Invited Speaker Abstracts最新文献

{"title":"Abstract ES5-3: Late recurrence in ER-positive breast cancer","authors":"J. Gralow","doi":"10.1158/1538-7445.SABCS18-ES5-3","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-ES5-3","url":null,"abstract":"The risk of recurrence in early stage, ER-positive breast cancer patients persists for 15-20+ years after diagnosis, and never declines to zero. Rates of late recurrence can be reduced by extending tamoxifen therapy beyond 5 years, with additional tamoxifen or a switch to an aromatase inhibitor. The benefits of extending aromatase inhibitors beyond 5 years remains unclear. The benefit of extended adjuvant endocrine therapy for the average early stage breast cancer patient is small. Extended therapy can be associated with serious increased risks, including thromboembolic events and endometrial cancer with tamoxifen, and fractures and possibly cardiovascular events with aromatase inhibitors. Quality of life can also be impacted, including vasomotor symptoms, sexual dysfunction, and arthralgias. Determining which patients have high residual risk of recurrence beyond 5 years, and importantly whether additional therapy is likely to mitigate that risk, has been the subject of considerable recent research. Tumor size, nodal status and grade of the primary tumor at the time of diagnosis have been shown to be associated with risk of late recurrence in ER-positive breast cancer. Several multi-parameter molecular biomarker assays performed on the primary tumor are able to separate patients into groups at low and high risk for recurrence beyond 5 years when using retrospective data sets. To date, no specific assay has been felt to have high enough level evidence to recommend inclusion in treatment guidelines or use in decision-making regarding continuing, stopping or switching endocrine therapy. Recent studies have evaluated whether there are better determinants of late risk of recurrence, beyond the biology of the primary tumor, that can be performed years after the original diagnosis. Assays that may predict the presence of dormant tumor cells and late relapse include Circulating Tumor Calls (CTCs), Disseminated Tumor Cells (DTCs) in the bone marrow, and circulating tumor DNA, proteins or metabolites. While early data is promising, further research is needed before incorporating into clinical decision-making. Identifying a biomarker to determine patients most likely to benefit from longer duration endocrine therapy, or additional therapeutic approaches, could help in reducing late relapse as well as minimizing the risk of side effects and overtreatment. Citation Format: Gralow J. Late recurrence in ER-positive breast cancer [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr ES5-3.","PeriodicalId":224797,"journal":{"name":"Invited Speaker Abstracts","volume":"723 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116130510","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 MS2-2: Missed opportunities - The perils of under-treatment","authors":"R. Freedman","doi":"10.1158/1538-7445.SABCS18-MS2-2","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-MS2-2","url":null,"abstract":"","PeriodicalId":224797,"journal":{"name":"Invited Speaker Abstracts","volume":"29 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114960570","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 ES7-3: Indications for radiation treatments after neoadjuvant chemotherapy while awaiting the results of clinical trials","authors":"T. Buchholz","doi":"10.1158/1538-7445.sabcs18-es7-3","DOIUrl":"https://doi.org/10.1158/1538-7445.sabcs18-es7-3","url":null,"abstract":"","PeriodicalId":224797,"journal":{"name":"Invited Speaker Abstracts","volume":"64 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133240405","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 ES10-1: Recurrent ESR1 mutations activating mutations in breast cancer","authors":"R. Jeselsohn","doi":"10.1158/1538-7445.SABCS18-ES10-1","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-ES10-1","url":null,"abstract":"","PeriodicalId":224797,"journal":{"name":"Invited Speaker Abstracts","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128798576","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 BL1: Modeling Immune Response: Lessons Learned from Mouse Models of Cancer Development","authors":"L. Coussens","doi":"10.1158/1538-7445.SABCS18-BL1","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-BL1","url":null,"abstract":"The concept that leukocytes are critical components of solid tumors is now generally accepted, however, their role(s) in regulating aspects of cancer progression, and/or response to cytotoxic, targeted and/or immune therapy is only beginning to be understood. Utilizing de novo mouse models of mammary tumor development, we now appreciate that CD4+ T lymphocytes differentially regulate myeloid cell recruitment, activation and effector function, and in turn, activated tumor-infiltrating myeloid cells foster malignancy and repress anti-tumor immunity by a diversity of mechanisms. Treatment of tumor-bearing mice with therapeutic agents disrupting lymphocyte-myeloid interactions, myeloid activation, or myeloid functionality generally slow primary tumor growth kinetics when combined with cytotoxic therapy; however, their impact on metastases is variable. Similar to organ-specific regulatory programs co-opted to foster primary tumor growth, regulation of metastatic seeding and outgrowth is also regulated by tissue- and organ-specific mechanisms. Based on this, it stands to reason that therapeutic strategies may not be efficacious in both primary and metastatic locations. To be presented will be our recent insights into organ-specific regulation of primary and metastatic mammary cancer development by adaptive and innate immune cells regulating pro- and/or anti-tumor immunity, and new studies evaluating how attenuating protumor properties of select lymphoid and myeloid cells can be exploited to enhance therapeutic responses to cytotoxic and immune-based therapy. LMC acknowledges generous support from the NIH / NCI, the Department of Defense Breast Cancer Research Program Era of Hope Scholar Expansion Award, Susan G. Komen Foundation, the Breast Cancer Research Foundation, the Brenden-Colson Center for Pancreatic Health, and a Stand Up To Cancer – Lustgarten Foundation Pancreatic Cancer Convergence Dream Team Translational Research Grant. Citation Format: Coussens L. Modeling Immune Response: Lessons Learned from Mouse Models of Cancer Development [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr BL1.","PeriodicalId":224797,"journal":{"name":"Invited Speaker Abstracts","volume":"27 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"117075056","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 CS1-1: Polygenic risk scores for breast cancer: Ready or not?","authors":"D. Evans","doi":"10.1158/1538-7445.SABCS18-CS1-1","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-CS1-1","url":null,"abstract":"There are increasing attempts to try to stratify cancer risks to enable more targeted early detection and prevention strategies and in particular to balance the risks and benefits of population screening for breast cancer. An increasing number of common genetic variants called Single Nucleotide Polymorphisms (SNPs) have been identified which alter breast cancer risk. Although individually their effect sizes are small they can be used multiplicatively to provide a polygenic risk score (PRS) that accurately predicts risk in both the familial and population setting. Although the first 18 SNPs produce a highly calibrated PRS that is ready for use there are now PRSs of 143 or even 313 SNPs that increase risk stratification although with some loss of calibration. Using data from 9362 women in the Predicting the Risk Of Cancer At Screening (PROCAS) study (500 prospective cancers) and 2000 women in the FH-Risk familial cohort (500 prospective cancers) we have validated the PRS alongside mammographic density (density residual-DR) and standard risk factors to assess future risk of different types of breast cancer. The combined score accurately predicts breast cancers rates with 18-21% of women being predicted in the moderate or high risk categories (≥5% 10 year risk) that developed 41.5-45% of the stage 2+ cancers. In contrast SNP143 is able to identify alongside density and standard risk factors 21% of the general population at Conclusions: A combined approach using Tyrer-Cuzick, mammographic density and a PRS provides accurate risk stratification not only overall but also for worse prognosis cancers. This provides support for reducing screening intervals in the high and increasing them in the low risk groups. It is high time these highly informative tests were used in risk stratification Citation Format: Evans D. Polygenic risk scores for breast cancer: Ready or not? [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr CS1-1.","PeriodicalId":224797,"journal":{"name":"Invited Speaker Abstracts","volume":"43 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122641772","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 ES10-3: Blockade of estrogen signaling boosts antitumor immunity by inhibiting tumor-induced pathological myelopoiesis","authors":"J. Conejo-Garcia","doi":"10.1158/1538-7445.sabcs18-es10-3","DOIUrl":"https://doi.org/10.1158/1538-7445.sabcs18-es10-3","url":null,"abstract":"","PeriodicalId":224797,"journal":{"name":"Invited Speaker Abstracts","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126648467","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 MS2-1: Overtreatment: First, do no harm","authors":"R. Jagsi","doi":"10.1158/1538-7445.SABCS18-MS2-1","DOIUrl":"https://doi.org/10.1158/1538-7445.SABCS18-MS2-1","url":null,"abstract":"","PeriodicalId":224797,"journal":{"name":"Invited Speaker Abstracts","volume":"20 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115318996","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 BS1-1: High resolution intravital imaging of the mechanism of how breast cancer initiates and sustains systemic dissemination","authors":"J. Condeelis","doi":"10.1158/1538-7445.sabcs18-bs1-1","DOIUrl":"https://doi.org/10.1158/1538-7445.sabcs18-bs1-1","url":null,"abstract":"","PeriodicalId":224797,"journal":{"name":"Invited Speaker Abstracts","volume":"165 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126744584","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 ES8-1: Windows of susceptibility across the lifecourse and breast cancer","authors":"L. Kushi","doi":"10.1158/1538-7445.sabcs18-es8-1","DOIUrl":"https://doi.org/10.1158/1538-7445.sabcs18-es8-1","url":null,"abstract":"","PeriodicalId":224797,"journal":{"name":"Invited Speaker Abstracts","volume":"35 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134301947","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}