Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2551
Pamela Valera, Luis Alzate-Duque, Nicholas Acuna
{"title":"Abstract 2551: The development of cancer digital videos to increase participation in marginalized communities","authors":"Pamela Valera, Luis Alzate-Duque, Nicholas Acuna","doi":"10.1158/1538-7445.AM2021-2551","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2551","url":null,"abstract":"","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"82 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90630065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2543
Luis Alzate-Duque, Pamela Valera, V. Cueto, Ashna Shome, A. Natale-Pereira
{"title":"Abstract 2543: Venue-based recruitment to increase colorectal screening rates using fecal immunochemical test in Essex County, New Jersey","authors":"Luis Alzate-Duque, Pamela Valera, V. Cueto, Ashna Shome, A. Natale-Pereira","doi":"10.1158/1538-7445.AM2021-2543","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2543","url":null,"abstract":"","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"59 4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83059163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2520
S. Tornaas, Siren Fromreid, H. Aarstad, O. Vintermyr, D. Costea, H. Dongre
{"title":"Abstract 2520: Detection of transcriptional active HPV 16/18 in patients with oropharyngeal squamous cell carcinoma by dual immunohistochemistry p16INK4and in situ hybridization E6/E7 mRNA in archival material older than 25 years","authors":"S. Tornaas, Siren Fromreid, H. Aarstad, O. Vintermyr, D. Costea, H. Dongre","doi":"10.1158/1538-7445.AM2021-2520","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2520","url":null,"abstract":"","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87194297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2612
R. Elespuru, Catherine G. Fischer
Cancer risk assessment is performed generally in relation to assessment of the safety of new medical products or environmental exposures, especially when DNA modification is a factor. The risk assessment paradigms used for products subject to regulatory review are independent of specific cancers, multiple exposures, and individual risk factors. A default cancer risk assessment for regulatory review includes “uncertainty factors” to account for differential susceptibility and other variables involved in extrapolating from experimental systems to human risk. However, there is a growing amount of evidence that suggests differing risk for different types of cancer as well as the importance of combinations of risk factors not limited to genetic or environmental effects. In the era of personalized medicine and cancer genomics, can we begin to assess personalized cancer risk, instead of overall cancer risk? What models would assist in this paradigm shift? There are several cancers for which specific genetic, environmental, viral and other associations have been established and could be used in personalized cancer risk assessments, including colon, liver, and lung cancer. A search was conducted on PubMed for available literature on epidemiology, genetic susceptibility, and risk factors associated with the major types of cancer, including ~25 pathological types of cancer in 17 different organs. Risk factors associated with each included chemical exposures and tobacco, as well as genetic, epigenetic, microbial, viral, dietary, exercise, and other factors known for involvement in the development of cancer in humans. The diversity of cancers and evidence for specific risk factors is summarized. Common risk factors, including smoking and obesity, are supplemented with a substantial set of individual, often non-overlapping risk factors for diverse cancers. Surprisingly, little evidence was found that genetic-environmental interactions are significant risk factors for most cancers. From this assessment we can begin to ask whether and for what cancers a personalized risk approach seems feasible. Disclaimer: The findings and conclusions in this presentation are those of the authors and should not be construed to represent any agency determination or policy. Citation Format: Rosalie K. Elespuru, Catherine Fischer. Personalized cancer risk and prevention: analysis of risk factors for specific cancers and integration into cancer risk assessment paradigms [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2612.
癌症风险评估通常与评估新医疗产品的安全性或环境暴露有关,特别是当DNA修饰是一个因素时。用于接受监管审查的产品的风险评估范式独立于特定的癌症、多重暴露和个人风险因素。监管审查的默认癌症风险评估包括“不确定性因素”,以解释从实验系统推断人类风险时涉及的不同易感性和其他变量。然而,越来越多的证据表明,不同类型的癌症有不同的风险,以及不限于遗传或环境影响的风险因素组合的重要性。在个体化医疗和癌症基因组学时代,我们能否开始评估个体化癌症风险,而不是整体癌症风险?哪些模型将有助于这种范式转变?有几种癌症已经与特定的基因、环境、病毒和其他因素建立了联系,可以用于个性化的癌症风险评估,包括结肠癌、肝癌和肺癌。在PubMed上检索了与主要癌症类型相关的流行病学、遗传易感性和危险因素的现有文献,包括17个不同器官的约25种病理类型的癌症。与每种疾病相关的风险因素包括化学物质暴露和烟草,以及遗传、表观遗传、微生物、病毒、饮食、运动和其他已知与人类癌症发展有关的因素。总结了癌症的多样性和特定危险因素的证据。常见的危险因素,包括吸烟和肥胖,补充了大量不同癌症的个体,通常不重叠的危险因素。令人惊讶的是,几乎没有证据表明遗传-环境相互作用是大多数癌症的重要危险因素。根据这一评估,我们可以开始问,针对哪些癌症,个性化的风险方法是否可行。免责声明:本报告中的发现和结论是作者的观点,不应被解释为代表任何机构的决定或政策。引文格式:Rosalie K. Elespuru, Catherine Fischer。个性化癌症风险与预防:分析特定癌症的危险因素并将其纳入癌症风险评估范式[摘要]。见:美国癌症研究协会2021年年会论文集;2021年4月10日至15日和5月17日至21日。费城(PA): AACR;癌症杂志,2021;81(13 -增刊):2612。
{"title":"Abstract 2612: Personalized cancer risk and prevention: analysis of risk factors for specific cancers and integration into cancer risk assessment paradigms","authors":"R. Elespuru, Catherine G. Fischer","doi":"10.1158/1538-7445.AM2021-2612","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2612","url":null,"abstract":"Cancer risk assessment is performed generally in relation to assessment of the safety of new medical products or environmental exposures, especially when DNA modification is a factor. The risk assessment paradigms used for products subject to regulatory review are independent of specific cancers, multiple exposures, and individual risk factors. A default cancer risk assessment for regulatory review includes “uncertainty factors” to account for differential susceptibility and other variables involved in extrapolating from experimental systems to human risk. However, there is a growing amount of evidence that suggests differing risk for different types of cancer as well as the importance of combinations of risk factors not limited to genetic or environmental effects. In the era of personalized medicine and cancer genomics, can we begin to assess personalized cancer risk, instead of overall cancer risk? What models would assist in this paradigm shift? There are several cancers for which specific genetic, environmental, viral and other associations have been established and could be used in personalized cancer risk assessments, including colon, liver, and lung cancer. A search was conducted on PubMed for available literature on epidemiology, genetic susceptibility, and risk factors associated with the major types of cancer, including ~25 pathological types of cancer in 17 different organs. Risk factors associated with each included chemical exposures and tobacco, as well as genetic, epigenetic, microbial, viral, dietary, exercise, and other factors known for involvement in the development of cancer in humans. The diversity of cancers and evidence for specific risk factors is summarized. Common risk factors, including smoking and obesity, are supplemented with a substantial set of individual, often non-overlapping risk factors for diverse cancers. Surprisingly, little evidence was found that genetic-environmental interactions are significant risk factors for most cancers. From this assessment we can begin to ask whether and for what cancers a personalized risk approach seems feasible. Disclaimer: The findings and conclusions in this presentation are those of the authors and should not be construed to represent any agency determination or policy. Citation Format: Rosalie K. Elespuru, Catherine Fischer. Personalized cancer risk and prevention: analysis of risk factors for specific cancers and integration into cancer risk assessment paradigms [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2612.","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"111 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83368560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2554
N. Smith, Sarah Malarkey, Pamela Valera, Luis Alzate-Duque, Humberto Baquerizo
Background: The cancer health justice lab [CHJL] formed in 2019, is a multidisciplinary lab comprised of underrepresented undergraduate, graduate, and postgraduate students and diverse professionals in public health, social work, nutrition, medicine, nursing, and criminal justice. Using a social determinants of health framework, CHJL focuses on mentoring and training students from underrepresented backgrounds to increase participation in cancer health disparities research and practice. Methods: In collaboration with the Northeast Regional Alliance HCOP Academy Program (NERA), a program that supports minority and economically disadvantaged undergraduate and high school students interested in health careers, and the Rutgers Bloustein School of Public Policy and Planning, CHJL recruits 3-4 interns per semester. Didactics include leading journal clubs focusing on social determinants of health, health disparities, adverse childhood experiences, and health equity topics. Responsibilities include developing, designing, and implementing a community-based initiative that serves vulnerable populations, grant writing, and peer-reviewed article publications in high impact journals. Results: CHJL currently has 24 members - 14 members are active, including seven interns. Two former interns have been hired as research assistants and are currently pursuing a master's degree in public health. Past members are pursuing postgraduate level education in public health and biomedical sciences. CHJL has generated seven peer-reviewed articles on areas including: systematic reviews of digital cancer education, mental health and social ties of people who are incarcerated and implementing evidence-based practices in state prisons. Current projects include research to understand smoking and vaping behaviors among sexual and gender minority groups;Cancer 101 videos, a short video on COVID-19 for Spanish speakers;auto-complete searches language bias in COVID-19, medication-assisted treatment in jails, group-based counseling, and smoking cessation treatment in prisons, and colorectal cancer screening in urban populations. Conclusion: CHJL addresses health inequities through education, mentoring, advocacy, training, and research. It serves as a model to increase diversity in the health-related workforce and a mechanism for historically underrepresented groups in medicine and public health to contribute to science. This multidisciplinary approach may be useful in educating the next generation of public health and health-related professionals. Furthermore, CHJL could serve as a venue to reduce social isolation and feelings of otherness that may contribute to health inequities.
{"title":"Abstract 2554: A health and justice lab to address cancer related health disparities and social determinants of health in marginalized communities: The Cancer Health Justice Lab","authors":"N. Smith, Sarah Malarkey, Pamela Valera, Luis Alzate-Duque, Humberto Baquerizo","doi":"10.1158/1538-7445.AM2021-2554","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2554","url":null,"abstract":"Background: The cancer health justice lab [CHJL] formed in 2019, is a multidisciplinary lab comprised of underrepresented undergraduate, graduate, and postgraduate students and diverse professionals in public health, social work, nutrition, medicine, nursing, and criminal justice. Using a social determinants of health framework, CHJL focuses on mentoring and training students from underrepresented backgrounds to increase participation in cancer health disparities research and practice. Methods: In collaboration with the Northeast Regional Alliance HCOP Academy Program (NERA), a program that supports minority and economically disadvantaged undergraduate and high school students interested in health careers, and the Rutgers Bloustein School of Public Policy and Planning, CHJL recruits 3-4 interns per semester. Didactics include leading journal clubs focusing on social determinants of health, health disparities, adverse childhood experiences, and health equity topics. Responsibilities include developing, designing, and implementing a community-based initiative that serves vulnerable populations, grant writing, and peer-reviewed article publications in high impact journals. Results: CHJL currently has 24 members - 14 members are active, including seven interns. Two former interns have been hired as research assistants and are currently pursuing a master's degree in public health. Past members are pursuing postgraduate level education in public health and biomedical sciences. CHJL has generated seven peer-reviewed articles on areas including: systematic reviews of digital cancer education, mental health and social ties of people who are incarcerated and implementing evidence-based practices in state prisons. Current projects include research to understand smoking and vaping behaviors among sexual and gender minority groups;Cancer 101 videos, a short video on COVID-19 for Spanish speakers;auto-complete searches language bias in COVID-19, medication-assisted treatment in jails, group-based counseling, and smoking cessation treatment in prisons, and colorectal cancer screening in urban populations. Conclusion: CHJL addresses health inequities through education, mentoring, advocacy, training, and research. It serves as a model to increase diversity in the health-related workforce and a mechanism for historically underrepresented groups in medicine and public health to contribute to science. This multidisciplinary approach may be useful in educating the next generation of public health and health-related professionals. Furthermore, CHJL could serve as a venue to reduce social isolation and feelings of otherness that may contribute to health inequities.","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88464614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2567
Karen A. Corleto, Tara N. Mahmood, Danilo Landrock, S. Hursting, C. Fabian, B. Kimler, Erin D. Giles
Introduction: Many women at high risk for breast cancer will not take standard selective estrogen receptor modulators (SERMs) for cancer prevention due to concern of side effects, especially vasomotor symptoms. Duavee®, a tissue selective complex of the SERM bazedoxifene (BZA; 20mg) + conjugated estrogen (CE; 0.45mg), is FDA approved for relief of hot-flashes. Preclinical and early phase human studies suggest Duavee® has potential for breast cancer prevention, with favorable change in mammographic fibroglandular volume and proliferation. Given the >40% incidence of obesity in postmenopausal women, and that obesity increases breast cancer risk, the current study was aimed at identifying the effects of obesity on response to Duavee® in a rodent model of obesity and postmenopausal breast cancer. Methods: This study used our well-characterized rat model of diet-induced obesity and postmenopausal ER-positive breast cancer. Rats were injected with N-methylnitrosourea (MNU, 50 mg/kg) at 7 weeks of age to induce mammary tumors and fed a high fat diet (HF; 46% kcal fat) to promote obesity. Lean and obese rat were selected based on % body fat at 16 weeks. Tumors were monitored by manual palpation weekly and measured using digital calipers. Tumor-bearing rats were ovariectomized (OVX) when a tumor reached 0.7cm3. Rats were then maintained on ad libitum HF diet or HF diet plus a daily oral dose of Duavee® (3mg BZA+ 0.07mg CE/kg body weight) for 8 weeks. Body composition was analyzed biweekly (qMR) and fat pads weighed at study end to determine regional fat distribution. Results: Like menopause in women, OVX induces weight gain in this model. Duavee® significantly blunted the OVX-induced weight gain in both lean (-65%, p Conclusions: These data suggest that Duavee® may provide beneficial effects on body composition and metabolism in obese OVX animals without promotion of tumor growth. Further analyses will include study of direct effects of Duavee® on tumors, the tumor microenvironment, and systemic markers of insulin resistance and mammary cancer risk in our rat model of pre-and postmenopausal obesity and breast cancer. Citation Format: Karen A. Corleto, Tara N. Mahmood, Danilo Landrock, Stephen D. Hursting, Carol J. Fabian, Bruce F. Kimler, Erin D. Giles. Duavee® improves metabolic health without increasing cancer risk: findings from a preclinical model of obesity and postmenopausal breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2567.
导论:由于担心副作用,尤其是血管舒缩症状,许多乳腺癌高危妇女不愿使用标准的选择性雌激素受体调节剂(SERMs)来预防癌症。Duavee®是一种SERM bazedoxifene (BZA;20mg) +共轭雌激素(CE;0.45毫克),被FDA批准用于缓解潮热。临床前和早期人类研究表明,Duavee®具有预防乳腺癌的潜力,有利于改变乳腺纤维腺的体积和增殖。鉴于绝经后妇女肥胖发生率>40%,肥胖增加乳腺癌风险,本研究旨在确定肥胖对Duavee®在肥胖和绝经后乳腺癌啮齿动物模型中的反应的影响。方法:本研究采用我们的特征良好的饮食性肥胖和绝经后雌激素受体阳性乳腺癌大鼠模型。7周龄大鼠注射n -甲基亚硝基脲(MNU, 50 mg/kg)诱导乳腺肿瘤,并饲喂高脂饲料(HF;46%卡路里脂肪),促进肥胖。16周时根据体脂百分比选择瘦鼠和肥鼠。每周用手触诊监测肿瘤,并用数字卡尺测量。当肿瘤达到0.7cm3时,切除荷瘤大鼠卵巢。然后,大鼠在8周内自由饲喂HF饲粮或HF饲粮加每日口服剂量的Duavee®(3mg BZA+ 0.07mg CE/kg体重)。每两周分析体成分(qMR),并在研究结束时称重脂肪垫,以确定区域脂肪分布。结果:与女性更年期一样,OVX在该模型中引起体重增加。结论:这些数据表明,Duavee®可能对肥胖OVX动物的身体组成和代谢有有益的影响,而不会促进肿瘤的生长。进一步的分析将包括研究Duavee®对绝经前和绝经后肥胖和乳腺癌大鼠模型中肿瘤、肿瘤微环境、胰岛素抵抗和乳腺癌风险的系统性标志物的直接影响。引文格式:Karen A. Corleto, Tara N. Mahmood, Danilo Landrock, Stephen D. Hursting, Carol J. Fabian, Bruce F. Kimler, Erin D. Giles。Duavee®改善代谢健康而不增加癌症风险:来自肥胖和绝经后乳腺癌的临床前模型的发现[摘要]。见:美国癌症研究协会2021年年会论文集;2021年4月10日至15日和5月17日至21日。费城(PA): AACR;癌症杂志,2021;81(13 -增刊):摘要第2567期。
{"title":"Abstract 2567: Duavee® improves metabolic health without increasing cancer risk: findings from a preclinical model of obesity and postmenopausal breast cancer","authors":"Karen A. Corleto, Tara N. Mahmood, Danilo Landrock, S. Hursting, C. Fabian, B. Kimler, Erin D. Giles","doi":"10.1158/1538-7445.AM2021-2567","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2567","url":null,"abstract":"Introduction: Many women at high risk for breast cancer will not take standard selective estrogen receptor modulators (SERMs) for cancer prevention due to concern of side effects, especially vasomotor symptoms. Duavee®, a tissue selective complex of the SERM bazedoxifene (BZA; 20mg) + conjugated estrogen (CE; 0.45mg), is FDA approved for relief of hot-flashes. Preclinical and early phase human studies suggest Duavee® has potential for breast cancer prevention, with favorable change in mammographic fibroglandular volume and proliferation. Given the >40% incidence of obesity in postmenopausal women, and that obesity increases breast cancer risk, the current study was aimed at identifying the effects of obesity on response to Duavee® in a rodent model of obesity and postmenopausal breast cancer. Methods: This study used our well-characterized rat model of diet-induced obesity and postmenopausal ER-positive breast cancer. Rats were injected with N-methylnitrosourea (MNU, 50 mg/kg) at 7 weeks of age to induce mammary tumors and fed a high fat diet (HF; 46% kcal fat) to promote obesity. Lean and obese rat were selected based on % body fat at 16 weeks. Tumors were monitored by manual palpation weekly and measured using digital calipers. Tumor-bearing rats were ovariectomized (OVX) when a tumor reached 0.7cm3. Rats were then maintained on ad libitum HF diet or HF diet plus a daily oral dose of Duavee® (3mg BZA+ 0.07mg CE/kg body weight) for 8 weeks. Body composition was analyzed biweekly (qMR) and fat pads weighed at study end to determine regional fat distribution. Results: Like menopause in women, OVX induces weight gain in this model. Duavee® significantly blunted the OVX-induced weight gain in both lean (-65%, p Conclusions: These data suggest that Duavee® may provide beneficial effects on body composition and metabolism in obese OVX animals without promotion of tumor growth. Further analyses will include study of direct effects of Duavee® on tumors, the tumor microenvironment, and systemic markers of insulin resistance and mammary cancer risk in our rat model of pre-and postmenopausal obesity and breast cancer. Citation Format: Karen A. Corleto, Tara N. Mahmood, Danilo Landrock, Stephen D. Hursting, Carol J. Fabian, Bruce F. Kimler, Erin D. Giles. Duavee® improves metabolic health without increasing cancer risk: findings from a preclinical model of obesity and postmenopausal breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2567.","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"25 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90663504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2613
Z. Su, Yu-Hsin Chen Chen, Tien-Yuan Wu
Most cancer cases are closely related to many risk factors such as environment and diets. Carcinogenesis may also be controlled by epigenetic regulation. Salvia miltiorrhiza Bunge (Danshen) is a common Chinese herbal medicine, and it has been reported that it has anti-cancer, anti-inflammatory, anti-coagulant, and anti-thrombotic activities. In this study, we studied the effect and epigenetic mechanisms of cryptotanshinone (CTS) and dihydrotanshinone (DHTS), the major active ingredients in Danshen, against human colorectal cancer HCT116 cells. The results showed that CTS and DHTS suppressed the proliferation of HCT116 cells for 72-hour treatment and induced mRNA and protein expressions of p21 and DLEC1. Pro-apoptosis proteins such as PARP, caspase-3, and caspase-9 are cleaved and activated in HCT116 cells treating CTS and DHTS. Moreover, CTS and DHTS also increased the protein levels of epigenetics regulating enzymes, including histone deacetylases (HDACs) and DNA methyltransferases (DNMTs) in HCT116 cells. Therefore, it is suggested that CTS and DHTS may affect tumor suppressor genes, such as p21 and DLEC1, by regulating epigenetic mechanisms, which induce apoptosis of colorectal cancer HCT116 cells. Citation Format: Zheng-Yuan Su, Yu-Hsin Chen Chen, Tien-Yuan Wu. Cryptotanshinone and dihydrotanshinone epigenetically suppress human colorectal cancer cell growth [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2613.
{"title":"Abstract 2613: Cryptotanshinone and dihydrotanshinone epigenetically suppress human colorectal cancer cell growth","authors":"Z. Su, Yu-Hsin Chen Chen, Tien-Yuan Wu","doi":"10.1158/1538-7445.AM2021-2613","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2613","url":null,"abstract":"Most cancer cases are closely related to many risk factors such as environment and diets. Carcinogenesis may also be controlled by epigenetic regulation. Salvia miltiorrhiza Bunge (Danshen) is a common Chinese herbal medicine, and it has been reported that it has anti-cancer, anti-inflammatory, anti-coagulant, and anti-thrombotic activities. In this study, we studied the effect and epigenetic mechanisms of cryptotanshinone (CTS) and dihydrotanshinone (DHTS), the major active ingredients in Danshen, against human colorectal cancer HCT116 cells. The results showed that CTS and DHTS suppressed the proliferation of HCT116 cells for 72-hour treatment and induced mRNA and protein expressions of p21 and DLEC1. Pro-apoptosis proteins such as PARP, caspase-3, and caspase-9 are cleaved and activated in HCT116 cells treating CTS and DHTS. Moreover, CTS and DHTS also increased the protein levels of epigenetics regulating enzymes, including histone deacetylases (HDACs) and DNA methyltransferases (DNMTs) in HCT116 cells. Therefore, it is suggested that CTS and DHTS may affect tumor suppressor genes, such as p21 and DLEC1, by regulating epigenetic mechanisms, which induce apoptosis of colorectal cancer HCT116 cells. Citation Format: Zheng-Yuan Su, Yu-Hsin Chen Chen, Tien-Yuan Wu. Cryptotanshinone and dihydrotanshinone epigenetically suppress human colorectal cancer cell growth [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2613.","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"56 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90834178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2529
Isaacson B. Adelani, S. Rotimi, C. Yates, M. Campbell
Introduction: Vitamin D in its hormonal form, 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) binds to the vitamin D receptor (VDR) to regulate genes, for example, in skeletal mineralization. However, it also has other potent biological functions in regulating apoptosis, proliferation, and inflammation. In carcinogenesis, 1,25(OH)2D3 may be exploited to regulate these crucial pathways. It is also clear that a frequent cancer disparity exists amongst African American (AA) men with prostate cancer compared to European Americans (EA). AA men show a higher incidence rate and two to three times increased risk of mortality than EA counterparts. Various groups have suggested that 1,25(OH)2D3 levels and/or VDR functions are risk factors linked with increased prostate cancer incidence in AA men. Incidentally, reports showed that VD plays a crucial role in regulating circadian rhythm (CR). There is, therefore, a need to understand and evaluate 1,25(OH)2D3-dependent CR regulation and the association with racial disparity in prostate cancer. This study aimed to determine if there are differentially expressed VD metabolic enzymes in AA and EA and evaluate if the differential expression correlates with CR genes. Methods: The Cancer Genome Atlas Research Network (TCGA), 2015 database was queried for expression of VD metabolizing enzymes and CR genes. The search was carried out on prostate adenocarcinoma expressions of AA and EA. VD metabolizing enzymes queried are CYP2R1, CYP24A1, CYP27B1, CYP27A1, while CR genes queried include ARNTL, CLOCK, CRY1, CRY2, CSNK1E, NPAS2, PER1, PER2, PER3, and TIMELESS. Prostate adenocarcinoma racial differential expressions of AA and EA were evaluated, and a correlation study was done using the Pearson correlation. Results: VD metabolic enzyme, CYP2R1, and CR gene, ARNTL were significantly upregulated in AA compared to EA counterparts. Although CYPR1 correlates negatively with CLOCK, CRY2, and PER3 in both races, CYPR1 specifically showed a positive correlation with CR gene CRY1 in EA and negative correlations with CR genes NPAS2 and CSNK1E in AA. However, a significant correlation between CYP2R1 and ARNTL in EA and AA was not observed. Conclusion: The data suggest a relationship between racial influence and prostate cancer associated with VD metabolism and CR regulation. Hence, it is crucial to elucidate CYP2R1 regulation in prostate cancer related to VD levels and CR regulation, especially with a focus on racial disparities. Citation Format: Isaacson Bababode Adelani, Solomon Oladapo Rotimi, Clayton Yates, Moray Campbell. Specific racial CYP2R1 correlation with circadian rhythm genes in prostate adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2529.
{"title":"Abstract 2529: Specific racial CYP2R1 correlation with circadian rhythm genes in prostate adenocarcinoma","authors":"Isaacson B. Adelani, S. Rotimi, C. Yates, M. Campbell","doi":"10.1158/1538-7445.AM2021-2529","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2529","url":null,"abstract":"Introduction: Vitamin D in its hormonal form, 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) binds to the vitamin D receptor (VDR) to regulate genes, for example, in skeletal mineralization. However, it also has other potent biological functions in regulating apoptosis, proliferation, and inflammation. In carcinogenesis, 1,25(OH)2D3 may be exploited to regulate these crucial pathways. It is also clear that a frequent cancer disparity exists amongst African American (AA) men with prostate cancer compared to European Americans (EA). AA men show a higher incidence rate and two to three times increased risk of mortality than EA counterparts. Various groups have suggested that 1,25(OH)2D3 levels and/or VDR functions are risk factors linked with increased prostate cancer incidence in AA men. Incidentally, reports showed that VD plays a crucial role in regulating circadian rhythm (CR). There is, therefore, a need to understand and evaluate 1,25(OH)2D3-dependent CR regulation and the association with racial disparity in prostate cancer. This study aimed to determine if there are differentially expressed VD metabolic enzymes in AA and EA and evaluate if the differential expression correlates with CR genes. Methods: The Cancer Genome Atlas Research Network (TCGA), 2015 database was queried for expression of VD metabolizing enzymes and CR genes. The search was carried out on prostate adenocarcinoma expressions of AA and EA. VD metabolizing enzymes queried are CYP2R1, CYP24A1, CYP27B1, CYP27A1, while CR genes queried include ARNTL, CLOCK, CRY1, CRY2, CSNK1E, NPAS2, PER1, PER2, PER3, and TIMELESS. Prostate adenocarcinoma racial differential expressions of AA and EA were evaluated, and a correlation study was done using the Pearson correlation. Results: VD metabolic enzyme, CYP2R1, and CR gene, ARNTL were significantly upregulated in AA compared to EA counterparts. Although CYPR1 correlates negatively with CLOCK, CRY2, and PER3 in both races, CYPR1 specifically showed a positive correlation with CR gene CRY1 in EA and negative correlations with CR genes NPAS2 and CSNK1E in AA. However, a significant correlation between CYP2R1 and ARNTL in EA and AA was not observed. Conclusion: The data suggest a relationship between racial influence and prostate cancer associated with VD metabolism and CR regulation. Hence, it is crucial to elucidate CYP2R1 regulation in prostate cancer related to VD levels and CR regulation, especially with a focus on racial disparities. Citation Format: Isaacson Bababode Adelani, Solomon Oladapo Rotimi, Clayton Yates, Moray Campbell. Specific racial CYP2R1 correlation with circadian rhythm genes in prostate adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2529.","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89602565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2557
Zhi-ming Zhao, Xiaomo Li, Fei Wang, T. Ma, Rong Liu
{"title":"Abstract 2557: Germline mutation landscape in a large cohort of Chinese pancreatic cancer patients","authors":"Zhi-ming Zhao, Xiaomo Li, Fei Wang, T. Ma, Rong Liu","doi":"10.1158/1538-7445.AM2021-2557","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2557","url":null,"abstract":"","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89557297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}