, Medical Biophysics.

Subjects/Keywords: Cancer; DNA damage; PTEN; tumor suppressor; 0307

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bassi, C. (2015). Nuclear PTEN Controls DNA Repair and Sensitivity to Genotoxic Stress. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/69214

Chicago Manual of Style (16^th Edition):

Bassi, Christian. “Nuclear PTEN Controls DNA Repair and Sensitivity to Genotoxic Stress.” 2015. Doctoral Dissertation, University of Toronto. Accessed March 08, 2021. http://hdl.handle.net/1807/69214.

MLA Handbook (7^th Edition):

Bassi, Christian. “Nuclear PTEN Controls DNA Repair and Sensitivity to Genotoxic Stress.” 2015. Web. 08 Mar 2021.

Vancouver:

Bassi C. Nuclear PTEN Controls DNA Repair and Sensitivity to Genotoxic Stress. [Internet] [Doctoral dissertation]. University of Toronto; 2015. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/1807/69214.

Council of Science Editors:

Bassi C. Nuclear PTEN Controls DNA Repair and Sensitivity to Genotoxic Stress. [Doctoral Dissertation]. University of Toronto; 2015. Available from: http://hdl.handle.net/1807/69214

Michigan State University

29. Gjidoda, Alison Marie. Transcriptional regulation of RNA polymerase III-transcribed genes by the retinoblastoma tumor suppressor protein.

Degree: 2012, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:1541

►

Thesis M.S. Michigan State University. Biochemistry and Molecular Biology 2012.

The Retinoblastoma Tumor Suppressor Protein (Rb) is a critical regulator of cellular proliferation. In the… (more)

Subjects/Keywords: RNA polymerases; Tumor suppressor proteins; Biochemistry

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gjidoda, A. M. (2012). Transcriptional regulation of RNA polymerase III-transcribed genes by the retinoblastoma tumor suppressor protein. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:1541

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Gjidoda, Alison Marie. “Transcriptional regulation of RNA polymerase III-transcribed genes by the retinoblastoma tumor suppressor protein.” 2012. Thesis, Michigan State University. Accessed March 08, 2021. http://etd.lib.msu.edu/islandora/object/etd:1541.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Gjidoda, Alison Marie. “Transcriptional regulation of RNA polymerase III-transcribed genes by the retinoblastoma tumor suppressor protein.” 2012. Web. 08 Mar 2021.

Vancouver:

Gjidoda AM. Transcriptional regulation of RNA polymerase III-transcribed genes by the retinoblastoma tumor suppressor protein. [Internet] [Thesis]. Michigan State University; 2012. [cited 2021 Mar 08]. Available from: http://etd.lib.msu.edu/islandora/object/etd:1541.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Gjidoda AM. Transcriptional regulation of RNA polymerase III-transcribed genes by the retinoblastoma tumor suppressor protein. [Thesis]. Michigan State University; 2012. Available from: http://etd.lib.msu.edu/islandora/object/etd:1541

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

The Ohio State University

30. Smith, Laura Taylor. An Epigenetic approach for identifying novel tumor associated genes from regions of Loss of Heterozygosity in human neoplasias.

Degree: PhD, Medical Microbiology and Immunology, 2005, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1116959843

► The incidence of cancer is expected to be 1 in every 3 individuals. Onset of the disease in the population has been attributed to multiple… (more)

▼ The incidence of cancer is expected to be 1 in every 3 individuals. Onset of the disease in the population has been attributed to multiple genetic and environmental factors. Pathways leading to the development and progression of carcinomas, including head and neck squamous cell carcinomas (HNSCC) and non-small cell lung cancer (NSCLC), remain largely unknown. Common genetic alterations have been identified for many neoplasias, but many of the important genes of activation (oncogenes) or inactivation (tumor suppressor genes) have not yet been identified or characterized. This lack of identified cancer targets is in part due to limitations in detection techniques, as well as limited by the type of aberrations screened for. For example, researchers often search for mutations within a chromosomal region that is lost in order to identify candidate tumor suppressor genes. Epigenetic mechanisms, such as histone modifications and DNA methylation, have also become accepted modes of transcriptional inactivation in human malignancies, but are still in their beginning stages of evaluation in HNSCC, and have not been widely applied as an approach to identify tumor suppressor genes. The majority of DNA methylation studies in HNSCC have focused on genes previously identified as being inactivated in other cancer types. Efforts using genome-wide methylation scanning techniques, such as Restriction Landmark Genomic Scanning (RLGS) have identified novel methylation targets in HNSCC. Better understanding of the role of DNA methylation in human malignancies, as well as the targets of this epigenetic inactivation, may allow for more efficient and earlier detection screenings, as well as providing an additional mechanism for identifying important cancer-related genes. In the introductory chapter one, limited information from the literature regarding DNA methylation and HNSCC is reviewed, demonstrating the void that remains in the molecular etiology of the disease. Chapter two describes the difficulty and limitations of traditional experiments used to identify tumor suppressor genes from within regions of loss of heterozygosity (LOH). Often neglected in these studies that look for genetic mutations, DNA methylation has proven to be as important for gene silencing in cancer. In this chapter, a novel application of the genome-wide methylation technique Restriction Landmark Genomic Scanning (RLGS) is used to identify genes frequently hypermethylated in a localized region of the genome frequently lost in the progression of human neoplasia for which no tumor suppressor gene has been elucidated. TCF21 is shown to be targeted for hypermethylation in the majority of HNSCC and NSCLC samples. Chapter three describes further characterization of DNA methylation of TCF21, and determines the effect of such methylation on transcription. DNA methylation along the CpG island of TCF21 is tumor specific, and removal of methylation results in transcriptional upregulation. Chapters four and five summarize the antagonistic cancer properties elicited by TCF21… Advisors/Committee Members: Plass, Christoph (Advisor).

Subjects/Keywords: Biology, Genetics; epigenetics; DNA methylation; tumor suppressor gene; metastasis suppressor gene

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Smith, L. T. (2005). An Epigenetic approach for identifying novel tumor associated genes from regions of Loss of Heterozygosity in human neoplasias. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1116959843

Chicago Manual of Style (16^th Edition):

Smith, Laura Taylor. “An Epigenetic approach for identifying novel tumor associated genes from regions of Loss of Heterozygosity in human neoplasias.” 2005. Doctoral Dissertation, The Ohio State University. Accessed March 08, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1116959843.

MLA Handbook (7^th Edition):

Smith, Laura Taylor. “An Epigenetic approach for identifying novel tumor associated genes from regions of Loss of Heterozygosity in human neoplasias.” 2005. Web. 08 Mar 2021.

Vancouver:

Smith LT. An Epigenetic approach for identifying novel tumor associated genes from regions of Loss of Heterozygosity in human neoplasias. [Internet] [Doctoral dissertation]. The Ohio State University; 2005. [cited 2021 Mar 08]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1116959843.

Council of Science Editors:

Smith LT. An Epigenetic approach for identifying novel tumor associated genes from regions of Loss of Heterozygosity in human neoplasias. [Doctoral Dissertation]. The Ohio State University; 2005. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1116959843

Open Access Theses and Dissertations