Prevention, Early Detection, and Interception最新文献

{"title":"Abstract 5091: Inhibition of mutagenicity of 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine ( PhIP) by aqueous extract (crude) and organic extract (pulegone) ofCalamintha nepeta.","authors":"Yanlingxue Wan, R. Hayes, Joshua Li, K. Ferrer, Padma T. Uppula, B. Y. Wong","doi":"10.1158/1538-7445.SABCS18-5091","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-5091","url":null,"abstract":"","PeriodicalId":20357,"journal":{"name":"Prevention, Early Detection, and Interception","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79634346","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 3993A: Real-world utilization of PD-L1 IHC testing and results across multiple tumor types","authors":"G. Krigsfeld, Emily A. Prince, K. Zerba, V. Chizhevsky, J. W. Ragheb, James White","doi":"10.1158/1538-7445.AM2019-3993A","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2019-3993A","url":null,"abstract":"Background: A number of programmed death ligand 1 (PD-L1) immunohistochemistry (IHC) diagnostic (Dx) tests have been approved by the FDA to guide treatment (Tx) with programmed death-1/PD-L1 inhibitors. Here, we evaluate the utilization of the Dako PD-L1 IHC 28-8 and 22C3 pharmDx and Ventana PD-L1 (SP142) assays on real-world samples across multiple tumor types, characterize PD-L1 testing practices among physicians who order a PD-L1 test, and investigate how PD-L1 test results impact physicians’ Tx decision-making and use of immuno-oncology (I-O) Tx. Methods: 55,652 samples with clinical characteristics were provided by Symphony Health Solutions. NeoGenomics Laboratories, Inc assessed PD-L1 expression between October 2015–April 2018, according to manufacturers’ protocols at time of study. Clinical characteristics were matched to PD-L1 test results using unique identifiers for the 4714 patients (pts) whose diagnoses and treatment could be determined. Results: Across tumor types, 56% of pts received a test prior to first-line (1L) Tx. Most lung cancer (57%) or melanoma (MEL; 65%) pts had a PD-L1 test prior to 1L Tx, while most squamous cell carcinoma of the head and neck (70%) or urothelial carcinoma (73%) pts had a PD-L1 test after Tx initiation, in line with drug and complementary Dx approvals for these tumor types during the testing period. The percentage of lung cancer pts whose PD-L1 expression was tested prior to 1L Tx rose from 32% during Q4 2015–Q3 2016 to 63% during Q4 2016–Q1 2018, in line with FDA approval of a companion PD-L1 IHC Dx for non-small cell lung cancer. Regardless of PD-L1 test used, most lung cancer (73%) or MEL (93%) pts received I-O Tx, defined as nivolumab (NIVO; + ipilimumab [IPI] for MEL only), pembrolizumab (pembro) ± chemotherapy, atezolizumab, or IPI alone. Moreover, the majority of lung cancer pts who had ≥1% PD-L1 expression or MEL regardless of PD-L1 expression received 1L I-O Tx irrespective of the PD-L1 test used. Analysis of PD-L1 expression, Dx test used, and Tx received showed that, for MEL pts tested with 22C3, 28%, 17%, and 0% of pts received NIVO or IPI, while 28%, 43%, and 43% received NIVO+IPI, at the expression cutoffs of 0%, 1–49%, and ≥50%, respectively. Lung cancer pts with 1–49% PD-L1 expression, as determined by a 22C3 test, received NIVO or pembro monotherapy at similar rates (12–18%). Of those who had ≥50% PD-L1 expression, as determined by the 28-8 test only, 52% received pembro monotherapy vs other Tx. Conclusions: Since FDA approval of the first PD-L1 IHC Dx in 2015, analyses of PD-L1 testing practices and physicians’ Tx decision behavior at a US national reference laboratory have shown that physicians’ adoption of PD-L1 testing is responsive to FDA approvals and that most testing for lung cancer and MEL occurs before 1L Tx initiation. In lung cancer or MEL pts who had a PD-L1 test result available, Tx decisions do not appear to be tied to the specific intended use of the PD-L1 assay that was ","PeriodicalId":20357,"journal":{"name":"Prevention, Early Detection, and Interception","volume":"65 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82832491","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 644: Ancestral paternal obesity: Systemic versus local effects on offspring mammary tissue development and tumorigenesis","authors":"C. C. Fontelles, A. Wärri, R. S. D. Cruz, M. I. Cruz, Ersilia Barin, S. Assis","doi":"10.1158/1538-7445.AM2019-644","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2019-644","url":null,"abstract":"Background: Obesity and overweight are risk factors for breast cancer, particularly in the post-menopausal years. We recently reported that having a history of ancestral overweight from the paternal lineage is enough to increase breast cancer susceptibility in daughters. Using a mouse model, we demonstrated that paternal consumption of an obesity inducing diet (OID) altered mammary gland development, increased mammary carcinogenesis and disrupted metabolic parameters in the female offspring, compared to the female offspring of fathers who consumed only control (CO) diet. Given both the systemic and local the mammary tissue alterations observed, we aimed to investigate in more details why daughters of overweight fathers are at increased risk for breast cancer. More specifically, we used mammary gland transplantation experiments to study whether this ancestrally-induced breast cancer predisposition is linked to systemic factors and/or mammary tissue confined changes in daughters. Material and methods: Male mice were exposed either to a control (CO) or to high-fat (OID) diet. CO and OID male mice were then mated with female mice fed CO diet exclusively. Female offspring of both CO and OID male mice underwent a mammary gland transplantation surgery. Briefly, female offspring had their mammary fat pad area between the nipple and the proximal lymph node excised. Afterwards, mammary tissue fragments (1 mm3) of a donor mouse, either CO or OID female offspring, were implanted into a pocket made in the cleared fat pad. The transplantations were performed from CO female offspring donors to both CO [CO(CO)] and OID [OID(CO)] female offspring hosts, as well as from OID female offspring donors to both CO [CO(OID)] and OID [OID(OID)] female offspring hosts. Approximately 10 weeks post-surgery, the mammary glands were collected, photographed and analyzed using ImageJ software to determine branching density, epithelial elongation and number of Terminal End Buds. Cell proliferation was assessed by ki-67 and cell apoptosis was measured on ImageJ software. Results: Our preliminary data shows that CO(OID) had more (p≤0.05) articulated mammary branching morphogenesis than CO(CO). OID(CO) displayed marginal increase (p≤0.09) in the mammary gland area, as well as in the mammary ductal elongation, compared to CO(OID). Additionally, the number of apoptotic cells within mammary ducts and lobules is higher in CO(OID) compared to OID(CO). In contrast, the number of proliferating cells is higher in OID(CO) mammary gland compared to CO(OID). Conclusion: Altogether, our findings suggest that daughters of overweight fathers have both systemic and mammary gland confined factors alterations that ultimately lead to higher breast cancer risk in adulthood. However, further data is needed to corroborate this hypothesis. Our ongoing mammary tumor transplantation studies should provide further insight. Citation Format: Camile C. Fontelles, Anni Warri, Raquel S. Da Cruz, Maria I. Cruz, E","PeriodicalId":20357,"journal":{"name":"Prevention, Early Detection, and Interception","volume":"48 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83211633","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 3318: Development of a cfDNA based trans-omics approach for early cancer detection","authors":"Yuying Wang, Heng Zhao, Kaijian Ling, Jianchao Zheng, Zhilong Li, Shuangshuang Chen, Jia Li, Chichuan Liu, Guanghui Yang, Hongpo Zhou, Jiaxi Peng, Lili Ye, Liuhong Zeng, Jianlong Sun, Ruijingfang Jiang, L. Deng, Yanzhou Wang, Kezhong Chen, Zhiqing Liang, Fan Yang, T. Shi, M. Ye","doi":"10.1158/1538-7445.SABCS18-3318","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-3318","url":null,"abstract":"","PeriodicalId":20357,"journal":{"name":"Prevention, Early Detection, and Interception","volume":"30 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87983255","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 662: Impact of chemotherapy on the intestinal microbiome and epithelial barrier in PDX models of lung cancer","authors":"Cindy Pensec, D. Guenot, L. Calvet, C. Mignard, O. Duchamp, T. Carton, S. Leuillet, H. Blottière, F. Vacon","doi":"10.1158/1538-7445.AM2019-662","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2019-662","url":null,"abstract":"Introduction In the field of lung cancer treatments, significant progresses have been realized during last decade, such as targeted therapies and immunotherapies. Nevertheless, chemotherapy remains the gold standard for cancer. Pemetrexed is a chemotherapeutic agent commonly used in advanced lung cancer. This drug has a broad-spectrum effect that can induce significant side effects in patients. However, the impact of pemetrexed on gut microbiota and gastrointestinal inflammation in PDX mice remains unknown, although the role of the microbiota in carcinogenesis and modulation of efficacy or toxicity of chemotherapy agents has been demonstrated. The aim of this new study was to explore the impact of pemetrexed on the gut microbiota and the integrity of intestinal epithelial barrier and inflammation markers of PDX models following treatment. Methods Upon establishment of the PDX model, mice were treated with pemetrexed for 2 weeks. Stool specimens were collected at 3 time-points: before, after and one week after treatment. Gut microbiota composition was studied by 16S rRNA gene sequencing. The colon integrity of the epithelial barrier was evaluated by a histological examination, a permeability measurement and a selected cytokines expression. In parallel, body weight was recorded and tissues were sampled for assessment of toxicity and inflammation. Results Pemetrexed induced a significant body weight loss after each treatment cycle reflecting toxicity as known in clinical results. We have found that pemetrexed and tumor induced several modifications on microbiota composition, and the more important perturbation was the significant increase of the relative abundance of Enterobacteriaceae. A significant alteration of epithelial barrier integrity associated with early inflammation and infiltration of leukocytes into mucosal tissues was observed following treatment. Moreover, we have shown that pemetrexed effect on the microbiota was reproducible on several models of lung PDX models of lung carcinoma, and that dysbiosis seem proportional to the effectiveness of chemotherapy. Conclusion This work is a preliminary approach, that confirms the relationship between microbiota and chemotherapy. A better understanding of gut microbiota alterations induced by chemotherapy could help reduce side effects. It is essential to expand our knowledge about the chemotherapy impact on microbiota in order to minimize the side effects, avoid infection complications, and improve therapy efficiency. Citation Format: Cindy Pensec, Dominique Guenot, Loreley Calvet, Caroline Mignard, Olivier Duchamp, Thomas Carton, Sebastien Leuillet, Herve M. Blottiere, Francoise Le Vacon. Impact of chemotherapy on the intestinal microbiome and epithelial barrier in PDX models of lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 662.","PeriodicalId":20357,"journal":{"name":"Prevention, Early Detection, and Interception","volume":"42 2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89272617","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 5083: BSCHL-2046, a lead chalcone derivative from a newly synthesized library, is a potent neddylation inhibitor against the growth of prostate cancer cell lines","authors":"Matthew Tippin, Dongjun Fu, Liankun Song, Victor Pham, Xaolin Zi","doi":"10.1158/1538-7445.SABCS18-5083","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-5083","url":null,"abstract":"","PeriodicalId":20357,"journal":{"name":"Prevention, Early Detection, and Interception","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88518614","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 5074: Optimizing erlotinib plus sulindac dosing regimens in a preclinical model of FAP","authors":"A. Ulusan, P. Rajendran, W. Dashwood, Altaf Mohammed, S. Sei, P. Brown, Eduardo Vilar-Sánchez, R. Dashwood","doi":"10.1158/1538-7445.AM2019-5074","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2019-5074","url":null,"abstract":"Introduction Colorectal cancer (CRC) involves sporadic cases and hereditary syndromes, such as familial adenomatous polyposis (FAP). In FAP patients, surgical intervention often is coupled to prevention strategies using nonsteroidal anti-inflammatory drugs. However, none of the current therapeutic options is fully effective. A recent trial in FAP patients combined standard of care Sulindac (SUL) treatment with daily Tarceva/erlotinib (ERL), and had good efficacy in reducing adenomatous polyp burden. Toxicity concerns, however, raised questions over the combination strategy for long-term prevention (Samadder et al. 2016). Using the Apc‐mutant polyposis in rat colon (Pirc) model as a mimic of human FAP, we sought to optimize the dosing regimens for SUL+ERL for an improved safety profile, while retaining efficacy in the GI tract. Methods In a short-term pharmacodynamic biomarker study, rats (n=7) were fed AIN control diet or AIN diet containing 250 ppm SUL, either alone or in combination with ERL, given by oral gavage at 6 or 12 mg/kg (daily), 21 mg/kg (twice weekly), or 42 mg/kg (once weekly). Colon and small intestine (SI) polyps were resected at 0.5, 1, 2, 3, 7, 10, and 14 days after dosing, and assessed by immunoblotting (IB) or RT-qPCR for changes in pErk/Erk, pAkt/Akt, and other biomarkers. In a follow-up efficacy study, rats (n=10) were given SUL, ERL, or ERL+SUL using dosing regimens that were dictated by recovery times for pErk in the biomarker study. Colon and SI polyps were recorded at necropsy for location, incidence, multiplicity, and volume. Tumors and adjacent normal tissues were taken for histopathology and molecular analyses. Results The biomarker study revealed that pErk was inhibited in Pirc colon polyps for up to 10 days after discontinuing ERL treatment, with full recovery on or around day 14. Nuclear β-catenin, c-Myc, Mmp-7 and Cyclin D1 also were attenuated by ERL+SUL in colon polyps. In the efficacy study, results accrued via endoscopy at 3, 4 and 5 months were remarkably consistent with data obtained during final necropsy, at 6 months. Compared to AIN controls, multiple ERL+SUL groups exhibited significant suppression of polyps in the colon (78-98% inhibition, p Conclusions These studies have the potential to define safe and effective dosing strategies for SUL+ERL, improving efficacy against colon and SI polyps, while circumventing toxicity and resistance. Outcomes from the current work, plus an ongoing one-year toxicity/resistance trial in Pirc, should be directly translatable to the clinical management of FAP patients exhibiting similar pathology and phenotype. Supported by NCI Contract Number HHSN261201500018I, Task Order HHSN26100004. Citation Format: Ahmetmursel Ulusan, Praveen Rajendran, Wan-Mohaiza Dashwood, Altaf Mohammed, Shizuko Sei, Powel H. Brown, Eduardo Vilar-Sanchez, Roderick H. Dashwood. Optimizing erlotinib plus sulindac dosing regimens in a preclinical model of FAP [abstract]. In: Proceedings of the America","PeriodicalId":20357,"journal":{"name":"Prevention, Early Detection, and Interception","volume":"32 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83104195","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 LB-251: The cancer clinical trial landscape in the EU and the Nordic countries","authors":"J. Pouwels, S. Soidinsalo, Heidi M. Haikala, P. Jaakola, T. Jalava, H. Joensuu, M. Mustonen, P. Korhonen, P. Kovanen, A. Lehtonen, J. Mattson, O. Monni, J. Westermarck, J. Klefström","doi":"10.1158/1538-7445.SABCS18-LB-251","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-LB-251","url":null,"abstract":"Background. Cancer clinical trials seek to determine the safety and efficacy of new treatment modalities. Due to the impact of cancer clinical trials on health care, economic activity and cancer research, many large-scale efforts have been undertaken around the world to create clinical trial-facilitating environments. The Nordic countries (Norway, Sweden, Denmark, Iceland and Finland) are among the countries with the highest 5-year net survival for cancer patients, which is a testimony to their high standard of early diagnosis, cancer care and functional public health care system. However, the contribution of the Nordic countries to the international cancer clinical trial landscape has remained largely unexplored. Methods. We mined www.clinicaltrials.gov for cancer clinical trials starting between the 1st of January 2000 and the 31st of December 2017. Trials were designated Cancer Clinical Trials if the trial indication contained one of 17 cancer-specific words (e.g. “cancer”, “neoplasia”, “malignancy”). The trial databases of all European Free Trade Association (EFTA; the EU, Switzerland, Norway, Iceland and Liechtenstein) countries was downloaded and subsequently mined for specific terms, i.e. cancer indication, study location and intervention type. A trial was counted for every country with a study center and thus the same trial can be counted for multiple countries. Results. Here, we present an analysis of the cancer clinical trial landscape in the EFTA and the Nordic countries. While in the EFTA the number of cancer clinical trials strongly increased from 2000-2014, that number has not grown between 2014 and 2017, unlike in the USA or China. Comparison of the number of cancer clinical trials in different EFTA countries showed strong variation, and indicated that Sweden, Finland and Norway have been involved in far fewer cancer clinical trials than expected for countries of their economic size or socio-economic status. Denmark is the only Nordic country to perform much better than the EFTA average. Discussion. We show that despite a high standard of care, most Nordic countries are lagging behind in cancer clinical trials compared to countries of similar socio-economic stature. This low number of cancer clinical trials may slow down uptake of new cancer drugs to routine care, prevent patients from receiving state-of-the-art therapies, increase health care costs, and inhibit scientific progress and commercial activity. We provide recommended actions to increase the number of cancer clinical trials, with special focus on Finland as part of the national growth strategy in the health sector. Note: This abstract was not presented at the meeting. Citation Format: Jeroen Pouwels, Sebastian Soidinsalo, Heidi Haikala, Panu Jaakola, Tarja Jalava, Heikki Joensuu, Mika Mustonen, Pasi Korhonen, Panu Kovanen, Anne Lehtonen, Johanna Mattson, Outi Monni, Jukka Westermarck, Juha Klefstrom. The cancer clinical trial landscape in the EU and the Nordic countries ","PeriodicalId":20357,"journal":{"name":"Prevention, Early Detection, and Interception","volume":"51 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87335491","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 5080: Decursinol intercepts LNCaP human prostate cancer xenograft growth bypassing androgen receptor-prostate specific antigen axis","authors":"Sangyub Kim, Chongtao Qin, Deepkamal N. Karelia, Arati Sharma, Cheng Jiang, Junxuan Lu","doi":"10.1158/1538-7445.SABCS18-5080","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-5080","url":null,"abstract":"","PeriodicalId":20357,"journal":{"name":"Prevention, Early Detection, and Interception","volume":"113 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91454401","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 5070: Sulforaphane is a novel inhibitor of breast cancer-induced osteolytic bone resorption","authors":"S. Pore, Joseph D Latoche, C. Anderson, Juraj Adamik, D. Galson, K. Weiss, Boeun Lee, R. Watters, P. Kumta, Shivendra V. Singh","doi":"10.1158/1538-7445.SABCS18-5070","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-5070","url":null,"abstract":"","PeriodicalId":20357,"journal":{"name":"Prevention, Early Detection, and Interception","volume":"711 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76902278","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}