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You searched for +publisher:"University of Arizona" +contributor:("Martinez, Jesse D."). Showing records 1 – 22 of 22 total matches.

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University of Arizona

1. Gomes, Cecil. The Role of 14-3-3 Gamma in Promoting Genomic Instability .

Degree: 2018, University of Arizona

 The 14-3-3 family members are a group of highly conserved scaffolding proteins that are present in all eukaryotes. Despite having limited endogenous activity, the 14-3-3s… (more)

Subjects/Keywords: 14-3-3; cancer; nsclc

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APA (6th Edition):

Gomes, C. (2018). The Role of 14-3-3 Gamma in Promoting Genomic Instability . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/628052

Chicago Manual of Style (16th Edition):

Gomes, Cecil. “The Role of 14-3-3 Gamma in Promoting Genomic Instability .” 2018. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/628052.

MLA Handbook (7th Edition):

Gomes, Cecil. “The Role of 14-3-3 Gamma in Promoting Genomic Instability .” 2018. Web. 12 Nov 2019.

Vancouver:

Gomes C. The Role of 14-3-3 Gamma in Promoting Genomic Instability . [Internet] [Doctoral dissertation]. University of Arizona; 2018. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/628052.

Council of Science Editors:

Gomes C. The Role of 14-3-3 Gamma in Promoting Genomic Instability . [Doctoral Dissertation]. University of Arizona; 2018. Available from: http://hdl.handle.net/10150/628052


University of Arizona

2. Su, Hsin-Yuan. Therapeutic Potential of EGFR Derived Peptides in Breast Cancer .

Degree: 2013, University of Arizona

 The epidermal growth factor receptor (EGFR) belongs to the erbB family of receptor tyrosine kinases which consists of four members (EGFR, ErbB2, ErbB3 and ErbB4).… (more)

Subjects/Keywords: EGFR; juxtamembrane domain; MUC1; nuclear EGFR; peptide; Cancer Biology; breast cancer

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APA (6th Edition):

Su, H. (2013). Therapeutic Potential of EGFR Derived Peptides in Breast Cancer . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/293486

Chicago Manual of Style (16th Edition):

Su, Hsin-Yuan. “Therapeutic Potential of EGFR Derived Peptides in Breast Cancer .” 2013. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/293486.

MLA Handbook (7th Edition):

Su, Hsin-Yuan. “Therapeutic Potential of EGFR Derived Peptides in Breast Cancer .” 2013. Web. 12 Nov 2019.

Vancouver:

Su H. Therapeutic Potential of EGFR Derived Peptides in Breast Cancer . [Internet] [Doctoral dissertation]. University of Arizona; 2013. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/293486.

Council of Science Editors:

Su H. Therapeutic Potential of EGFR Derived Peptides in Breast Cancer . [Doctoral Dissertation]. University of Arizona; 2013. Available from: http://hdl.handle.net/10150/293486


University of Arizona

3. Akhenblit, Paul. Interrogating Tumor Metabolism with AcidoCEST MRI .

Degree: 2016, University of Arizona

 Tumor metabolism is a highly dysregulated process that is identified as a unique target for therapy. Current philosophy proposes that tumor metabolism is a plastic… (more)

Subjects/Keywords: Molecular Imaging; Tumor Acidosis; Tumor Metabolism; Cancer Biology; acidoCEST MRI

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APA (6th Edition):

Akhenblit, P. (2016). Interrogating Tumor Metabolism with AcidoCEST MRI . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/612606

Chicago Manual of Style (16th Edition):

Akhenblit, Paul. “Interrogating Tumor Metabolism with AcidoCEST MRI .” 2016. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/612606.

MLA Handbook (7th Edition):

Akhenblit, Paul. “Interrogating Tumor Metabolism with AcidoCEST MRI .” 2016. Web. 12 Nov 2019.

Vancouver:

Akhenblit P. Interrogating Tumor Metabolism with AcidoCEST MRI . [Internet] [Doctoral dissertation]. University of Arizona; 2016. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/612606.

Council of Science Editors:

Akhenblit P. Interrogating Tumor Metabolism with AcidoCEST MRI . [Doctoral Dissertation]. University of Arizona; 2016. Available from: http://hdl.handle.net/10150/612606


University of Arizona

4. Das, Lipsa. Regulation of Intracellular Trafficking of Laminin Binding Integrins in Prostate Cancer .

Degree: 2017, University of Arizona

 Laminin binding integrins (α6β1 and α3β1) are persistently but differentially expressed throughout prostate cancer progression and metastasis. Prostate cancer primarily invades through laminin rich nerve… (more)

Subjects/Keywords: Cancer; Endosomes; Integrin; Laminin; Rab11; Trafficking

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APA (6th Edition):

Das, L. (2017). Regulation of Intracellular Trafficking of Laminin Binding Integrins in Prostate Cancer . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/625651

Chicago Manual of Style (16th Edition):

Das, Lipsa. “Regulation of Intracellular Trafficking of Laminin Binding Integrins in Prostate Cancer .” 2017. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/625651.

MLA Handbook (7th Edition):

Das, Lipsa. “Regulation of Intracellular Trafficking of Laminin Binding Integrins in Prostate Cancer .” 2017. Web. 12 Nov 2019.

Vancouver:

Das L. Regulation of Intracellular Trafficking of Laminin Binding Integrins in Prostate Cancer . [Internet] [Doctoral dissertation]. University of Arizona; 2017. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/625651.

Council of Science Editors:

Das L. Regulation of Intracellular Trafficking of Laminin Binding Integrins in Prostate Cancer . [Doctoral Dissertation]. University of Arizona; 2017. Available from: http://hdl.handle.net/10150/625651


University of Arizona

5. Gaitonde, Supriya Vishwaraj. Mechanisms involved in p53 regulation .

Degree: 2000, University of Arizona

 Inactivation of the tumor suppressor protein p53 is a very important and common step in the process of carcinogenesis. The overall purpose of this project… (more)

Subjects/Keywords: Biology; Cell.

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APA (6th Edition):

Gaitonde, S. V. (2000). Mechanisms involved in p53 regulation . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/298798

Chicago Manual of Style (16th Edition):

Gaitonde, Supriya Vishwaraj. “Mechanisms involved in p53 regulation .” 2000. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/298798.

MLA Handbook (7th Edition):

Gaitonde, Supriya Vishwaraj. “Mechanisms involved in p53 regulation .” 2000. Web. 12 Nov 2019.

Vancouver:

Gaitonde SV. Mechanisms involved in p53 regulation . [Internet] [Doctoral dissertation]. University of Arizona; 2000. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/298798.

Council of Science Editors:

Gaitonde SV. Mechanisms involved in p53 regulation . [Doctoral Dissertation]. University of Arizona; 2000. Available from: http://hdl.handle.net/10150/298798


University of Arizona

6. Powell, Ashley Ann. Bile acid biological activity in colon cancer cells: From hydrophobicity to gene activation .

Degree: 2002, University of Arizona

 Bile acids, known for millennia to play a role in health and disease, are currently being studied for their pivotal contribution to the development and… (more)

Subjects/Keywords: Biology, Cell.; Health Sciences, Oncology.

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APA (6th Edition):

Powell, A. A. (2002). Bile acid biological activity in colon cancer cells: From hydrophobicity to gene activation . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/280045

Chicago Manual of Style (16th Edition):

Powell, Ashley Ann. “Bile acid biological activity in colon cancer cells: From hydrophobicity to gene activation .” 2002. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/280045.

MLA Handbook (7th Edition):

Powell, Ashley Ann. “Bile acid biological activity in colon cancer cells: From hydrophobicity to gene activation .” 2002. Web. 12 Nov 2019.

Vancouver:

Powell AA. Bile acid biological activity in colon cancer cells: From hydrophobicity to gene activation . [Internet] [Doctoral dissertation]. University of Arizona; 2002. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/280045.

Council of Science Editors:

Powell AA. Bile acid biological activity in colon cancer cells: From hydrophobicity to gene activation . [Doctoral Dissertation]. University of Arizona; 2002. Available from: http://hdl.handle.net/10150/280045

7. Paz, Edwin Alfredo. Molecular Mechanisms of Polyamine Metabolism Affecting Oncogenic Signaling .

Degree: 2013, University of Arizona

 Eukaryotic cells tightly regulate metabolism in order to sustain normal processes. Dysregulation of cellular metabolism is associated with multiple diseases including cancer. Polyamine metabolism is… (more)

Subjects/Keywords: DFMO; eIF5A; let-7; oncometabolite; polyamines; LIN28; Cancer Biology

…Theses and Dissertations of the University of Arizona Graduate College, I present my work in… 

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APA (6th Edition):

Paz, E. A. (2013). Molecular Mechanisms of Polyamine Metabolism Affecting Oncogenic Signaling . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/299021

Chicago Manual of Style (16th Edition):

Paz, Edwin Alfredo. “Molecular Mechanisms of Polyamine Metabolism Affecting Oncogenic Signaling .” 2013. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/299021.

MLA Handbook (7th Edition):

Paz, Edwin Alfredo. “Molecular Mechanisms of Polyamine Metabolism Affecting Oncogenic Signaling .” 2013. Web. 12 Nov 2019.

Vancouver:

Paz EA. Molecular Mechanisms of Polyamine Metabolism Affecting Oncogenic Signaling . [Internet] [Doctoral dissertation]. University of Arizona; 2013. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/299021.

Council of Science Editors:

Paz EA. Molecular Mechanisms of Polyamine Metabolism Affecting Oncogenic Signaling . [Doctoral Dissertation]. University of Arizona; 2013. Available from: http://hdl.handle.net/10150/299021

8. Havas, Aaron Paul. Defining Mechanisms of Sensitivity and Resistance to Histone Deacetylase Inhibitors to Develop Effective Thereaputic Strategies for the Treatment of Aggressive Diffuse Large B-Cell Lymphoma .

Degree: 2016, University of Arizona

 Diffuse large B-cell lymphoma (DLBCL) is the most common form of non-Hodgkin lymphoma (NHL). The current standard of care is the combination of rituximab with… (more)

Subjects/Keywords: Diffuse Large B-cell lymphoma; Histone deacetylase inhibitor; microtubule targeting agents; non-Hodgkin lymphoma; cell cycle regulation

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APA (6th Edition):

Havas, A. P. (2016). Defining Mechanisms of Sensitivity and Resistance to Histone Deacetylase Inhibitors to Develop Effective Thereaputic Strategies for the Treatment of Aggressive Diffuse Large B-Cell Lymphoma . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/622977

Chicago Manual of Style (16th Edition):

Havas, Aaron Paul. “Defining Mechanisms of Sensitivity and Resistance to Histone Deacetylase Inhibitors to Develop Effective Thereaputic Strategies for the Treatment of Aggressive Diffuse Large B-Cell Lymphoma .” 2016. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/622977.

MLA Handbook (7th Edition):

Havas, Aaron Paul. “Defining Mechanisms of Sensitivity and Resistance to Histone Deacetylase Inhibitors to Develop Effective Thereaputic Strategies for the Treatment of Aggressive Diffuse Large B-Cell Lymphoma .” 2016. Web. 12 Nov 2019.

Vancouver:

Havas AP. Defining Mechanisms of Sensitivity and Resistance to Histone Deacetylase Inhibitors to Develop Effective Thereaputic Strategies for the Treatment of Aggressive Diffuse Large B-Cell Lymphoma . [Internet] [Doctoral dissertation]. University of Arizona; 2016. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/622977.

Council of Science Editors:

Havas AP. Defining Mechanisms of Sensitivity and Resistance to Histone Deacetylase Inhibitors to Develop Effective Thereaputic Strategies for the Treatment of Aggressive Diffuse Large B-Cell Lymphoma . [Doctoral Dissertation]. University of Arizona; 2016. Available from: http://hdl.handle.net/10150/622977


University of Arizona

9. Junk, Damian Jerome. Determining the Role of p53 Mutation in Human Breast Cancer Progression Using Recombinant Mutant/Wild-Type p53 Heterozygous Human Mammary Epithelial Cell Culture Models .

Degree: 2008, University of Arizona

 Breast cancer is the most frequently diagnosed form of cancer in women and the second leading cause of cancer-related deaths. Breast cancer is a heterogeneous… (more)

Subjects/Keywords: mutant p53; breast cancer; epigenetics; migration; invasion

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APA (6th Edition):

Junk, D. J. (2008). Determining the Role of p53 Mutation in Human Breast Cancer Progression Using Recombinant Mutant/Wild-Type p53 Heterozygous Human Mammary Epithelial Cell Culture Models . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/193600

Chicago Manual of Style (16th Edition):

Junk, Damian Jerome. “Determining the Role of p53 Mutation in Human Breast Cancer Progression Using Recombinant Mutant/Wild-Type p53 Heterozygous Human Mammary Epithelial Cell Culture Models .” 2008. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/193600.

MLA Handbook (7th Edition):

Junk, Damian Jerome. “Determining the Role of p53 Mutation in Human Breast Cancer Progression Using Recombinant Mutant/Wild-Type p53 Heterozygous Human Mammary Epithelial Cell Culture Models .” 2008. Web. 12 Nov 2019.

Vancouver:

Junk DJ. Determining the Role of p53 Mutation in Human Breast Cancer Progression Using Recombinant Mutant/Wild-Type p53 Heterozygous Human Mammary Epithelial Cell Culture Models . [Internet] [Doctoral dissertation]. University of Arizona; 2008. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/193600.

Council of Science Editors:

Junk DJ. Determining the Role of p53 Mutation in Human Breast Cancer Progression Using Recombinant Mutant/Wild-Type p53 Heterozygous Human Mammary Epithelial Cell Culture Models . [Doctoral Dissertation]. University of Arizona; 2008. Available from: http://hdl.handle.net/10150/193600


University of Arizona

10. Bair III, Warner B. The Regulation of Growth Factor Receptors EGFR and IGF-IR and the Growth Factor VEGF by Thioredoxin-1 .

Degree: 2005, University of Arizona

 Thioredoxin-1 (Trx-1) is a redox protein that is overexpressed in many tumors where it is associated with tumor growth, inhibited apoptosis and decreased patient survival.… (more)

Subjects/Keywords: EGFR; VEGF; IGF-IR; Sp1; Trx-1

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APA (6th Edition):

Bair III, W. B. (2005). The Regulation of Growth Factor Receptors EGFR and IGF-IR and the Growth Factor VEGF by Thioredoxin-1 . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/193665

Chicago Manual of Style (16th Edition):

Bair III, Warner B. “The Regulation of Growth Factor Receptors EGFR and IGF-IR and the Growth Factor VEGF by Thioredoxin-1 .” 2005. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/193665.

MLA Handbook (7th Edition):

Bair III, Warner B. “The Regulation of Growth Factor Receptors EGFR and IGF-IR and the Growth Factor VEGF by Thioredoxin-1 .” 2005. Web. 12 Nov 2019.

Vancouver:

Bair III WB. The Regulation of Growth Factor Receptors EGFR and IGF-IR and the Growth Factor VEGF by Thioredoxin-1 . [Internet] [Doctoral dissertation]. University of Arizona; 2005. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/193665.

Council of Science Editors:

Bair III WB. The Regulation of Growth Factor Receptors EGFR and IGF-IR and the Growth Factor VEGF by Thioredoxin-1 . [Doctoral Dissertation]. University of Arizona; 2005. Available from: http://hdl.handle.net/10150/193665


University of Arizona

11. Basu Roy, Upal Kunal. Regulation and Function of Caveolin-1 in Colorectal Carcinogenesis .

Degree: 2007, University of Arizona

 Colon cancer is the second leading cause of cancer deaths in the United States of America. It is caused by the accumulation of mutations in… (more)

Subjects/Keywords: Molecular & Cellular Biology

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APA (6th Edition):

Basu Roy, U. K. (2007). Regulation and Function of Caveolin-1 in Colorectal Carcinogenesis . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/194031

Chicago Manual of Style (16th Edition):

Basu Roy, Upal Kunal. “Regulation and Function of Caveolin-1 in Colorectal Carcinogenesis .” 2007. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/194031.

MLA Handbook (7th Edition):

Basu Roy, Upal Kunal. “Regulation and Function of Caveolin-1 in Colorectal Carcinogenesis .” 2007. Web. 12 Nov 2019.

Vancouver:

Basu Roy UK. Regulation and Function of Caveolin-1 in Colorectal Carcinogenesis . [Internet] [Doctoral dissertation]. University of Arizona; 2007. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/194031.

Council of Science Editors:

Basu Roy UK. Regulation and Function of Caveolin-1 in Colorectal Carcinogenesis . [Doctoral Dissertation]. University of Arizona; 2007. Available from: http://hdl.handle.net/10150/194031


University of Arizona

12. Mehta, Dipti J. 15-deoxy-delta-12, 14-prostaglandin J2 (15d-PGJ2) Mediated Signaling in Colon Cancer .

Degree: 2006, University of Arizona

 Normal tissue structure and function are maintained by a dynamic interaction between epithelial cells and the stroma consisting of fibroblasts, adipose, vasculature and resident immune… (more)

Subjects/Keywords: 15d-PGJ2; K-RAS; Apoptosis; Adipogenesis; carcinogenesis; colon

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APA (6th Edition):

Mehta, D. J. (2006). 15-deoxy-delta-12, 14-prostaglandin J2 (15d-PGJ2) Mediated Signaling in Colon Cancer . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/194039

Chicago Manual of Style (16th Edition):

Mehta, Dipti J. “15-deoxy-delta-12, 14-prostaglandin J2 (15d-PGJ2) Mediated Signaling in Colon Cancer .” 2006. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/194039.

MLA Handbook (7th Edition):

Mehta, Dipti J. “15-deoxy-delta-12, 14-prostaglandin J2 (15d-PGJ2) Mediated Signaling in Colon Cancer .” 2006. Web. 12 Nov 2019.

Vancouver:

Mehta DJ. 15-deoxy-delta-12, 14-prostaglandin J2 (15d-PGJ2) Mediated Signaling in Colon Cancer . [Internet] [Doctoral dissertation]. University of Arizona; 2006. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/194039.

Council of Science Editors:

Mehta DJ. 15-deoxy-delta-12, 14-prostaglandin J2 (15d-PGJ2) Mediated Signaling in Colon Cancer . [Doctoral Dissertation]. University of Arizona; 2006. Available from: http://hdl.handle.net/10150/194039


University of Arizona

13. Pochampalli, Mamata Rani. Characterization of Effects of Muc1 Expression on Epidermal Growth Factor Receptor Signaling in Breast Cancer .

Degree: 2006, University of Arizona

 EGF receptors are key regulators of cell survival and growth in normal and transformed tissues. Ligand binding results in formation of homo/hetero dimers of these… (more)

Subjects/Keywords: MUC1; EGFR; MOUSE MODELS; HUMAN BREAST CANCER CELL LINES; BREAST CANCER

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APA (6th Edition):

Pochampalli, M. R. (2006). Characterization of Effects of Muc1 Expression on Epidermal Growth Factor Receptor Signaling in Breast Cancer . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/194355

Chicago Manual of Style (16th Edition):

Pochampalli, Mamata Rani. “Characterization of Effects of Muc1 Expression on Epidermal Growth Factor Receptor Signaling in Breast Cancer .” 2006. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/194355.

MLA Handbook (7th Edition):

Pochampalli, Mamata Rani. “Characterization of Effects of Muc1 Expression on Epidermal Growth Factor Receptor Signaling in Breast Cancer .” 2006. Web. 12 Nov 2019.

Vancouver:

Pochampalli MR. Characterization of Effects of Muc1 Expression on Epidermal Growth Factor Receptor Signaling in Breast Cancer . [Internet] [Doctoral dissertation]. University of Arizona; 2006. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/194355.

Council of Science Editors:

Pochampalli MR. Characterization of Effects of Muc1 Expression on Epidermal Growth Factor Receptor Signaling in Breast Cancer . [Doctoral Dissertation]. University of Arizona; 2006. Available from: http://hdl.handle.net/10150/194355


University of Arizona

14. Chandramouli, Anupama. The Role of Prostaglandin E2/EP4 Prostanoid Receptor Signaling in Colorectal Carcinogenesis .

Degree: 2009, University of Arizona

 Colorectal cancer, among other tumors, is characterized by elevated levels of prostaglandins due to the up-regulation of cyclooxygenase -2 (COX-2), a key enzyme in the… (more)

Subjects/Keywords: Colorectal Cancer; CREB; Cyclooxygenase 2; EP4 prostanoid receptor; Prostaglandin E2; S100P

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APA (6th Edition):

Chandramouli, A. (2009). The Role of Prostaglandin E2/EP4 Prostanoid Receptor Signaling in Colorectal Carcinogenesis . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/195443

Chicago Manual of Style (16th Edition):

Chandramouli, Anupama. “The Role of Prostaglandin E2/EP4 Prostanoid Receptor Signaling in Colorectal Carcinogenesis .” 2009. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/195443.

MLA Handbook (7th Edition):

Chandramouli, Anupama. “The Role of Prostaglandin E2/EP4 Prostanoid Receptor Signaling in Colorectal Carcinogenesis .” 2009. Web. 12 Nov 2019.

Vancouver:

Chandramouli A. The Role of Prostaglandin E2/EP4 Prostanoid Receptor Signaling in Colorectal Carcinogenesis . [Internet] [Doctoral dissertation]. University of Arizona; 2009. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/195443.

Council of Science Editors:

Chandramouli A. The Role of Prostaglandin E2/EP4 Prostanoid Receptor Signaling in Colorectal Carcinogenesis . [Doctoral Dissertation]. University of Arizona; 2009. Available from: http://hdl.handle.net/10150/195443


University of Arizona

15. Jean-Louis, Samira. Membrane Perturbation By Bile Acids and Their Potential Role in Signaling .

Degree: 2005, University of Arizona

 Secondary bile acids have long been postulated to be tumor promoters in the colon but their mechanism of action are yet to be delineated. Though… (more)

Subjects/Keywords: Bile Acid; DCA; Membrane Perturbation; Cholesterol; EGFR; Signaling

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APA (6th Edition):

Jean-Louis, S. (2005). Membrane Perturbation By Bile Acids and Their Potential Role in Signaling . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/193551

Chicago Manual of Style (16th Edition):

Jean-Louis, Samira. “Membrane Perturbation By Bile Acids and Their Potential Role in Signaling .” 2005. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/193551.

MLA Handbook (7th Edition):

Jean-Louis, Samira. “Membrane Perturbation By Bile Acids and Their Potential Role in Signaling .” 2005. Web. 12 Nov 2019.

Vancouver:

Jean-Louis S. Membrane Perturbation By Bile Acids and Their Potential Role in Signaling . [Internet] [Doctoral dissertation]. University of Arizona; 2005. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/193551.

Council of Science Editors:

Jean-Louis S. Membrane Perturbation By Bile Acids and Their Potential Role in Signaling . [Doctoral Dissertation]. University of Arizona; 2005. Available from: http://hdl.handle.net/10150/193551


University of Arizona

16. Mayelzadeh, Foroozan. DNA Binding and Selective Gene Induction by Different Forms of the P53 Protein .

Degree: 2006, University of Arizona

 When cells are challenged by genotoxic stress, the tumor suppressor protein p53 promotes adaptive responses, including cell cycle arrest, DNA repair, or apoptosis. How these… (more)

Subjects/Keywords: Genetics

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APA (6th Edition):

Mayelzadeh, F. (2006). DNA Binding and Selective Gene Induction by Different Forms of the P53 Protein . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/193992

Chicago Manual of Style (16th Edition):

Mayelzadeh, Foroozan. “DNA Binding and Selective Gene Induction by Different Forms of the P53 Protein .” 2006. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/193992.

MLA Handbook (7th Edition):

Mayelzadeh, Foroozan. “DNA Binding and Selective Gene Induction by Different Forms of the P53 Protein .” 2006. Web. 12 Nov 2019.

Vancouver:

Mayelzadeh F. DNA Binding and Selective Gene Induction by Different Forms of the P53 Protein . [Internet] [Doctoral dissertation]. University of Arizona; 2006. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/193992.

Council of Science Editors:

Mayelzadeh F. DNA Binding and Selective Gene Induction by Different Forms of the P53 Protein . [Doctoral Dissertation]. University of Arizona; 2006. Available from: http://hdl.handle.net/10150/193992


University of Arizona

17. Morgan, Sherif. The Bile Acid, Deoxycholic Acid, Modulates IGF-IR Function in Colon Cancer Cells .

Degree: 2009, University of Arizona

 Deoxycholic acid (DCA) is a secondary bile acid postulated to be involved in the etiology and the progression of colorectal cancer, but its specific mechanisms… (more)

Subjects/Keywords: apoptosis; bile acids; colon cancer; deoxycholic acid; insulin-like growth factor-I receptor

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APA (6th Edition):

Morgan, S. (2009). The Bile Acid, Deoxycholic Acid, Modulates IGF-IR Function in Colon Cancer Cells . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/194122

Chicago Manual of Style (16th Edition):

Morgan, Sherif. “The Bile Acid, Deoxycholic Acid, Modulates IGF-IR Function in Colon Cancer Cells .” 2009. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/194122.

MLA Handbook (7th Edition):

Morgan, Sherif. “The Bile Acid, Deoxycholic Acid, Modulates IGF-IR Function in Colon Cancer Cells .” 2009. Web. 12 Nov 2019.

Vancouver:

Morgan S. The Bile Acid, Deoxycholic Acid, Modulates IGF-IR Function in Colon Cancer Cells . [Internet] [Doctoral dissertation]. University of Arizona; 2009. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/194122.

Council of Science Editors:

Morgan S. The Bile Acid, Deoxycholic Acid, Modulates IGF-IR Function in Colon Cancer Cells . [Doctoral Dissertation]. University of Arizona; 2009. Available from: http://hdl.handle.net/10150/194122


University of Arizona

18. Pourpak, Alan. Ethonafide-Induced Cytotoxicity is Mediated by Topoisomerase II Inhibition in Human Prostate Cancer Cells .

Degree: 2006, University of Arizona

 Ethonafide is an anthracene-containing derivative of amonafide that belongs to the azonafide series of anticancer agents. The lack of cross-resistance in MDR-expressing cancer cell lines… (more)

Subjects/Keywords: Ethonafide; Topoisomerase II; Prostate cancer

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APA (6th Edition):

Pourpak, A. (2006). Ethonafide-Induced Cytotoxicity is Mediated by Topoisomerase II Inhibition in Human Prostate Cancer Cells . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/194367

Chicago Manual of Style (16th Edition):

Pourpak, Alan. “Ethonafide-Induced Cytotoxicity is Mediated by Topoisomerase II Inhibition in Human Prostate Cancer Cells .” 2006. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/194367.

MLA Handbook (7th Edition):

Pourpak, Alan. “Ethonafide-Induced Cytotoxicity is Mediated by Topoisomerase II Inhibition in Human Prostate Cancer Cells .” 2006. Web. 12 Nov 2019.

Vancouver:

Pourpak A. Ethonafide-Induced Cytotoxicity is Mediated by Topoisomerase II Inhibition in Human Prostate Cancer Cells . [Internet] [Doctoral dissertation]. University of Arizona; 2006. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/194367.

Council of Science Editors:

Pourpak A. Ethonafide-Induced Cytotoxicity is Mediated by Topoisomerase II Inhibition in Human Prostate Cancer Cells . [Doctoral Dissertation]. University of Arizona; 2006. Available from: http://hdl.handle.net/10150/194367


University of Arizona

19. Feldman, Rebecca A. A Novel Mechanism for UDCA-Induced Growth Suppression .

Degree: 2008, University of Arizona

 Bile acids have been studied for many years for their role in either promoting (Deoxycholic Acid) or suppressing (Ursodeoxycholic Acid) colon tumor development in animal… (more)

Subjects/Keywords: bile acids; UDCA; Colon Cancer; Chemoprevention

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APA (6th Edition):

Feldman, R. A. (2008). A Novel Mechanism for UDCA-Induced Growth Suppression . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/195775

Chicago Manual of Style (16th Edition):

Feldman, Rebecca A. “A Novel Mechanism for UDCA-Induced Growth Suppression .” 2008. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/195775.

MLA Handbook (7th Edition):

Feldman, Rebecca A. “A Novel Mechanism for UDCA-Induced Growth Suppression .” 2008. Web. 12 Nov 2019.

Vancouver:

Feldman RA. A Novel Mechanism for UDCA-Induced Growth Suppression . [Internet] [Doctoral dissertation]. University of Arizona; 2008. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/195775.

Council of Science Editors:

Feldman RA. A Novel Mechanism for UDCA-Induced Growth Suppression . [Doctoral Dissertation]. University of Arizona; 2008. Available from: http://hdl.handle.net/10150/195775


University of Arizona

20. Henderson, Meredith C. UA62784; a Putative Inhibitor of CENP-E Kinesin-like Protein and its Effects on Human Pancreatic Cancer Cells .

Degree: 2008, University of Arizona

 UA62784 is a novel fluorenone identified in a biologic screen of compounds that are selectively cytotoxic in DPC4 (deleted in pancreatic cancer)-deleted pancreatic cancer cells.… (more)

Subjects/Keywords: cancer; pancreatic; kinesin; CENP-E; DPC4

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APA (6th Edition):

Henderson, M. C. (2008). UA62784; a Putative Inhibitor of CENP-E Kinesin-like Protein and its Effects on Human Pancreatic Cancer Cells . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/196030

Chicago Manual of Style (16th Edition):

Henderson, Meredith C. “UA62784; a Putative Inhibitor of CENP-E Kinesin-like Protein and its Effects on Human Pancreatic Cancer Cells .” 2008. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/196030.

MLA Handbook (7th Edition):

Henderson, Meredith C. “UA62784; a Putative Inhibitor of CENP-E Kinesin-like Protein and its Effects on Human Pancreatic Cancer Cells .” 2008. Web. 12 Nov 2019.

Vancouver:

Henderson MC. UA62784; a Putative Inhibitor of CENP-E Kinesin-like Protein and its Effects on Human Pancreatic Cancer Cells . [Internet] [Doctoral dissertation]. University of Arizona; 2008. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/196030.

Council of Science Editors:

Henderson MC. UA62784; a Putative Inhibitor of CENP-E Kinesin-like Protein and its Effects on Human Pancreatic Cancer Cells . [Doctoral Dissertation]. University of Arizona; 2008. Available from: http://hdl.handle.net/10150/196030


University of Arizona

21. Rial, Nathaniel S. The Adenomatous Polyposis Coli Tumor Suppressor Gene Suppresses Deoxycholic Acid Induction of the Chemotactic Cytokine CXCL8 in Human Colorectal Cancer .

Degree: 2007, University of Arizona

 Elevated deoxycholic acid (DCA) and mutations in the Adenomatous Polyposis Coli (APC) tumor suppressor gene have been associated with increased risk of colorectal cancer (CRC).… (more)

Subjects/Keywords: APC; DCA; CXCL8; colorectal cancer

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

APA (6th Edition):

Rial, N. S. (2007). The Adenomatous Polyposis Coli Tumor Suppressor Gene Suppresses Deoxycholic Acid Induction of the Chemotactic Cytokine CXCL8 in Human Colorectal Cancer . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/194449

Chicago Manual of Style (16th Edition):

Rial, Nathaniel S. “The Adenomatous Polyposis Coli Tumor Suppressor Gene Suppresses Deoxycholic Acid Induction of the Chemotactic Cytokine CXCL8 in Human Colorectal Cancer .” 2007. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/194449.

MLA Handbook (7th Edition):

Rial, Nathaniel S. “The Adenomatous Polyposis Coli Tumor Suppressor Gene Suppresses Deoxycholic Acid Induction of the Chemotactic Cytokine CXCL8 in Human Colorectal Cancer .” 2007. Web. 12 Nov 2019.

Vancouver:

Rial NS. The Adenomatous Polyposis Coli Tumor Suppressor Gene Suppresses Deoxycholic Acid Induction of the Chemotactic Cytokine CXCL8 in Human Colorectal Cancer . [Internet] [Doctoral dissertation]. University of Arizona; 2007. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/194449.

Council of Science Editors:

Rial NS. The Adenomatous Polyposis Coli Tumor Suppressor Gene Suppresses Deoxycholic Acid Induction of the Chemotactic Cytokine CXCL8 in Human Colorectal Cancer . [Doctoral Dissertation]. University of Arizona; 2007. Available from: http://hdl.handle.net/10150/194449


University of Arizona

22. Wozniak, Ryan Joseph. Mechanisms Underlying the Pharmacologic Reversal of Genetic and Epigenetic Components of Tumor Suppressor Gene Silencing in Human Breast Cancer .

Degree: 2006, University of Arizona

 In women, tumors of the breast remain the most frequently diagnosed malignancy and the second leading cause of cancer-related deaths. One of the hallmarks of… (more)

Subjects/Keywords: Pharmacology; Cancer; Genetics; Epigenetics

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

APA (6th Edition):

Wozniak, R. J. (2006). Mechanisms Underlying the Pharmacologic Reversal of Genetic and Epigenetic Components of Tumor Suppressor Gene Silencing in Human Breast Cancer . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/195193

Chicago Manual of Style (16th Edition):

Wozniak, Ryan Joseph. “Mechanisms Underlying the Pharmacologic Reversal of Genetic and Epigenetic Components of Tumor Suppressor Gene Silencing in Human Breast Cancer .” 2006. Doctoral Dissertation, University of Arizona. Accessed November 12, 2019. http://hdl.handle.net/10150/195193.

MLA Handbook (7th Edition):

Wozniak, Ryan Joseph. “Mechanisms Underlying the Pharmacologic Reversal of Genetic and Epigenetic Components of Tumor Suppressor Gene Silencing in Human Breast Cancer .” 2006. Web. 12 Nov 2019.

Vancouver:

Wozniak RJ. Mechanisms Underlying the Pharmacologic Reversal of Genetic and Epigenetic Components of Tumor Suppressor Gene Silencing in Human Breast Cancer . [Internet] [Doctoral dissertation]. University of Arizona; 2006. [cited 2019 Nov 12]. Available from: http://hdl.handle.net/10150/195193.

Council of Science Editors:

Wozniak RJ. Mechanisms Underlying the Pharmacologic Reversal of Genetic and Epigenetic Components of Tumor Suppressor Gene Silencing in Human Breast Cancer . [Doctoral Dissertation]. University of Arizona; 2006. Available from: http://hdl.handle.net/10150/195193

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