Advanced search options

Advanced Search Options 🞨

Browse by author name (“Author name starts with…”).

Find ETDs with:

in
/  
in
/  
in
/  
in

Written in Published in Earliest date Latest date

Sorted by

Results per page:

Sorted by: relevance · author · university · dateNew search

You searched for +publisher:"Penn State University" +contributor:("Karam E El Bayoumy, Dissertation Advisor/Co-Advisor"). Showing records 1 – 3 of 3 total matches.

Search Limiters

Last 2 Years | English Only

No search limiters apply to these results.

▼ Search Limiters


Penn State University

1. Zhang, Shang-min. Oral Cancer Induced by The Tobacco Carcinogen Dibenzo[a,l]pyrene in Mice.

Degree: 2013, Penn State University

Oral cancer is the most common type of head and neck cancer, which is the sixth most common cancer worldwide. More than 90% of oral cancers are a type called oral squamous cell carcinoma (OSCC). Tobacco use is the most important risk factor. Chronic and/or heavy use of alcohol is another major risk factor. Early detection and prevention of oral cancer is very pivotal. Progress in the prevention and control of oral cancer has been hampered by the lack of appropriate animal models that could reflect human exposure. Therefore, experimental animal models that can accurately represent the cellular and molecular changes associated with the initiation and progression of human oral cancer are of crucial importance to better understand the mechanisms of oral carcinogenesis and to identify novel chemopreventive, as well as chemotherapeutic agents. We recently developed a novel mouse model to study oral carcinogenesis. We showed for the first time that direct application of DB[a,l]P into the oral cavity, induced SCC in oral tissues; (±)-anti-DB[a,l]PDE-diol epoxide, the ultimate metabolite of DB[a,l]P, is a remarkably potent carcinogen in the oral cavity (both oral tissues and tongue). The mechanisms that can account for oral cancer-induced by this tobacco carcinogen are the focus of this dissertation. Our working hypothesis is that both genetic and epigenetic alterations induced by DB[a,l]P can contribute to the development of oral cancer. To test our hypothesis, we focused initially on assessing the effect of this carcinogen on genetic alterations. We have developed a new stable isotope dilution HPLC-MS/MS method to identify and quantify DB[a,l]PDE-dA and -dG adducts in oral tissue of mice. Our method is sensitive enough to detect DNA adducts in vivo. We detected (-)-anti-cis- and (-)-anti-trans-DB[a,l]PDE-N6-dA and (-)-anti-cis- and (-)-anti-trans-DB[a,l]PDE-N2-dG adducts in oral and tongue tissues of mice treated with DB[a,l]P; the results indicate that the levels of dA adducts are significantly higher than dG adducts and that DB[a,l]P is predominantly metabolized to (-)-anti-DB[a,l]PDE. Using immunohistochemistry (IHC), we have shown over-expression of p53 and COX-2 protein in OSCC and dysplastic tissues induced by DB[a,l]P and DB[a,l]PDE in mice. P53 protein overexpression detected by IHC may result from p53 gene mutation or exposure to genotoxic stress. To determine whether p53 over-expression is, in part, due to p53 mutations, Exons 5 to 8 of p53 from representative tumor tissues, were analyzed by polymerase chain reaction single-strand conformation polymorphisms (PCR-SSCP) and direct sequencing. G:C→T:A transversion was detected in Exon 5, leading to mutation of codon 155 Arg to Leu; A:T → T:A transversion was detected in Exon 7, resulting in mutation of codon 232 Lys to stop codon. To further test our hypothesis, we examined the epigenetic effect of DB[a,l]P exposure. Methylation specific PCR and bisulfite sequencing were used to examine methylation alteration of p16 and RAR-β promoters. Promoter… Advisors/Committee Members: Karam E El Bayoumy, Dissertation Advisor/Co-Advisor, Kristin Ann Eckert, Committee Member, John Peter Richie Jr., Committee Member, Thomas E Spratt, Committee Member.

Subjects/Keywords: Oral Cancer; Tobacco Carcinogen; DB[a; l]P; DNA adducts; LC-MS/MS; p53 mutations; epigenetics; alcohol; chemoprevention

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Zhang, S. (2013). Oral Cancer Induced by The Tobacco Carcinogen Dibenzo[a,l]pyrene in Mice. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/18930

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):

Zhang, Shang-min. “Oral Cancer Induced by The Tobacco Carcinogen Dibenzo[a,l]pyrene in Mice.” 2013. Thesis, Penn State University. Accessed February 28, 2021. https://submit-etda.libraries.psu.edu/catalog/18930.

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

MLA Handbook (7th Edition):

Zhang, Shang-min. “Oral Cancer Induced by The Tobacco Carcinogen Dibenzo[a,l]pyrene in Mice.” 2013. Web. 28 Feb 2021.

Vancouver:

Zhang S. Oral Cancer Induced by The Tobacco Carcinogen Dibenzo[a,l]pyrene in Mice. [Internet] [Thesis]. Penn State University; 2013. [cited 2021 Feb 28]. Available from: https://submit-etda.libraries.psu.edu/catalog/18930.

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

Council of Science Editors:

Zhang S. Oral Cancer Induced by The Tobacco Carcinogen Dibenzo[a,l]pyrene in Mice. [Thesis]. Penn State University; 2013. Available from: https://submit-etda.libraries.psu.edu/catalog/18930

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


Penn State University

2. Skibinski, Christine G. preclinical investigations into the role of omega-3 fatty acids for breast cancer prevention.

Degree: 2015, Penn State University

As discussed in Chapter 1, Breast cancer is the second leading cause of cancer death in women in the United States, with about 2 million women at high risk for developing the disease. A current strategy, approved by the FDA, for breast cancer prevention is the daily administration of selective estrogen receptor modulators(SERMS), tamoxifen and raloxifene. These SERMS have proven to be effective at reducing breast cancer incidence in women that are at high risk by 50% and 38%, respectively. However, these agents are poorly accepted as oral chemopreventives even by women at high risk for breast cancer because of concerns of side effects which include thromboembolic events and an increase in endometrial cancers. Furthermore, both agents are ineffective against the more aggressive estrogen receptor negative tumors. A series of experiments have been conducted in our laboratories to test the hypothesis that chemoprevention can be improved by combining SERMS with agents with different mechanisms of action. Such an approach can allow the use of low doses of SERMS and thus reduce their side effects. Literature data provide some support of the protective effects of omega-3 fatty acids against the development of several cancers, including breast cancer. However, the results remain inconsistent which could be due to confounding variables. These confounding variables which have been reported by our group include omega-3:omega-6(n-3:n-6) ratio and caloric intake. A previous study conducted in our laboratories showed that high ratios of omega-3:omega-6 fatty acids(25:1 n-3:n-6) are required to inhibit mammary carcinogenesis in the rat and such high ratios of omega-3:omega-6 fatty acids potentiated the chemopreventive efficacy of tamoxifen. Studies conducted in Chapter 2 were aimed to test the hypothesis that by using a proteomics approach, novel proteins can be identified that can provide insights into the molecular mechanism by which high ratios of omega-3:omega-6 fatty acids inhibit mammary carcinogenesis. We further hypothesize that proteins identified in a minimally invasive fashion can be used for early detection and to monitor the efficacy of the chemopreventive agents. We used an isobaric Tagging for Relative and Absolute Quantitation (iTRAQ) method to provide insights into the mechanism, at the protein level, responsible for the chemopreventive action of the high omega-3:omega-6 fatty acid ratios in the absence and presence of tamoxifen in the 1-methyl-1-nitrosourea(MNU)-induced mammary tumor model in the rat; selective proteins were further validated by western blotting. Compared to control (n-3:n-6, 1:1) diet, both 10:1 and 25:1 n-3:n-6 diets upregulated plasma vitamin D binding protein, gelsolin, and 14-3-3 sigma, reported to have tumor suppressive effects, whereas alpha-1B-glycoprotein which has been reported to be elevated in the serum of breast cancer patients was decreased. Compared to 25:1 n-3:n-6, the 25:1 n-3:n-6 plus tamoxifen diet downregulated apolipoprotein E, haptoglobin, and… Advisors/Committee Members: Karam E El Bayoumy, Dissertation Advisor/Co-Advisor, Arunangshu Das, Committee Member, Thomas E Spratt, Committee Member, Andrea Manni, Committee Member, Mark Kester, Committee Member.

Subjects/Keywords: Docosahexaenoic Acid; Liposome; Breast Cancer Prevention

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Skibinski, C. G. (2015). preclinical investigations into the role of omega-3 fatty acids for breast cancer prevention. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/26720

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):

Skibinski, Christine G. “preclinical investigations into the role of omega-3 fatty acids for breast cancer prevention.” 2015. Thesis, Penn State University. Accessed February 28, 2021. https://submit-etda.libraries.psu.edu/catalog/26720.

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

MLA Handbook (7th Edition):

Skibinski, Christine G. “preclinical investigations into the role of omega-3 fatty acids for breast cancer prevention.” 2015. Web. 28 Feb 2021.

Vancouver:

Skibinski CG. preclinical investigations into the role of omega-3 fatty acids for breast cancer prevention. [Internet] [Thesis]. Penn State University; 2015. [cited 2021 Feb 28]. Available from: https://submit-etda.libraries.psu.edu/catalog/26720.

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

Council of Science Editors:

Skibinski CG. preclinical investigations into the role of omega-3 fatty acids for breast cancer prevention. [Thesis]. Penn State University; 2015. Available from: https://submit-etda.libraries.psu.edu/catalog/26720

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


Penn State University

3. Facompre, Nicole Danielle. Organoselenium-mediated alteration of prostate cancer cell signaling pathways .

Degree: 2010, Penn State University

Prostate cancer is the most commonly diagnosed malignancy and second leading cause of cancer related death in men in the United States. The lack of treatment for “worried well” patients with prostatic intraepithelial neoplasia (a premalignant condition) combined with issues of recurrence and hormone resistance present significant obstacles to prostate cancer survivorship. The long latency of prostate cancer provides opportunity to intervene with mechanistically-based agents at various stages of disease progression. A number of signaling cascades have been shown to play important roles in prostate cancer development and progression, including the androgen receptor, PI3K/Akt, and mammalian target of rapamycin (mTOR) signaling pathways. Crosstalk between the androgen receptor and Akt pathways is thought to contribute to progression and hormone refractory disease. Studies have also implicated the mammalian target of rapamycin (mTOR) signaling pathway in the progression of prostate cancer and its transition to androgen independence, suggesting mTOR as a potential target for new therapies. Selenium, an essential nutrient and known antioxidant, has been shown in epidemiologic and preclinical studies to be protective against prostate cancer. However, clinical intervention trials with selenium have thus far had contradictory outcomes and the anti-cancer mechanisms of selenium compounds are not well understood. Studies consistently show that dose and form are critical factors in the actions of selenium compounds. In the present investigation we compare the effects of two structurally distinct organoselenium compounds naturally occurring selenomethionine (SM) and synthetic 1,4-phenylenebis(methylene)selenocyanate (p-XSC) on cell growth, apoptosis, and signaling in androgen responsive (AR) and androgen independent (AI) human prostate cancer cells. We have found that, in contrast to SM, p-XSC dose-dependently inhibits viability, induces apoptosis, and modulates critical signaling molecules in both AR and AI cells. p-XSC effectively inhibits androgen receptor expression and transcriptional activity, Akt phosphorylation, and Akt-specific phosphorylation of the androgen receptor. We also show that p-XSC preferentially inhibits mTOR complex 2 (mTORC2) signaling in AI cells, a novel potential target for selenium in prostate cancer. Based on these findings, we hypothesized that the combination of p-XSC with rapamycin, which primarily targets mTOR complex 1 (mTORC1), may be a superior approach to inhibit prostate cancer cell growth than either agent alone. Drug combination strategies can offer a number of advantages to single-agent therapies including the enhancement of efficacy, the reduction of dose and toxicity, and the management of drug resistance. Our data show that inhibition of AI cell viability and mTOR signaling is significantly enhanced by combining p-XSC and rapamycin, compared with each agent individually. We propose that these agents achieve this effect, in part, by targeting the two distinct arms of the… Advisors/Committee Members: Karam E El Bayoumy, Dissertation Advisor/Co-Advisor, Karam E El Bayoumy, Committee Chair/Co-Chair, Raghu Sinha, Committee Member, Jeffrey Maurice Peters, Committee Member, Thomas E Spratt, Committee Member, Sergei A Grigoryev, Committee Member.

Subjects/Keywords: androgen receptor; selenium; prostate cancer; Akt

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Facompre, N. D. (2010). Organoselenium-mediated alteration of prostate cancer cell signaling pathways . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/11123

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):

Facompre, Nicole Danielle. “Organoselenium-mediated alteration of prostate cancer cell signaling pathways .” 2010. Thesis, Penn State University. Accessed February 28, 2021. https://submit-etda.libraries.psu.edu/catalog/11123.

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

MLA Handbook (7th Edition):

Facompre, Nicole Danielle. “Organoselenium-mediated alteration of prostate cancer cell signaling pathways .” 2010. Web. 28 Feb 2021.

Vancouver:

Facompre ND. Organoselenium-mediated alteration of prostate cancer cell signaling pathways . [Internet] [Thesis]. Penn State University; 2010. [cited 2021 Feb 28]. Available from: https://submit-etda.libraries.psu.edu/catalog/11123.

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

Council of Science Editors:

Facompre ND. Organoselenium-mediated alteration of prostate cancer cell signaling pathways . [Thesis]. Penn State University; 2010. Available from: https://submit-etda.libraries.psu.edu/catalog/11123

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

.