Prevention Research最新文献

{"title":"Abstract 2539: DNA content and chromatin texture measurement to predict malignant transformation in low-grade oral dysplasia","authors":"Madhurima Datta, D. Laronde, M. Rosin, A. Carraro, Korbelik Jagoda, A. Harrison, Zhaoyang Chen, M. Guillaud","doi":"10.1158/1538-7445.AM2021-2539","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2539","url":null,"abstract":"","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"138 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74672686","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}

{"title":"Abstract 2552: Adapting a novel cancer care delivery model: identifying barriers unique to care coordination for LGBTQ cancer survivors","authors":"Nicolás O. Francone, J. Alhalel, William J. Dunne, Sankirtana M Danner, Nihmotallahi Adebayo, T. Madorsky, Cassandra Osei, J. Rivera, Julia Trossman, C. Weldon, Elizabeth Adetoro, Melissa A Simon","doi":"10.1158/1538-7445.AM2021-2552","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2552","url":null,"abstract":"","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"155 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73731158","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}

{"title":"Abstract 2534: Underlying mechanism of response to neddylation inhibition in a subset of glioblastoma","authors":"S. Ferdosi, B. Taylor, Matthew Lee, N. Tang, S. Peng, R. Bybee, G. Reid, L. Hartman, K. Garcia-Mansfield, Ritin Sharma, P. Pirrotte, F. Furnari, Harshil Dhruv, M. Berens","doi":"10.1158/1538-7445.AM2021-2534","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2534","url":null,"abstract":"","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"35 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76973966","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}

{"title":"Abstract 2556: The somatic variant of HLRCC, an unrecognized type of RCC","authors":"M. Merino, E. Dikoglu, S. Gurram, M. Linehan, R. Srinivasan","doi":"10.1158/1538-7445.AM2021-2556","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2556","url":null,"abstract":"","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88879009","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}

{"title":"Abstract 2598: Towards an electrochemical serum-based platform for early diagnosis and stratification of glioma","authors":"Christopher Rinaldi, A. G. Theakstone, D. Corrigan, Paul Brennan, M. Baker","doi":"10.1158/1538-7445.AM2021-2598","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2598","url":null,"abstract":"Development of an electrochemical diagnostic test would provide quantitative detection of biomarkers characteristic of clinical serum samples that may facilitate early detection and triage of glioma patients in the clinical setting. Today, 32 individuals will receive a confirmatory diagnosis of a brain tumor in the UK, equivalent to 3% of all patients diagnosed with cancer annually. Implications for patients and families are tragic, brain cancer is responsible for >5,000 mortalities annually in the UK, with 20.1 mean years of life lost to the disease per patient, greater than any other cancer. Presently, ~22% of brain cancer patients receive diagnosis through GP referral, with over a third of patients attending their health practice on five occasions prior to diagnosis. Brain tumor symptoms are diverse and often non-specific in the absence of epileptic seizures, with an extremely poor positive predictive value. Consequently, suspected patients experience significant diagnostic delays, with significant time spent in primary care settings. Heightened symptoms often translates to emergency presentation, where >60% of brain cancer patients currently receive diagnosis, associated with reduced survival compared to non-emergency pathways. Hence, earlier detection of brain cancer patients is a clinical need within primary care settings to prevent significant diagnostic delays and improve patient outcomes. Introduction of a widespread screening program with medical imaging modalities is not economically viable for early detection of brain cancer given high test costs and low incidence in the general population. However, a recent health economic study suggested a blood-based test may prove cost saving to NHS services if employed to triage brain tumor patients for medical imaging in primary and secondary care. Blood is fundamental to physiological function of cells and their perpetual interaction provides a rich source of endogenous molecules that may reflect biochemical events of gliomagenesis. Our current work towards development of a blood-based electrochemical platform for brain cancer focuses on screening of clinical serum samples for a large panel of cytokines from confirmed patients with glioma tumor types. Thereafter, our work demonstrates electrochemical detection of elevated cytokine biomarkers identified within our serum samples. Previously, we demonstrated the potential of this platform technology for early detection of Hodgkin lymphoma, with successful discrimination between cancerous and non-cancerous patient samples, which we now hope to extend to early detection of brain cancer. Implementation of a low-cost, point-of-care triage blood test for brain cancer would have significant clinical and economical benefits, ultimately facilitating the promotion of early detection strategies in primary care to enable timely cancer diagnosis and improve patient outcomes. Citation Format: Christopher Rinaldi, Ashton G. Theakstone, Damion Corrigan, Paul Bre","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90968989","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}

{"title":"Abstract 2562: EGCG targeting of adipogenesis reveals a STAT3-mediated paracrine oncogenic control of triple-negative breast cancer cell invasive phenotype","authors":"N. G. Suárez, Sahily Rodriguez Torres, B. Annabi","doi":"10.1158/1538-7445.AM2021-2562","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2562","url":null,"abstract":"Background: Obese subjects have an increased risk of developing triple-negative breast cancer (TNBC), in part associated with the chronic low-grade inflammation state. On the other hand, epidemiological data indicates that increased consumption of polyphenol-rich fruits and vegetables plays a key role in reducing incidence of some cancers. Objectives: Here, we tested whether green tea-derived epigallocatechin-3-gallate (EGCG) could alter adipogenesis involved in the maturation of pre-adipocytes, and how this impacts the paracrine regulation of the mature adipocytes secretome on the TNBC invasive phenotype. Methods: Differentiation was performed and conditioned media (CM) from preadipocytes and mature adipocytes harvested. Human TNBC-derived MDA-MB-231 real-time cell migration was performed using the exCELLigence system. Differential gene arrays and RT-qPCR were used to assess gene expression levels. Western blotting was used to assess protein expression levels. In vitro vasculogenic mimicry (VM) was assessed with Matrigel. Results: EGCG was found to inhibit the induction of numerous key adipogenic biomarkers, including lipoprotein lipase, adiponectin, leptin, fatty acid synthase, and fatty acid binding protein 4. Increased MDA-MB-231 chemotaxis and VM were found in response to mature adipocytes secretome, and this was correlated with the induction of the STAT3 signaling pathway. This invasive phenotype was prevented by EGCG, JAK/STAT inhibitors Tofacitinib and AG490, as well as upon STAT3 gene silencing. Conclusion: Adipocytes secretome plays a key role in the paracrine regulation of TNBC cells invasive phenotype. Dietary catechin-mediated interventions may, in part through the inhibition of adipogenesis and modulation of adipocytes secretome, prevent the onset of an obesogenic environment that favors TNBC development. Citation Format: Narjara Gonzalez Suarez, Sahily Rodriguez Torres, Borhane Annabi. EGCG targeting of adipogenesis reveals a STAT3-mediated paracrine oncogenic control of triple-negative breast cancer cell invasive phenotype [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 2562.","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87164234","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}

{"title":"Abstract 2576: Calorie restriction reverses the tumorigenic effects of obesity to a greater extent than bariatric surgery in a murine model of breast cancer","authors":"Kristina K Camp, Emily L Rossi, Tori L. McFarlane, Steven S Doerstling, Subreen A Khatib, Elaine M Glenny, M. Coleman, Laura W. Bowers, Erika T Rezeli, R. Seeley, A. Lewis, J. Parker, A. Fodor, F. Fouladi, S. Hursting","doi":"10.1158/1538-7445.AM2021-2576","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2576","url":null,"abstract":"","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"196 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75896121","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}

{"title":"Abstract 2589: Gene signature of fluvastatin resistance for prevention of breast cancer and predicting resistance to statins","authors":"A. Bhardwaj, Z. Ju, Matthew D Embury, Jing Wang, I. Bedrosian","doi":"10.1158/1538-7445.AM2021-2589","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2589","url":null,"abstract":"Introduction: Cholesterol biosynthesis pathway is highly regulated and inhibition of the pathway with statins is known to cause restorative upregulation of several genes in the pathway. The goal of this study is to investigate if the statin mediated upregulation in the cholesterol biosynthesis pathway genes associates with the resistance to fluvastatin in a model of hormonally insensitive breast cancer Methods: A published gene signature of statin resistance was validated 1) a cell line based model of breast cancer progression consisting of inherently fluvastatin sensitive and inherently fluvastatin resistant cell lines and also compared to our experimentally derived acquired signature of fluvastatin resistance using 2) an isogenic set of cell lines consisting of a fluvastatin sensitive cell line (MCF10.AT1), and an acquired resistant cell line (MCF10.AT- R) and lastly validated using 3) SV40 C3 tag, a mouse model of hormone receptor negative breast cancer. Clariom RNA profiling were processed and mined by IPA analysis to identify the fluvastatin resistance signature that were validated by qPCR. Fluvastatin resistance was determined in vitro by colony formation assay and in vivo in a mouse model of breast cancer. Results: We found more than 75% of the published 17 gene panel fluvastatin resistance gene signature (consisting of cholesterol biosynthesis pathway genes) to be significantly upregulated in an inherently resistant cell line, DCIS cell line, relative to fluvastatin sensitive preneoplastic, MCF10.AT1 cell line. We found this inherent statin resistance gene signature to be also relevant in the MCF10.AT-R resistant cells as we found 13 of these genes to map to top 3 upregulated pathways that are steroid biosynthesis, steroid hormone biosynthesis and terpenoid backbone biosynthesis pathway. Next, we tested if 17 gene statin resistance signature associates with presence of tumors in the mammary glands of fluvastatin treated mice and found upregulation of more than 50% of the genes in the resistance signature in the tumor bearing mammary glands. Lastly, we studied if a 10-day period of fluvastatin treatment to SV40C3 Tag mice, a spontaneous mouse model of breast cancer, can also trigger the upregulation of these cholesterol biosynthesis pathway genes and provide an early signal of statin resistance. These experiments showed that a 10-day period is not long enough to cause a feedback upregulation in steroid biosynthesis pathway genes and thus can9t be used a surrogate timepoint to detect resistance to fluvastatin. Conclusions: Upregulation of multiple steroid biosynthesis pathway genes after fluvastatin treatment suggests an opportunity of dual targeting of the cholesterol biosynthesis pathway in order to sensitize the fluvastatin resistant breast cancer cells. Citation Format: Anjana Bhardwaj, Zhenlin Ju, Matthew Embury, Jing Wang, Isabelle Bedrosian. Gene signature of fluvastatin resistance for prevention of breast cancer and predicting resis","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77052818","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}

{"title":"Abstract 2583: Effects of garlic compound diallyl trisulfide on head and neck cancer cells and cancer stem cells in vitro and in vivo","authors":"Sivapar V Mathan, Su-Hyeong Kim, Shivendra V. Singh, R. Singh","doi":"10.1158/1538-7445.AM2021-2583","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2583","url":null,"abstract":"Head and neck cancer (HNC) is the seventh most prevalent cancer worldwide. The five-year survival rate is less than fifty percent despite significant advances in therapeutic approaches. Early diagnosis and treatment can help in prevention and disease management. Studies have reported that dietary intake of Allium vegetables or processed garlic that contains diallyl trisulfide (DATS) lowered the risk of various cancers. However, it has not been investigated for its efficacy and molecular mechanisms against HNC. Herein, we investigated the effect of DATS on HNC UMSCC-22A, UMSCC-22B, and Cal33 cells in vitro. DATS treatment significantly reduced the cell viability of HNC cells. DATS induced significant G2/M phase cell cycle arrest, which resulted in the accumulation of cyclin B1 and induced levels of p21. DATS-induced M phase arrest was attenuated by N-acetyl cysteine (NAC) treatment, which suggested that DATS mediates growth-suppressive effects by reactive oxygen species (ROS) generation. DATS treatment induced mitochondrial dysfunction. DATS induced ROS production led to apoptosis, which was attenuated by NAC treatment. DATS increased proapoptotic protein cleaved caspase-3, cleaved PARP, and Bax/Bcl2 ratio and decreased the levels of antiapoptotic protein XIAP. DATS induced ROS mediated DNA damage which was attenuated by NAC treatment. Further, DATS mediated increase in level of cleaved PARP, accumulation of Cyclin B1 and decrease in XIAP was attenuated by NAC treatment. DATS (1-10 μM) treatment resulted in inhibition of self renewal of HNC cancer stem cells (HNC CSCs) sphere formation. DATS reduced aldehyde dehydrogenase 1 (ALDH1) activity and CD133high/CD44high HNC CSC fraction. DATS-treated SCID mice tumor xenograft also revealed it9s in vivo efficacy on HNC CSCs. Further, DATS treatment reduced the tumor weight, volume and reduced the levels of Ki67 cell proliferation marker in UMSCC22B head and neck cancer CD1 nude mice tumor xenograft. DATS treatment decreased tumor incidence and inhibited tumor promotion and progression in twenty two week C57BL6 4-Nitroquinoline 1-oxide (4-NQO)-induced mouse oral carcinogenesis model. DATS treatment reduced the cell proliferation marker Ki67 and increased TUNEL positive apoptotic cells in treatment groups compared to control group. Collectively, DATS inhibited cell proliferation, induced cell cycle arrest, and cell death via apoptosis involving DNA damage, mitochondrial dysfunction, and ROS generation. DATS treatment also reduced the HNC CSC fraction, sphere formation and ALDH1 activity. More importantly, DATS inhibited cancer incidence and progression in 4-NQO oral carcinogenesis study. Further, DATS inhibited HNC tumor growth and HNC CSC fraction in vivo. Thus, DATS could be a potential chemopreventive and chemotherapeutic agent against head and neck cancer. Citation Format: Sivapar V. Mathan, Su-Hyeong Kim, Shivendra V. Singh, Rana P. Singh. Effects of garlic compound diallyl trisulfide on head and neck ","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78240840","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}

{"title":"Abstract 2558: Understanding the shared roles of obesity and genetic mutation in the development of endometrial cancer","authors":"M. Wilson, Jake J. Reske, R. Chandler","doi":"10.1158/1538-7445.AM2021-2558","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2558","url":null,"abstract":"","PeriodicalId":20290,"journal":{"name":"Prevention Research","volume":"59 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79979480","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}