bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 2576: Radiation therapy delay and risk of ipsilateral breast tumors in women with ductal carcinoma in situ
Authors: Liu Ying , Yun Shumei , Lian Min , Colditz Graham 
Published: July 2016

Abstract
Objectives: To examine the relationship between radiation therapy delay and risk of subsequent breast events in the ipsilateral breast and to identify factors that are associated with delay in women with ductal carcinoma in situ (DCIS).
Methods: From the Missouri Cancer Registry, we identified the women who were diagnosed with first primary DCIS between 1996 and 2011 and treated with breast conserving surgery (BCS). Radiation therapy delay was defined as the first radiation therapy that was delivered greater than eight weeks after BCS. Propensity scores were calculated for radiation therapy delay and no radiation therapy during the first course of treatment. A propensity score-adjusted Cox proportional hazards regression analysis was conducted to estimate the hazard ratio (HR) of ipsilateral breast tumors. Logistic regression analysis was conducted to identify factors associated with delay.
Results: Among 5,916 patients, 1,053 (17.8%) received radiation therapy greater than eight weeks after BCS and 1,702 (28.8%) did not receive radiation therapy during the first course of treatment. During the 72- month follow-up, 182 (3.1%) developed ipsilateral breast tumors. After adjustment for propensity scores, the HR of ipsilateral breast tumors was 1.26 (95% CI, 1.00-1.59; p = 0.049) for radiation therapy delay and 1.35 (95% CI, 1.03-1.76; p = 0.03) for no radiation therapy compared with timely radiation therapy. Radiation therapy delay was associated with black race, being non-married and on Medicaid, later years of diagnosis, larger tumor size micropapillary architecture, and positive surgical margin.
Conclusions: Receipt of radiation therapy greater than eight weeks after BCS was associated with a significantly increased risk of ipsilateral breast tumors in women with DCIS. Timeliness of radiation therapy should be improved, particularly for black and Medicaid patients.
Citation Format: Ying Liu, Shumei Yun, Min Lian, Graham Colditz. Radiation therapy delay and risk of ipsilateral breast tumors in women with ductal carcinoma in situ. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2576.
Abstract 2586: Evaluation of risk-based colposcopy in the ALTS trial
Authors: Liu Angela H. , Schiffman Mark , Gage Julia C. , Castle Philip E. , Wentzensen Nicolas 
Published: July 2016

Abstract
Objective: Women referred to colposcopy have a wide spectrum of underlying risk of precancer that could influence colposcopic practice and management. We sought to evaluate important risk-strata based on HPV status, cytology, and colposcopic impression in women undergoing colposcopy.
Methods: Among participants in the ASCUS-LSIL Triage Study, we stratified women from the immediate colposcopy and HPV triage study arms based on enrollment HPV typing, study cytology, and colposcopic impression. In each group, absolute risk of CIN3+ at enrollment colposcopy and cumulative risk over 2-year follow-up were estimated. Immediate CIN3+ risk of LSIL and HSIL cytology were used as thresholds for colposcopy referral and immediate treatment, respectively.
Results: We observed substantial differences in risk of precancer across strata. Women with HSIL cytology, who were HPV16-positive, and high-grade colpscopic impression had a 71% baseline and 78% 2-year risk of CIN3+, respectively. HPV16-positive women with HSIL cytology and low-grade impression, and women with high-grade impression and either HSIL cytology or HPV16 infection, also showed significant CIN3+ risk exceeding the risk of HSIL. In contrast, women with normal colposcopy, &lt;HSIL cytology, and absence of HPV16 infection had the lowest baseline CIN3+ risk (3.2%), below the colposcopy referral threshold in ALTS.
Conclusion: Risk assessment at colposcopy can inform colposcopy-biopsy practice and guide management. In the low-risk group, biopsy yields little additional disease and a normal colposcopy may confer higher reassurance that CIN3+ is not present; while in the highest risk groups, immediate treatment without biopsy confirmation could be considered according to current guidelines. Analyses evaluating the benefit of multiple biopsies in these risk strata are underway and will be presented at the meeting.
Citation Format: Angela H. Liu, Mark Schiffman, Julia C. Gage, Philip E. Castle, Nicolas Wentzensen. Evaluation of risk-based colposcopy in the ALTS trial. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2586.
Abstract 2588: Prediction of the 5-year risk of hepatocellular carcinoma during long-term antiviral therapy in the general Korean population
Authors: Shim Jae-Jun , Oh In Hwan , Kim Jung Wook , Lee Chang Kyun , Jang Jae Young , Lee Ju-Seog , Kim Byung-Ho 
Published: July 2016

Abstract
Oral antiviral therapy using nucleos(t)ide analogues can decrease risk for hepatocellular carcinoma (HCC) in patients with chronic hepatitis B. However, wide use of antiviral therapy is limited by stringent treatment indications in many countries. We compared preventive effect of antiviral therapy on HCC development between current and new extended indication for the treatment. We established Korean cohort with chronic hepatitis B virus (HBV) infection using the fifth National Health and Nutrition Examination Survey (KNHANES). The cohort represented 993,872 subjects with chronic HBV infection more than 40 years in Korea. We estimated five-year risk of HCC before and after antiviral therapy using a HCC prediction score (REACH-B). The National Health Insurance (NHI) in Korea, the European Association for the Study of the Liver (EASL) guideline, and a new extended indication were compared. During a 5-year period, predicted HCC cases were 2,725 per 100,000 individuals (0.55% / year). When the cohort was treated under the Korean NHI indication, EASL, and new extended indication, HCC risk decreased to 2,531 (-7.1%), 2,089 (-23.3%), and 1,122 (-58.8%) cases per 100,000 individuals, respectively (P &lt; 0.0001). As participation rate in antiviral therapy among eligible patients increased every 10%, HCC risk decreased to -0.74%, -2.39%, and -5.87%, respectively. New extended indication could decrease HCC risk eight times more than the current Korean NHI indication. Prediction of HCC development among chronic HBV infection is feasible in the virtual population level. Considering the large preventive effect of antiviral therapy, the treatment indications should be revised to increase eligible patients. Indications for antiviral treatment used in this study and predicted reduction of HCC riskKorean NHIEASLNew extended indicationLiver enzymeAST or ALT ≥ 80 IU/LALT ≥ ULN x 1AnyHBV DNA level≥ 20,000 IU/mL≥ 2,000 IU/mL≥ 2,000 IU/mLHCC risk reduction, mean (SD) (%)-7.14 (0.14)-23.33 (0.26)-58.82 (0.07)
Citation Format: Jae-Jun Shim, In Hwan Oh, Jung Wook Kim, Chang Kyun Lee, Jae Young Jang, Ju-Seog Lee, Byung-Ho Kim. Prediction of the 5-year risk of hepatocellular carcinoma during long-term antiviral therapy in the general Korean population. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2588.
Abstract 2592: The role of surgery in the treatment of epithelioid trophoblastic tumor: A single institution case series
Authors: Winder Abigail , Sobecki-Rausch Janelle , Maniar Kruti , Novak Karen , Kim Julie , Lurain John 
Published: July 2016

Abstract
Objective: Epithelioid trophoblastic tumor (ETT) is a rare variant of gestational trophoblastic neoplasia (GTN) that develops from chorionic-type intermediate trophoblasts, simulates carcinoma, often presents many years following a pregnancy event, is associated with low or normal human chorionic gonadotropin (hCG) levels, and is relatively resistant to chemotherapy. Our aim was to identify the role of surgery in the management of both localized and metastatic ETT.
Methods: A retrospective review of women with ETT treated at a gestational trophoblastic disease center from 2010-2015 identified five women. Medical records were abstracted for demographic data, clinical presentation, hCG levels, prior pregnancy information, disease sites, and treatment with chemotherapy and surgery.
Results: The five women with ETT ranged in age from 28 to 48 years. Clinical presentation was abnormal uterine bleeding prompting dilation and curettage, which established the diagnosis of ETT in three women. One woman presented with repeated spontaneous pneumothorax requiring thoracoscopic resection, which identified a 6 cm ETT in the lung. Another woman was initially treated with methotrexate for a presumed ectopic pregnancy without a response. Two women had no identifiable antecedent pregnancy, two women had spontaneous abortions 19 and 72 months prior to the diagnosis of ETT, and one woman had a normal term delivery 48 months earlier. Four of five women had metastatic disease to the lungs. Three of these women underwent pulmonary wedge resection as well as hysterectomy followed by paclitaxel-cisplatin/paclitaxel-etoposide (TP/TE) chemotherapy, while the other woman was treated with etoposide, methotrexate, actinomycin D/etoposide, cisplatin (EMA/EP) chemotherapy and hysterectomy. The one woman with nonmetastatic disease was treated with hysterectomy only. All five women are currently without evidence of disease.
Conclusions: Surgery, including hysterectomy and resection of metastatic disease, is an important component in the treatment of women with ETT. Adjuvant chemotherapy with a platinum-containing regimen, such as TP/TE or EMA/EP, should be used in women with metastatic disease. All five women with ETT in this series were cured using this approach, including the four with metastatic disease.
Citation Format: Abigail Winder, Janelle Sobecki-Rausch, Kruti Maniar, Karen Novak, Julie Kim, John Lurain. The role of surgery in the treatment of epithelioid trophoblastic tumor: A single institution case series. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2592.
Abstract 2597: Breast and ovarian cancer risks associated with cancer predisposition gene mutations identified by multigene panel testing
Authors: Couch Fergus J. , Goldgar David E. , Hart Steven N. , Hallberg Emily , Moore Raymond , Meeks Huong , Huether Robert , LaDuca Holly , Chao Elizabeth , Dolinsky Jill 
Published: July 2016

Abstract
Multigene panel testing (MGPT) for hereditary cancer is increasing in popularity in the USA. Many panels include genes identified as hereditary breast and/or ovarian cancer (HBOC) genes despite limited data regarding the precise cancer risks associated with mutations in these genes. Here we report on results from BreastNext and OvaNext panel testing of 20 genes (ATM, BARD1, BRCA1, BRCA2, BRIP1, CDH1, CHEK2, MLH1, MRE11A, MSH2, MSH6, NBN, NF1, PALB2, PMS2, PTEN, RAD50, RAD51C, RAD51D, TP53) in a cohort of 15,083 individuals. The majority of individuals were from high-risk breast and/or ovarian (Br/Ov) cancer families, with 92.4% of all probands meeting National Comprehensive Cancer Network HBOC testing criteria. Pathogenic mutations were identified in 9.4% of the overall cohort.
To estimate gene-specific breast and ovarian cancer risks, case-control analyses were performed comparing the frequencies of pathogenic mutations from Caucasian breast or ovarian cancer cases from BreastNext and OvaNext with frequencies from Caucasian, non-Finnish, non-TCGA controls from the Exome Aggregation Consortium (ExAC) database. Mutations in the well studied ATM and CHEK2 genes were associated with moderate risks (OR&gt;2) of breast cancer and mutations in PALB2 were associated with high-risks (OR&gt;5) of breast cancer, consistent with previous reports. In addition, the study suggested that pathogenic mutations in MSH6, RAD51D, CDH1, and NF1 are associated with moderate to high risks of breast cancer. In contrast, RAD51C, RAD51D, and BRIP1 mutations were associated with high risks of ovarian cancer, PALB2 mutations were associated with moderate risks, but ATM and CHEK2 mutations were not associated with increased ovarian cancer risk. In addition, modeling of missense mutations in the predisposition genes using in silico prediction algorithms suggested that missense mutations in CDH1, CHEK2, MSH2, and MSH6 are associated with moderate risks of breast cancer and missense mutations in RAD51C increase risks of ovarian cancer. This large breast and ovarian cancer case-control analysis provides useful data for many predisposition genes previously lacking risk estimates, and should prove useful for clinical risk management of patients after clinical panel testing.
Citation Format: Fergus J. Couch, David E. Goldgar, Steven N. Hart, Emily Hallberg, Raymond Moore, Huong Meeks, Robert Huether, Holly LaDuca, Elizabeth Chao, Jill Dolinsky. Breast and ovarian cancer risks associated with cancer predisposition gene mutations identified by multigene panel testing. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2597.
Abstract 2599: Association of periodontal disease and breast health in women undergoing screening mammography
Authors: Park Hannah Lui , Acheampong Teofilia , Nguyen Kathleen , Nguyen Cindy , Ziogas Argyrios , Kelly Richard , Alvarez Andrea , Larsen Kathryn M. , Goodman Deborah , Anton-Culver Hoda 
Published: July 2016

Abstract
It is well established that chronic and persistent inflammation contributes to cancer development. Chronic inflammation is often associated with periodontal disease, or gum disease. Periodontal disease, which can be prevented or ameliorated by following proper oral hygiene, is known to be associated with various systemic disorders including coronary heart disease and some cancers, including head and neck cancer and pancreatic cancer. However, little is known about its potential association with breast cancer, with only one report in which periodontal disease was a positive predictor for breast cancer in a Swedish cohort. To examine if a potential link exists between periodontal disease and breast cancer in a separate cohort, mammography patients from the UC Irvine Athena Breast Health Network cohort were recruited to participate in a survey that included questions about their periodontal health. Diagnosis of invasive breast cancer, DCIS, and benign breast diseases was determined through data extraction from electronic medical records. There was no association between periodontal disease and DCIS or invasive breast cancer. However, there was a significant difference in the frequency of breast cysts among women with periodontal disease compared to women without periodontal disease (p&lt;0.01). Women with periodontal disease were at least 4-fold more likely to have breast cysts, even after adjusting for potential confounders including age, race/ethnicity, and smoking history (p&lt;0.05). To our knowledge, this is the first report on an association between periodontal disease and breast cysts. Our data suggest that further studies on potential links between periodontal disease and breast health are warranted.
Citation Format: Hannah Lui Park, Teofilia Acheampong, Kathleen Nguyen, Cindy Nguyen, Argyrios Ziogas, Richard Kelly, Andrea Alvarez, Kathryn M. Larsen, Deborah Goodman, Hoda Anton-Culver. Association of periodontal disease and breast health in women undergoing screening mammography. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2599.
Abstract 2624: Possibility of prostate cancer prevention based on cancer stem cell theory
Authors: Shiozawa Nobuya , Sugahara Ryosuke , Sato Ayami , Ota Masako , Yano Tomohiro 
Published: July 2016

Abstract
Cancer stem cells are considered to be one of the causes of cancer. In recent years, stemness (stem like) of gene expression patterns in the development process of cancer has been observed. Stemness and pathology of cancer are closely related. Elucidation of the stemness regulation of cancer is an important key to the development of new cancer prevention methods. However, as far as we know, there exist no cancer prevention studies focusing on cancer stem cells. In this study, we have investigated the possibility of prostate cancer prevention with a focus on cancer stem cells. We utilized prostate cancer cell lines PC3, DU145 (androgen-independent) and LNCaP (androgen-dependent) cells. Then, using spheroid formed cells, mRNA expression levels of cancer stem cells markers were estimated by RT-real time-PCR. Cancer cells have several malignant phenotypes under hypoxia, and we investigated for the cancer stem cells induced malignant alteration under hypoxia. In addition, under hypoxia, we investigated cell viability effect under tocotrienol-rich fraction (TRF) from annatto. TRF almost consists of delta- tocotrienol (δ-T3) that has the strongest anti-cancer activity. We observed spheroid formation capacity and compared the spheroid sizes and mRNA levels of DU145, PC3 and LNCaP cells. Size of DU145 spheroid is smaller in comparison to spheroids of PC3 and LNCaP. mRNA expression levels of cancer stem cells marker were elevated in PC3 and LNCaP cells. This means that PC3 and LNCaP cells have higher concentration of cancer stem cells. Furthermore, stemness decreases with increase of passage number, the number of cultures. We confirmed the presence of stemness in the formation capacity of spheroid until passage 4. Under hypoxia, cell viability of cancer stem cells was elevated compared to normal cultured prostate cancer cells. In addition, under hypoxia and TRF treatment, cell viability of cancer stem cells decreased with increase in TRF concentration compared to control (0 μg/ml). Our results suggest that TRF suppress cell viability of prostate cancer stem cells under hypoxic states and is effective in prostate cancer prevention.
Citation Format: Nobuya Shiozawa, Ryosuke Sugahara, Ayami Sato, Masako Ota, Tomohiro Yano. Possibility of prostate cancer prevention based on cancer stem cell theory. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2624.
Abstract 2655: Oncogenic chromatin factors drive cell type-specific transcription within megadomains in NUT midline carcinoma
Authors: Kuroda Mitzi I. , Alekseyenko Artyom A. , Walsh Erica M. , Wang Xin , Grayson Adlai , Hsi Peter T. , Kharchenko Peter V. , French Christopher A. 
Published: July 2016

Abstract
NUT midline carcinoma (NMC), a subtype of squamous cell cancer, is one of the most aggressive human solid malignancies known. NMC is driven by the creation of a translocation oncoprotein, BRD4-NUT, which blocks differentiation and drives growth of NMC cells. BRD4-NUT forms distinctive nuclear foci in patient tumors, which we find correlate with ∼100 unprecedented, hyperacetylated expanses of chromatin that reach up to 2 Mb in size. These ‘megadomains’ appear to be the result of aberrant, feed-forward loops of acetylation and binding of acetylated histones. Megadomains drive transcription of underlying DNA in NMC patient cells and in naïve cells induced to express BRD4-NUT. Here we characterize the constituents of BRD4-NUT chromatin complexes using a crosslinking approach, BioTAP-XL. We find many transcriptional activating proteins known to associate with BRD4, along with novel interactors including p300/CBP and a previously uncharacterized BRD4-NUT Megadomain Associated Protein (BMAP1). BMAP1 is expressed in primary NMC tissue and a subset of more common head and neck squamous cell carcinomas (HNSQC). Concurrently, we discovered a patient-derived NMC harboring a novel BMAP1-NUT fusion. BMAP-NUT blocks differentiation, and like BRD4-NUT recruits p300 to form hyperacetylated megadomains, including at the MYC locus. Thus, our proteomic and genetic approaches have converged on a novel mechanism that involves reprogramming very large regulatory regions to drive oncogenic transcription.
Citation Format: Mitzi I. Kuroda, Artyom A. Alekseyenko, Erica M. Walsh, Xin Wang, Adlai Grayson, Peter T. Hsi, Peter V. Kharchenko, Christopher A. French. Oncogenic chromatin factors drive cell type-specific transcription within megadomains in NUT midline carcinoma. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2655.
Abstract 2659: A novel isoform of TET1 that lacks a CXXC domain is overexpressed in cancer
Authors: Good Charly R. , Madzo Jozef , Maegawa Shinji , Engel Nora , Jelinek Jaroslav , Issa Jean-Pierre 
Published: July 2016

Abstract
TET1 is a DNA demethylase that regulates DNA methylation, hydroxymethylation and gene expression patterns. It has a catalytic domain that oxidizes methylated cytosine into 5-hydroxymethylcytosine and can then be further oxidized or converted to un-methylated cytosine. TET1 has a CXXC domain that allows it to recognize and bind to long stretches of CpG dinucleotides, known as CpG islands (CGIs). Our previous work found TET1 to protect CGIs from aberrant methylation and that the CXXC domain limits its ability to regulate genes outside of CGIs. However, many of the methylation changes in cancer are outside CGIs. To determine if TET1 could possibly play a role in this hypomethylation, we searched for alternatively spliced forms of the protein. We identified a novel isoform of TET1 (TET1ALT) that lacks the CXXC domain but retains the demethylase domain. TET1ALT has a unique transcription start site from a strong alternate promoter upstream of exon 3, yielding a protein with a unique translation start site. We confirmed promoter activity using Luciferase constructs, and confirmed TET1ALT translation and function through overexpression experiments. Gene expression analyses by qPCR found that TET1ALT is silenced in mESCs but becomes activated in select embryonic and adult tissues while full length TET1 is favored in mESCs, but is repressed in adult tissues. Thus, there is an isoform switch during differentiation and TET1ALT is the major isoform expressed in adult cells. TET1ALT is over expressed in several cancer cell lines, including breast cancer. In conclusion, we have identified a novel isoform of TET1 that has the potential to regulate DNA methylation outside of CGIs and is the predominant isoform expressed in adult cells. We are investigating the hypothesis that TET1ALT may contribute to the methylation changes observed in cancer outside of CGIs, such as in gene bodies and in enhancers.
Citation Format: Charly R. Good, Jozef Madzo, Shinji Maegawa, Nora Engel, Jaroslav Jelinek, Jean-Pierre Issa. A novel isoform of TET1 that lacks a CXXC domain is overexpressed in cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2659.