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You searched for subject:(Adenocarcinoma metabolism 60). Showing records 1 – 3 of 3 total matches.

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1. Steg, Adam. Analysis of the hedgehog pathway in pancreatic adenocarcinoma.

Degree: PhD, 2008, University of Alabama – Birmingham

Pancreatic adenocarcinoma (PAC) is the fourth leading cause of cancer mortality in the United States. Despite the use of highly aggressive treatment regimens (surgery, chemotherapy and radiation), almost all patients succumb to metastatic disease within 6-10 months of diagnosis. The hedgehog (HH) signaling pathway was originally discov-ered to play a critical role in mammalian embryological development. Interestingly, re-cent studies have suggested that aberrant expression of this pathway is involved in the initiation and continued growth of PAC. Small molecules that antagonize the transmem-brane protein Smoothened (Smo), a critical signaling component of the HH pathway, have proven effective in decreasing PAC growth both in vitro and in vivo and show promise as a new therapeutic strategy. Data from our laboratory indicate the HH path-way is overexpressed in pancreatic cancers and Smo antagonism decreases pancreatic cancer cell growth in vitro. The major accomplishments of this dissertation research in-clude (1) the validation of a recently developed technique known as Taqman low-density array (TLDA) which can be used to analyze the expression of multiple genes in a single RNA sample, (2) the identification of novel, tumor-associated genes through an extensive characterization of the HH pathway and its transcriptional targets in PAC clinical speci-mens (both surgically resected tissues and fine-needle biopsies) and (3) the identification of genes associated with in vitro response to cyclopamine, a selective HH pathway inhibi-tor, in human pancreatic cancer cell lines. These findings contribute to the growing characterization of the HH pathway in pancreatic cancer etiology and may provide a basis for future clinical applications in which PAC patients most likely to respond to HH pathway antagonists could be identified based upon gene expression profiling, thereby maximizing the efficacy of this type of therapy.

xiii, 149 p. : ill., digital, PDF file

Pharmacology and Toxicology

Joint Health Sciences

Hedgehog Pancreatic Cancer GLI3

UNRESTRICTED

Advisors/Committee Members: Johnson, Martin R., Buchsbaum, Donald J.<br>, Frost, Andra R.<br>, Ruppert, J. Michael <br>, Smith, Jeffrey B..

Subjects/Keywords: Adenocarcinoma  – metabolism <; br>; Adenocarcinoma  – pathology <; br>; Hedgehog Proteins  – metabolism <; br>; Pancreatic Neoplasms  – metabolism <; br>; Pancreatic Neoplasms  – pathology

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

APA (6th Edition):

Steg, A. (2008). Analysis of the hedgehog pathway in pancreatic adenocarcinoma. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,290

Chicago Manual of Style (16th Edition):

Steg, Adam. “Analysis of the hedgehog pathway in pancreatic adenocarcinoma.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 11, 2019. http://contentdm.mhsl.uab.edu/u?/etd,290.

MLA Handbook (7th Edition):

Steg, Adam. “Analysis of the hedgehog pathway in pancreatic adenocarcinoma.” 2008. Web. 11 Dec 2019.

Vancouver:

Steg A. Analysis of the hedgehog pathway in pancreatic adenocarcinoma. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2019 Dec 11]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,290.

Council of Science Editors:

Steg A. Analysis of the hedgehog pathway in pancreatic adenocarcinoma. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,290

2. Huffman, Derek M. Calorie restriction, exercise and body fat : effects on cancer and markers of longevity.

Degree: PhD, 2007, University of Alabama – Birmingham

The benefits of calorie restriction (CR) have historically been attributed to a reduction in food intake. More recently, reduced fat stores have been proposed as an important mediator of CR, spurring interest into the potential for changes in energy expenditure and body composition as a CR mimetic. In order to better understand the relationship of body composition, energetics, cancer and longevity, four separate studies were performed. In Experimental Aim 1, a mouse model of prostate cancer (TRAMP) was used to determine if leanness rather than reduced food intake is responsible for the cancer-preventative effect of CR. It was found that increasing energy expenditure via thermoregulation under fixed-food intake conditions, resulted in smaller, leaner mice, which had less cancer incidence and progression. This finding suggests that in terms of cancer prevention, leanness rather calorie intake per se, is more closely associated with the benefits associated with CR. In Experimental Aim 2, results suggest that the longevity protein SIRT1 is elevated in mouse and human prostate cancer, and may be paradoxically implicated in tumor promotion. Experimental Aim 3 found that liver SIRT1 was not significantly affected by acute or chronic exercise. Finally, the results from Aim 4 found that exercised mice were significantly leaner than their weight-matched counterparts which were calorie restricted. However, CR and exercise had disparate effects on longevity biomarkers, including more favorable changes in the insulin/IGF-1 axis with CR, while exercisers had less DNA damage. The results of this experiment imply that the inability of exercise in prior studies to increase lifespan could be due to a failure to fully mimic the physiologic effects of CR. More studies are needed to determine if the inability of exercise to fully mimic CR is inherent to exercise itself, or if the life-prolonging action of CR work independently of changes in energy balance and body composition.

1 online resource (x, 183 p. : ill., digital, PDF file)

Nutrition Sciences;

Health Professions;

exercise cancer aging longevity caloric restriction obesity

UNRESTRICTED

Advisors/Committee Members: Nagy, Tim R., Bamman, Marcas M.<br>, Elgavish, Ada<br>, Grizzle, William E.<br>, Piyathilake, Chandrika J.<br>, Tollefsbol, Trygve O..

Subjects/Keywords: Adenocarcinoma<; br>; Aging<; br>; Biological Markers  – metabolism<; br>; Caloric Restriction<; br>; Gene Expression Regulation, Neoplastic<; br>; Physical Conditioning, Animal  – physiology<; br>; Prostatic Neoplasms<; br>; Sirtuins  – genetics

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

APA (6th Edition):

Huffman, D. M. (2007). Calorie restriction, exercise and body fat : effects on cancer and markers of longevity. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,596

Chicago Manual of Style (16th Edition):

Huffman, Derek M. “Calorie restriction, exercise and body fat : effects on cancer and markers of longevity.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 11, 2019. http://contentdm.mhsl.uab.edu/u?/etd,596.

MLA Handbook (7th Edition):

Huffman, Derek M. “Calorie restriction, exercise and body fat : effects on cancer and markers of longevity.” 2007. Web. 11 Dec 2019.

Vancouver:

Huffman DM. Calorie restriction, exercise and body fat : effects on cancer and markers of longevity. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2019 Dec 11]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,596.

Council of Science Editors:

Huffman DM. Calorie restriction, exercise and body fat : effects on cancer and markers of longevity. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,596

3. Rayburn, Elizabeth R. Novel immunomodulatory oligonucleotides for cancer therapy.

Degree: PhD, 2007, University of Alabama – Birmingham

Prostate and colon cancer are two of the most prevalent cancers in the United States. Cancer therapy, including surgery, chemotherapy, radiotherapy and biological therapy, often results in severe side effects. New therapies are urgently needed to improve patient survival and quality of life. A new immunotherapy is being developed that makes use of Toll-like receptor 9, which recognizes certain sequences of bacterial and synthetic DNA. TLR9 agonists stimulate the immune system, and have been suggested to have anti-cancer effects. The objective of my dissertation research was to investigate the anti-cancer effects and mechanisms of action of an immunomodulatory oligonucleotide (IMO) agonist of TLR9 that has novel structural and chemical modifications. The anti-tumor activity of the IMO was evaluated in models of prostate and colon cancer alone and in combination with conventional therapies. The expression of TLR9 in cancer cells was also examined, as were the in vitro effects of the IMO. Major discoveries of the dissertation research include: 1) treatment with the IMO led to potent anti-tumor effects, inhibiting tumor growth in all in vivo models of prostate and colon cancer; 2) combination with the IMO led to enhanced effects following treatment with chemotherapeutic agents or radiation; 3) both TLR9 mRNA and protein were expressed in these cancer cells; 4) the IMO increased apoptosis, and decreased proliferation and survival in prostate and colon cancer cells and 5) the IMO is effective against tumors regardless of their p53 or hormone receptor status. Additional studies have shown that the IMO has anti-cancer effects in models of breast and lung cancer, further demonstrating that TLR9 agonism presents a viable new option for cancer therapy. Future studies of TLR9 agonism focused on determining its mechanism(s) of action in cancer cells, and studies in other models of cancer would be of interest. In summary, the IMO has potent anti-tumor effects both as monotherapy and in combination with conventional chemotherapeutic agents and radiation, and appears to act directly on cancer cells via TLR9, suggesting that TLR9 agonism may supply the much-needed new therapeutic strategy that would improve survival and quality of life for patients.

xii, 153 p. : ill., digital, PDF file

Pharmacology and Toxicology

Joint Health Sciences

Immunomodulator Oligonucleotide Toll-like Receptor 9 Chemotherapy CpG Cancer

UNRESTRICTED

Advisors/Committee Members: Zhang, Ruiwen, Diasio, Robert B.<br>Posey, James A.<br>Tollefsbol, Trygve O.<br>Wang, Hui.

Subjects/Keywords: Adenocarcinoma  – drug therapy<; br>; Antineoplastic Agents  – therapeutic use<; br>; Antineoplastic Combined Chemotherapy Protocols  – therapeutic use<; br>; Apoptosis  – drug effects<; br>; Colonic Neoplasms  – drug therapy<; br>; Deoxycytidine  – analogs & derivatives<; br>; Immunologic Factors  – therapeutic use<; br>; Oligonucleotides  – therapeutic use<; br>; Prostatic Neoplasms  – drug therapy<; br>; Taxoids  – therapeutic use<; br>; Toll-Like Receptor 9  – agonists<; br>; Tumor Suppressor Protein p53  – metabolism

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

APA (6th Edition):

Rayburn, E. R. (2007). Novel immunomodulatory oligonucleotides for cancer therapy. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,463

Chicago Manual of Style (16th Edition):

Rayburn, Elizabeth R. “Novel immunomodulatory oligonucleotides for cancer therapy.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 11, 2019. http://contentdm.mhsl.uab.edu/u?/etd,463.

MLA Handbook (7th Edition):

Rayburn, Elizabeth R. “Novel immunomodulatory oligonucleotides for cancer therapy.” 2007. Web. 11 Dec 2019.

Vancouver:

Rayburn ER. Novel immunomodulatory oligonucleotides for cancer therapy. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2019 Dec 11]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,463.

Council of Science Editors:

Rayburn ER. Novel immunomodulatory oligonucleotides for cancer therapy. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,463

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