+publisher:"Texas A&M University" +contributor:("Allred, Clinton D")

Texas A&M University

1. Yang, Liyi. Estrogenic Properties of Sorghum Phenolics: Possible Role in Colon Cancer Prevention.

Degree: PhD, Food Science and Technology, 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/151237

► Consumption of whole grains has been linked to reduced risk of colon cancer. This study determined estrogenic activity of sorghum phenolic extracts of different phenolic… (more)

▼ Consumption of whole grains has been linked to reduced risk of colon cancer. This study determined estrogenic activity of sorghum phenolic extracts of different phenolic profiles and identified possible estrogenic compounds in sorghum in vitro, as well as evaluated the potential of estrogenic sorghum phenolic extracts to prevent colon carcinogenesis in vivo. The thermal stability of sorghum 3-deoxyanthocyanins was also studied, to determine their suitability as functional food colorants. White and TX430 (black) sorghum extracts showed estrogenic activity in cell models predominantly expressing estrogen receptor-α (ERα) or ERβ at 5 and 10 µg/mL, respectively. The same treatments led to induction of apoptosis in cells expressing ERβ. The red TX2911 sorghum did not possess these activities. Compositional analysis revealed differences in flavones and flavanones. Flavones with estrogen-like properties, i.e. luteolin and apigenin, were detected in White and TX430 (black) sorghum extracts, but not in red TX2911 extract. Naringenin, a flavanone known to antagonize ERα signalling, was only detected in the red TX2911 extract. Additional experiments with sorghum extracts of distinct flavones/flavanone ratio, as well as with pure apigenin and naringenin, suggested that flavones are the more potent ERβ agonists in sorghum. On the other hand, 3-deoxyanthocyanins were probably not estrogenic. Estrogenic white and black sorghum phenolic extracts (fed at 1% level in the diet) reduced the number of azoxymethane induced colon premalignant lesion (aberrant crypt foci) by 39.3% and 14.7%, respectively, in ovariectomized mice. Further studies are needed to elucidate the protective mechanisms induced by these sorghum extracts. Sorghum 3-deoxyanthocyanins retained good color stability after 30 minutes of heat treatment at 121 °C under pressure: More than 80% of color retained in pH 1 and 2 HCl and citric acid solutions, and 39-84% retained from pHs 3-7. Formic acid negatively affected the color stability at pH 1 and pH 2 due to its reducing capacity. Methoxylation decreased the thermal stability of 3-deoxyanthocyanins. The heat stability of 3-deoxyanthocyanins indicates good potential for food use. Overall, the inherent estrogenic activity of specific sorghum phenolic extracts is a likely mechanism for colon cancer prevention. Further studies are needed to assess physiologically relevant dietary level of sorghum phenolics for prevention of colon cancer, and effect of food processing on the activity and bioavailability of the chemopreventive components. Advisors/Committee Members: Awika, Joseph M. (advisor), Allred, Clinton D. (advisor), Talcott, Stephen T. (committee member), Rooney, Lloyd W. (committee member).

Subjects/Keywords: sorghum; polyphenols; estrogenic activity; colon cancer

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APA (6^th Edition):

Yang, L. (2013). Estrogenic Properties of Sorghum Phenolics: Possible Role in Colon Cancer Prevention. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151237

Chicago Manual of Style (16^th Edition):

Yang, Liyi. “Estrogenic Properties of Sorghum Phenolics: Possible Role in Colon Cancer Prevention.” 2013. Doctoral Dissertation, Texas A&M University. Accessed March 01, 2021. http://hdl.handle.net/1969.1/151237.

MLA Handbook (7^th Edition):

Yang, Liyi. “Estrogenic Properties of Sorghum Phenolics: Possible Role in Colon Cancer Prevention.” 2013. Web. 01 Mar 2021.

Vancouver:

Yang L. Estrogenic Properties of Sorghum Phenolics: Possible Role in Colon Cancer Prevention. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1969.1/151237.

Council of Science Editors:

Yang L. Estrogenic Properties of Sorghum Phenolics: Possible Role in Colon Cancer Prevention. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151237

Texas A&M University

2. Yoo, Gyhye. Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer.

Degree: PhD, Nutrition, 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/156457

► Estrogen is a female sex hormone that has a variety of biologic actions via modulation of gene expression through estrogen receptors (ERs). The protective effect… (more)

▼ Estrogen is a female sex hormone that has a variety of biologic actions via modulation of gene expression through estrogen receptors (ERs). The protective effect of estradiol (E2) and estrogen signaling in colon cancer has been demonstrated in epidemiological and clinical data as well as animal experiments. The overall aim of this series of studies is to determine the protective mechanism of estrogen signaling activated by E2 and phytoestrogens on colitis and colon cancer. First, the estrogenic effect of novel phytoestrogens, trigonelline (Trig) and 3,3-diindolylmethane (DIM) was determined in non-malignant colonocytes (YAMCs). Both molecules decreased cell growth of YAMCs, but their mechanisms of action were distinct from E2. Trig increased apoptosis by functional ERs without direct binding to ERs while DIM altered the expression of target genes of ERs via increased ER transcriptional activity. These data suggest that phytoestrogens could activate estrogen signaling through unique mechanisms. Second, the protective effect of estrogen signaling on colitis and colitis associated colon cancer (CAC) was demonstrated in vitro and in vivo. In the in vitro study, IL-6 induced cell growth was observed, and E2 and genistein (GEN) treatment inhibited IL-6 actions via an increase of apoptosis and modulation of gene expression related to estrogen signaling. In the in vivo colitis experiment, chronic inflammation damaged the colon, but E2 treatment increased the recovery of the damaged colon via an increase of cell proliferation with modulation of cytokines. However, GEN treatment exacerbated the damage on chronic inflammation. In the CAC model, E2 and GEN treatment suppressed the formation of aberrant crypt foci (ACF), premalignant lesions. These data suggest that E2 protects the colon and colon epithelial cells, and the protective mechanism of estrogen signaling differs depending on the type of injury and local conditions. Lastly, the interaction of estrogen signaling and the p53 pathway was studied using intestinal epithelial cell-specific p53 knockout mice (Tp53^ΔIEC). The protective effect of E2 in Tp53^ΔIEC mice was observed, suggesting that the suppression of ACF by estrogen signaling is partially independent of the p53 pathway. Overall, estrogen signaling has a protective property against colitis and colon cancer but the protective mechanism of estrogen signaling could be changed from apoptosis to proliferation depending on the condition of the colon. In addition, each phytoestrogen has a distinct and unique way of influencing the colon. These data help clarify the role and the mechanism of estrogen signaling on colon cancer. Advisors/Committee Members: Allred, Clinton D (advisor), Chapkin, Robert S (committee member), Talcott, Stephen T (committee member), Weeks, Brad R (committee member).

Subjects/Keywords: Estrogen Signaling; Phytoestrogens; Colitis; Colon Cancer; IL-6; p53

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

APA (6^th Edition):

Yoo, G. (2015). Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/156457

Chicago Manual of Style (16^th Edition):

Yoo, Gyhye. “Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer.” 2015. Doctoral Dissertation, Texas A&M University. Accessed March 01, 2021. http://hdl.handle.net/1969.1/156457.

MLA Handbook (7^th Edition):

Yoo, Gyhye. “Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer.” 2015. Web. 01 Mar 2021.

Vancouver:

Yoo G. Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer. [Internet] [Doctoral dissertation]. Texas A&M University; 2015. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1969.1/156457.

Council of Science Editors:

Yoo G. Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer. [Doctoral Dissertation]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/156457

Texas A&M University

3. Armstrong, Cameron Michelle. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.

Degree: PhD, Nutrition, 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/151883

► Epidemiological studies suggest pre-menopausal women have a reduced risk for sporadic and inflammation-associated colon cancer compared to post-menopausal women and men. The studies presented herein… (more)

▼ Epidemiological studies suggest pre-menopausal women have a reduced risk for sporadic and inflammation-associated colon cancer compared to post-menopausal women and men. The studies presented herein aim to determine the protective mechanisms of estradiol (E2) during sporadic and inflammation-associated colonic carcinogenesis. When investigating the role of E2 and fish oil at the earliest stage of sporadic colon cancer development, E2 had no effect on DNA adduct formation while dietary fish oil significantly reduced DNA adduct formation. Contrarily, E2 significantly induced apoptosis of damaged colonocytes while fish oil was not protective. In an in vivo model of inflammation-associated colon carcinogenesis with E2 administered following induction of DNA damage and initiation of inflammation, E2 treatment was associated with decreased colon tumor size and number in wild type (WT) but not estrogen receptor (ER) β knockout (ERβKO) mice. Interestingly, apoptosis was reduced and proliferation increased by E2 in these tumors in WT mice. This may be due to the altered ER expression in these tissues as the tumors developed, with ERβ expression decreasing concomitantly with ERα expression increasing. Contrary to the protective effect of E2 on inflammation-associated colon tumor formation, which was dependent on ERβ, during acute inflammation in the colon E2 was protective against inflammation in both WT and ERβKO mice and injury in ERβKO mice. The protection against inflammation is likely due to the reduction of pro-inflammatory cytokine expression by E2. Apoptosis and proliferation were decreased and increased in the proximal and distal colon respectively in ERβKO mice. In vitro studies further elucidated the roles of ERα and ERβ in colonocytes. E2 and ERβ, but not ERα, specific agonists reduced cell number and induce apoptosis in nonmalignant colonocytes. This effect was lost in the presence of mutated p53. In ERα overexpressed nonmalignant colonocytes, E2 had no effect on cell number while ERβ agonist and ERα agonists decreased and increased cell number respectively. These studies suggest that E2 is protective in the colon and ERβ is required for protection against carcinogenesis but not protection against inflammation. Additionally, the protection against colon carcinogenesis is likely p53 mediated. Advisors/Committee Members: Allred, Clinton D (advisor), Turner, Nancy D (committee member), Villalobos, Alice R (committee member), Weeks, Brad R (committee member).

Subjects/Keywords: colon cancer; estradiol; estrogen receptor; inflammation

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

APA (6^th Edition):

Armstrong, C. M. (2013). The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151883

Chicago Manual of Style (16^th Edition):

Armstrong, Cameron Michelle. “The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.” 2013. Doctoral Dissertation, Texas A&M University. Accessed March 01, 2021. http://hdl.handle.net/1969.1/151883.

MLA Handbook (7^th Edition):

Armstrong, Cameron Michelle. “The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.” 2013. Web. 01 Mar 2021.

Vancouver:

Armstrong CM. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1969.1/151883.

Council of Science Editors:

Armstrong CM. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151883

Texas A&M University

4. Weige, Charles. Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development.

Degree: PhD, Genetics, 2012, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838

► Hormone replacement therapy and estrogen replacement therapy have shown the ability to reduce risk of colon cancer development in clinical and animal studies, but in… (more)

▼ Hormone replacement therapy and estrogen replacement therapy have shown the ability to reduce risk of colon cancer development in clinical and animal studies, but in vitro research has been unable to reproduce an estradiol (E2) induced response in colon cancer cell lines. We demonstrated that young adult mouse colonocytes (YAMC, non-malignant colonocytes) exhibit an anti-proliferative response to E2 treatment. These cells demonstrate reduced cell culture growth and increased apoptosis in response to E2. YAMC cells containing an activated Ras mutation are considered to be malignantly transformed, and lose the ability to respond to E2 treatment. Fulvestrant (ICI) was used as an estrogen receptor antagonist to determine that these results were estrogen receptor mediated. Furthermore, this effect was demonstrated to require the presence of ER? through the use of a transgenic ERbeta knockout mouse. In these mice, the presence of E2 significantly reduced the formation of azoxymethane induced premalignant lesions. Since YAMC cells exhibit an anti-proliferative response to E2 treatment, we utilized isogenic YAMC cell lines with and without a dominant negative p53 mutation to demonstrate that this E2 induced action involves p53 activity. E2 treatment results in increased p53 transcriptional activity and a pro-apoptotic change in expression of p53 downstream targets. Presence of the dominant negative p53 mutant nullifies these effects of E2 treatment. The involvement of p53 in the previously described protection against AOM induced premalignant lesions, was investigated using wild type and heterozygous p53 knockout (Het p53KO) mice. The reduction in p53 protein corresponded to reduced effectiveness of E2 treatment on the prevention of premalignant lesion formation in Het p53KO mice. In summary, our data indicate that E2 treatment induces anti-proliferative responses in non-malignant colonocytes and protects against the formation of carcinogen-induced premalignant lesions. These effects require the presence of functional ER? and p53. Further studies are required to more thoroughly elucidate the specific interactions and downstream effects of ER? and p53 in response to E2 stimulation. Advisors/Committee Members: Allred, Clinton D. (advisor), Chapkin, Robert S. (committee member), Dabney, Alan R. (committee member), Lupton, Joanne R. (committee member).

Subjects/Keywords: Estrogen; estrogen receptor beta; colon cancer; p53; apoptosis; aberrant crypt foci

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

APA (6^th Edition):

Weige, C. (2012). Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838

Chicago Manual of Style (16^th Edition):

Weige, Charles. “Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development.” 2012. Doctoral Dissertation, Texas A&M University. Accessed March 01, 2021. http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838.

MLA Handbook (7^th Edition):

Weige, Charles. “Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development.” 2012. Web. 01 Mar 2021.

Vancouver:

Weige C. Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development. [Internet] [Doctoral dissertation]. Texas A&M University; 2012. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838.

Council of Science Editors:

Weige C. Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development. [Doctoral Dissertation]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838

5. Billimek, Autumn Renee. Estradiol and Genistein Alter Cellular Physiology of Non-Malignant Colonocytes.

Degree: MS, Nutrition, 2012, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2011-08-9858

► Many studies show that estradiol (E2) and consumption of soy and its primary phytoestrogen component genistein (GEN) can inhibit the formation of colon tumors. However,… (more)

Subjects/Keywords: Estradiol; Genistein; Colon Cancer

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

APA (6^th Edition):

Billimek, A. R. (2012). Estradiol and Genistein Alter Cellular Physiology of Non-Malignant Colonocytes. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2011-08-9858

Chicago Manual of Style (16^th Edition):

Billimek, Autumn Renee. “Estradiol and Genistein Alter Cellular Physiology of Non-Malignant Colonocytes.” 2012. Masters Thesis, Texas A&M University. Accessed March 01, 2021. http://hdl.handle.net/1969.1/ETD-TAMU-2011-08-9858.

MLA Handbook (7^th Edition):

Billimek, Autumn Renee. “Estradiol and Genistein Alter Cellular Physiology of Non-Malignant Colonocytes.” 2012. Web. 01 Mar 2021.

Vancouver:

Billimek AR. Estradiol and Genistein Alter Cellular Physiology of Non-Malignant Colonocytes. [Internet] [Masters thesis]. Texas A&M University; 2012. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2011-08-9858.

Council of Science Editors:

Billimek AR. Estradiol and Genistein Alter Cellular Physiology of Non-Malignant Colonocytes. [Masters Thesis]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2011-08-9858

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