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You searched for +publisher:"Temple University" +contributor:("Skorski, Tomasz"). Showing records 1 – 11 of 11 total matches.

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Temple University

1. Morales, Kimberly. RAD52 DNA Binding Activity Can Be Targeted to Eliminate CML Stem Cells.

Degree: PhD, 2012, Temple University

Biology

BCR-ABL1 transforms hematopoietic stem cells into leukemia stem cells (LSCs) to induce chronic myeloid leukemia in chronic phase. Expression of BCR-ABL1 stimulates production of… (more)

Subjects/Keywords: Molecular biology; Oncology; Cellular biology; BCR-ABL1; chronic myeloid leukemia; DNA repair; RAD52; stem cells

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

APA (6th Edition):

Morales, K. (2012). RAD52 DNA Binding Activity Can Be Targeted to Eliminate CML Stem Cells. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,190030

Chicago Manual of Style (16th Edition):

Morales, Kimberly. “RAD52 DNA Binding Activity Can Be Targeted to Eliminate CML Stem Cells.” 2012. Doctoral Dissertation, Temple University. Accessed September 22, 2020. http://digital.library.temple.edu/u?/p245801coll10,190030.

MLA Handbook (7th Edition):

Morales, Kimberly. “RAD52 DNA Binding Activity Can Be Targeted to Eliminate CML Stem Cells.” 2012. Web. 22 Sep 2020.

Vancouver:

Morales K. RAD52 DNA Binding Activity Can Be Targeted to Eliminate CML Stem Cells. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2020 Sep 22]. Available from: http://digital.library.temple.edu/u?/p245801coll10,190030.

Council of Science Editors:

Morales K. RAD52 DNA Binding Activity Can Be Targeted to Eliminate CML Stem Cells. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,190030


Temple University

2. Dasgupta, Yashodhara. NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS.

Degree: PhD, 2014, Temple University

Biology

BCR-ABL1 results from t(9;22)(q34;q11) reciprocal translocation resulting in BCR-ABL1 kinase expression, initiating chronic myeloid leukemia in chronic phase (CML-CP). At the initial stages of… (more)

Subjects/Keywords: Biology

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APA (6th Edition):

Dasgupta, Y. (2014). NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,239008

Chicago Manual of Style (16th Edition):

Dasgupta, Yashodhara. “NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS.” 2014. Doctoral Dissertation, Temple University. Accessed September 22, 2020. http://digital.library.temple.edu/u?/p245801coll10,239008.

MLA Handbook (7th Edition):

Dasgupta, Yashodhara. “NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS.” 2014. Web. 22 Sep 2020.

Vancouver:

Dasgupta Y. NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Sep 22]. Available from: http://digital.library.temple.edu/u?/p245801coll10,239008.

Council of Science Editors:

Dasgupta Y. NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,239008


Temple University

3. Pokiniewski, Katie Ann. Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization.

Degree: PhD, 2016, Temple University

Microbiology and Immunology

The Adeno-Associated Virus(AAV) is a small, single stranded DNA virus that has been developed as a gene transfer vector. Early clinical trials… (more)

Subjects/Keywords: Virology; Microbiology;

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APA (6th Edition):

Pokiniewski, K. A. (2016). Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,385837

Chicago Manual of Style (16th Edition):

Pokiniewski, Katie Ann. “Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization.” 2016. Doctoral Dissertation, Temple University. Accessed September 22, 2020. http://digital.library.temple.edu/u?/p245801coll10,385837.

MLA Handbook (7th Edition):

Pokiniewski, Katie Ann. “Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization.” 2016. Web. 22 Sep 2020.

Vancouver:

Pokiniewski KA. Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Sep 22]. Available from: http://digital.library.temple.edu/u?/p245801coll10,385837.

Council of Science Editors:

Pokiniewski KA. Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,385837


Temple University

4. McDevitt, Shane. Mechanistic Studies of Double-strand Break Repair Factors RAD52 and DNA Polymerase Theta.

Degree: PhD, 2018, Temple University

Biomedical Sciences

Small molecule disruption of RAD52 rings as a mechanism for precision medicine in BRCA deficient cancers Suppression of RAD52 causes synthetic lethality in… (more)

Subjects/Keywords: Molecular biology; Biochemistry;

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APA (6th Edition):

McDevitt, S. (2018). Mechanistic Studies of Double-strand Break Repair Factors RAD52 and DNA Polymerase Theta. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,518019

Chicago Manual of Style (16th Edition):

McDevitt, Shane. “Mechanistic Studies of Double-strand Break Repair Factors RAD52 and DNA Polymerase Theta.” 2018. Doctoral Dissertation, Temple University. Accessed September 22, 2020. http://digital.library.temple.edu/u?/p245801coll10,518019.

MLA Handbook (7th Edition):

McDevitt, Shane. “Mechanistic Studies of Double-strand Break Repair Factors RAD52 and DNA Polymerase Theta.” 2018. Web. 22 Sep 2020.

Vancouver:

McDevitt S. Mechanistic Studies of Double-strand Break Repair Factors RAD52 and DNA Polymerase Theta. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2020 Sep 22]. Available from: http://digital.library.temple.edu/u?/p245801coll10,518019.

Council of Science Editors:

McDevitt S. Mechanistic Studies of Double-strand Break Repair Factors RAD52 and DNA Polymerase Theta. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,518019


Temple University

5. Magimaidas, Andrew. The Role of the Stress Response Gene Gadd45b in Senescence.

Degree: PhD, 2015, Temple University

Molecular Biology and Genetics

The Gadd45 family of proteins (Gadd45a, Gadd45b, and Gadd45g) has been shown to act as stress sensors in response to various… (more)

Subjects/Keywords: Molecular biology; Genetics;

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APA (6th Edition):

Magimaidas, A. (2015). The Role of the Stress Response Gene Gadd45b in Senescence. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,376546

Chicago Manual of Style (16th Edition):

Magimaidas, Andrew. “The Role of the Stress Response Gene Gadd45b in Senescence.” 2015. Doctoral Dissertation, Temple University. Accessed September 22, 2020. http://digital.library.temple.edu/u?/p245801coll10,376546.

MLA Handbook (7th Edition):

Magimaidas, Andrew. “The Role of the Stress Response Gene Gadd45b in Senescence.” 2015. Web. 22 Sep 2020.

Vancouver:

Magimaidas A. The Role of the Stress Response Gene Gadd45b in Senescence. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Sep 22]. Available from: http://digital.library.temple.edu/u?/p245801coll10,376546.

Council of Science Editors:

Magimaidas A. The Role of the Stress Response Gene Gadd45b in Senescence. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,376546


Temple University

6. Mohamed-Hadley, Alisha. THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION.

Degree: PhD, 2011, Temple University

Molecular Biology and Genetics

The Gadd45 family of proteins is known to play a central role as cellular stress sensors that modulate the response of… (more)

Subjects/Keywords: Molecular Biology; Apoptosis; Cytokine; Gadd45a; Myc; Myeloid cells

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APA (6th Edition):

Mohamed-Hadley, A. (2011). THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,126332

Chicago Manual of Style (16th Edition):

Mohamed-Hadley, Alisha. “THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION.” 2011. Doctoral Dissertation, Temple University. Accessed September 22, 2020. http://digital.library.temple.edu/u?/p245801coll10,126332.

MLA Handbook (7th Edition):

Mohamed-Hadley, Alisha. “THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION.” 2011. Web. 22 Sep 2020.

Vancouver:

Mohamed-Hadley A. THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION. [Internet] [Doctoral dissertation]. Temple University; 2011. [cited 2020 Sep 22]. Available from: http://digital.library.temple.edu/u?/p245801coll10,126332.

Council of Science Editors:

Mohamed-Hadley A. THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION. [Doctoral Dissertation]. Temple University; 2011. Available from: http://digital.library.temple.edu/u?/p245801coll10,126332


Temple University

7. Bolton, Elisabeth Spring. Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP.

Degree: PhD, 2013, Temple University

Microbiology and Immunology

In chronic myelogenous leukemia (CML), activation of BCR-ABL, the product of the bcr-abl chimeric gene, leads to constitutive activation of pathways that… (more)

Subjects/Keywords: Biology; Molecular biology; Immunology;

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APA (6th Edition):

Bolton, E. S. (2013). Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,234916

Chicago Manual of Style (16th Edition):

Bolton, Elisabeth Spring. “Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP.” 2013. Doctoral Dissertation, Temple University. Accessed September 22, 2020. http://digital.library.temple.edu/u?/p245801coll10,234916.

MLA Handbook (7th Edition):

Bolton, Elisabeth Spring. “Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP.” 2013. Web. 22 Sep 2020.

Vancouver:

Bolton ES. Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2020 Sep 22]. Available from: http://digital.library.temple.edu/u?/p245801coll10,234916.

Council of Science Editors:

Bolton ES. Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,234916


Temple University

8. Whitfield, Fatima. Gamma-Delta T-Cells in Patients with Ovarian Carcinoma.

Degree: PhD, 2008, Temple University

Microbiology and Immunology

Ovarian cancer is the fifth most common cause of death from all cancers among women in the Western world and the most… (more)

Subjects/Keywords: Health Sciences, Immunology; Health Sciences, Oncology

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APA (6th Edition):

Whitfield, F. (2008). Gamma-Delta T-Cells in Patients with Ovarian Carcinoma. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,3422

Chicago Manual of Style (16th Edition):

Whitfield, Fatima. “Gamma-Delta T-Cells in Patients with Ovarian Carcinoma.” 2008. Doctoral Dissertation, Temple University. Accessed September 22, 2020. http://digital.library.temple.edu/u?/p245801coll10,3422.

MLA Handbook (7th Edition):

Whitfield, Fatima. “Gamma-Delta T-Cells in Patients with Ovarian Carcinoma.” 2008. Web. 22 Sep 2020.

Vancouver:

Whitfield F. Gamma-Delta T-Cells in Patients with Ovarian Carcinoma. [Internet] [Doctoral dissertation]. Temple University; 2008. [cited 2020 Sep 22]. Available from: http://digital.library.temple.edu/u?/p245801coll10,3422.

Council of Science Editors:

Whitfield F. Gamma-Delta T-Cells in Patients with Ovarian Carcinoma. [Doctoral Dissertation]. Temple University; 2008. Available from: http://digital.library.temple.edu/u?/p245801coll10,3422


Temple University

9. Radu, Maria. The role of p27 phosphorylation in mediating atRA sensitivity of ovarian carcinoma cells.

Degree: 2008, Temple University

Microbiology and Immunology

Ph.D.;

All trans retinoic acid (atRA) has been shown to inhibit the growth of CAOV3 ovarian carcinoma cells. This results from arrest… (more)

Subjects/Keywords: Health Sciences, Immunology; Biology, Cell; Health Sciences, Oncology; retinoic acid; p27; phosphorylation; cell cycle; growth arrest

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APA (6th Edition):

Radu, M. (2008). The role of p27 phosphorylation in mediating atRA sensitivity of ovarian carcinoma cells. (Thesis). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,5459

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

Chicago Manual of Style (16th Edition):

Radu, Maria. “The role of p27 phosphorylation in mediating atRA sensitivity of ovarian carcinoma cells.” 2008. Thesis, Temple University. Accessed September 22, 2020. http://digital.library.temple.edu/u?/p245801coll10,5459.

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

MLA Handbook (7th Edition):

Radu, Maria. “The role of p27 phosphorylation in mediating atRA sensitivity of ovarian carcinoma cells.” 2008. Web. 22 Sep 2020.

Vancouver:

Radu M. The role of p27 phosphorylation in mediating atRA sensitivity of ovarian carcinoma cells. [Internet] [Thesis]. Temple University; 2008. [cited 2020 Sep 22]. Available from: http://digital.library.temple.edu/u?/p245801coll10,5459.

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

Council of Science Editors:

Radu M. The role of p27 phosphorylation in mediating atRA sensitivity of ovarian carcinoma cells. [Thesis]. Temple University; 2008. Available from: http://digital.library.temple.edu/u?/p245801coll10,5459

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


Temple University

10. Zacharakis, Nikolaos. Identification of putative antigens in Systemic Sclerosis utilizing in vivo clonally expanded T cells.

Degree: PhD, 2014, Temple University

Microbiology and Immunology

Systemic sclerosis (SSc) is a chronic autoimmune disease of the connective tissue. Immune system dysregulation, excessive deposition of collagen and microvascular damage… (more)

Subjects/Keywords: Immunology;

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APA (6th Edition):

Zacharakis, N. (2014). Identification of putative antigens in Systemic Sclerosis utilizing in vivo clonally expanded T cells. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,249827

Chicago Manual of Style (16th Edition):

Zacharakis, Nikolaos. “Identification of putative antigens in Systemic Sclerosis utilizing in vivo clonally expanded T cells.” 2014. Doctoral Dissertation, Temple University. Accessed September 22, 2020. http://digital.library.temple.edu/u?/p245801coll10,249827.

MLA Handbook (7th Edition):

Zacharakis, Nikolaos. “Identification of putative antigens in Systemic Sclerosis utilizing in vivo clonally expanded T cells.” 2014. Web. 22 Sep 2020.

Vancouver:

Zacharakis N. Identification of putative antigens in Systemic Sclerosis utilizing in vivo clonally expanded T cells. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Sep 22]. Available from: http://digital.library.temple.edu/u?/p245801coll10,249827.

Council of Science Editors:

Zacharakis N. Identification of putative antigens in Systemic Sclerosis utilizing in vivo clonally expanded T cells. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,249827


Temple University

11. Reed, Katherine Sullivan. Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers.

Degree: PhD, 2018, Temple University

Biomedical Sciences

PARP inhibitors (PARPi) have been used to induce synthetic lethality in BRCA-deficient tumors in clinical trials with limited success due to the development… (more)

Subjects/Keywords: Oncology; Cellular biology;

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

APA (6th Edition):

Reed, K. S. (2018). Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,507327

Chicago Manual of Style (16th Edition):

Reed, Katherine Sullivan. “Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers.” 2018. Doctoral Dissertation, Temple University. Accessed September 22, 2020. http://digital.library.temple.edu/u?/p245801coll10,507327.

MLA Handbook (7th Edition):

Reed, Katherine Sullivan. “Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers.” 2018. Web. 22 Sep 2020.

Vancouver:

Reed KS. Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2020 Sep 22]. Available from: http://digital.library.temple.edu/u?/p245801coll10,507327.

Council of Science Editors:

Reed KS. Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,507327

.