bluuebunny/crossref_metadata_2025_split huggingface dataset:
Insurance disparity in the United States cancer survivors’ smoking rates: A trend study from NHIS 2008-2017.
Authors: Zhao Yannan , Zheng-Lin Binbin , Wang Biyun , Hu Xi-Chun , Jiang Changchuan 
Published: May 2019

1553 Background: Smoking rates have been decreasing in the U.S over the last decade. Smoking cessation is a critical part of cancer treatment and survivorship care. However, little is known about the trend of smoking rates in U.S. cancer survivors and how it varied by individuals’ insurance coverages. Methods: We conducted a retrospective study to evaluate the temporal trend of smoking rates using the National Health Interview Survey from 2008 through 2017. Adult cancer survivors (n = 20122) were included in the analysis. The outcomes were self-reported current smoking behavior. Insurance coverage was categorized into any private (age ≤65), other coverage (age ≤65), uninsured (age ≤65), Medicare + any private (age > 65), and other coverage (age > 65). We combined every two years data to improve statistical power in the subgroup analysis. Weighted analyses were performed with SAS 9.4 to account for the complex design. Results: The smoking rates in cancer survivors decreased from 18.4% in 2008 to 12.5% in 2017. However, the smoking rates varied remarkably by insurance status (p < 0.001). There was a decreasing trend of smoking rates in participants with any private (age ≤65) (17.3% in 2008/2009 to 12.0% in 2016/2017), Medicare + any private (age > 65) (7.5% in 2008/2009 to 5.9% in 2016/2017), and other coverage (age > 65) (13.2% in 2008/2009 to 9.2% in 2016/2017) whereas the current smoking rates remains high in cancer survivors with other coverage (age ≤65) (40.1% in 2008/2009 to 34.4% in 2016/2017) and uninsured (age ≤65) (43.4% in 2008/2009 to 43,1% in 2016/2017). Conclusions: Cancer survivors report less smoking behaviors over the last decade which is similar to the general population. However, the smoking rate remains dangerously high in non-elderly cancer survivors without any private insurance.
Comorbidity and racial differences in risk of mortality of men with breast cancer.
Authors: Parise Carol , Caggiano Vincent 
Published: May 2019

1554 Background: Black men with breast cancer have more concomitant disease and worse survival than white men. Less is known about concomitant disease and survival in Hispanic and Asian/Pacific Islander (API) men with breast cancer. The purpose of this study was to compare differences in survival and risk of mortality of white, black, Hispanic, and Asian/Pacific Islander (API) men with breast cancer with increasing comorbidity. Methods: We identified 1,497 cases of first primary male invasive breast cancer from the California Cancer Registry 2000-2015 with a documented Charlson Comorbidity Index (CCI). The CCI is a weighted index based on the presence of certain comorbid conditions following a cancer diagnosis and weighted by the severity of these conditions. A score of 0 indicates no significant comorbidity and scores of 2 or more are interpreted as a high comorbidity burden. Bivariate associations between race and AJCC stage, tumor grade, estrogen receptor (ER) status, human epidermal growth factor 2 (HER2), and socioeconomic status (SES) were compared using the χ2 Test of Independence. Kaplan Meier Survival analysis was used to compare unadjusted survival among the races. Cox Regression was used to assess risk of mortality for each race when adjusted for factors that had a statistically significant (p < 0.10) bivariate association with race/ethnicity. Analyses were conducted within each level of the CCI (0, 1, and 2 or more). Results: Among men with a CCI of 0 or 2, blacks had worse unadjusted survival than whites. There were no differences in survival for men with a CCI of 1. Stage, SES, ER, and type of surgery all had statistically significant bivariate associations with race/ethnicity. For men with a CCI of 0, Hispanics (HR = 0.367; 95% CI = 0.167, 0.801) and APIs (HR = 0.422; 95% CI = 0.189, 0.941) had a reduced risk of mortality when compared with whites. Black men had the same risk of mortality as white men. There were no differences in risk of mortality by race for men with a CCI of 1 or 2. Conclusions: Black men with breast cancer and no comorbidity have the same risk of mortality as white men while Hispanic and API men have lower risk of mortality. There are no racial disparities in adjusted risk of mortality in men with breast cancer with any concomitant disease.
Burden of thrombocytopenia in adult cancer patients receiving chemotherapy.
Authors: Soff Gerald A. , Shaw Jaime , Kilpatrick Karynsa , Marongiu Andrea , Park Joseph 
Published: May 2019

1555 Background: Thrombocytopenia is a common toxicity of chemotherapy, yet there are limited data on its occurrence in routine clinical practice. Methods: Using structured patient-level data from the Flatiron Health EHR-derived database, we assessed risk (3-month cumulative incidence) of chemotherapy-induced thrombocytopenia (CIT) in adult patients (2012-2017) based on platelet counts, overall and by each grade of CIT, cancer type, and chemotherapy regimen (Table); and the co-occurrence of other hematologic abnormalities. Results: Of 15,521 solid tumor patients who initiated chemotherapy, 13% had evidence of CIT within 3 months (platelet count <100x109/L), 4% had grade 3 (25 to <50x109/L) and 2% had grade 4 (<25x109/L) CIT. Of the solid tumors examined, incidence was highest in melanoma patients. In hematologic malignancies (N = 2,537), 3-month risk was even higher with nearly 30%, 16%, and 12% having any grade, grade 3 and 4 CIT, respectively; and the greatest risk being in multiple myeloma patients. Anthracycline-based regimens were associated with the highest risk of CIT (7% grade 3; 4% grade 4), followed by gemcitabine- and platinum-based regimens. Anemia often accompanied first evidence of CIT (49%); isolated thrombocytopenia occurred in 15%. Conclusions: This study provides a current snapshot of CIT risk in a large sample of adult patients undergoing chemotherapy in routine clinical practice, highlighting patients at highest risk for CIT and underscoring the complexity of managing cancer treatment. [Table: see text]
Breast cancer screening adherence at multiple timepoints over eight years among women in a familial cohort.
Authors: Schaeffer Marcy L. , May Betty J , Hogan Brenna C. , Orellana Mikiaila M. , McCullough Michelle C. , Armstrong Deborah Kay , Myers Kelly , Visvanathan Kala 
Published: May 2019

1557 Background: Since 2007, U.S. guidelines recommend cancer-free women with ≥20% lifetime breast cancer (BC) risk undergo BC screening with mammogram and breast MRI. There is limited long-term data on BC screening adherence among young, high-risk women. To address this knowledge gap, we examined utilization of multiple BC screening modalities over time. Methods: Eligible women were ≥ 30 years old, had no history of BC/ovarian cancer, an intact breast, are enrolled in the Breast and Ovarian Surveillance Service (BOSS) Cohort, and visited the Johns Hopkins Cancer Genetics Clinic for risk assessment within 2 months of cohort enrollment (N = 374). All screening was self-reported at baseline, 4, and 8 years. A subset has been validated. We categorized women by BC risk (Tyrer-Cuzick version) obtained at the clinic. We examined frequency of screening over follow-up, and defined adherence to annual mammography and breast MRI based on age- and risk-based guidelines. We modeled the association between BC risk and adherence at 4 and 8 years using logistic regression. Results: At baseline, the median age was 47 years, 31% had lifetime risk < 20%, and 69% had risk ≥20%. Frequency of mammography and clinical breast exam over follow-up was > 60%, while frequency of breast MRI and breast ultrasound was < 40%. Twenty-five percent of high-risk women at 4 years and 40% at 8 years did not report any mammography, breast MRI, or breast ultrasound. At 4 years, high-risk women were 85% less adherent [multivariable adjusted OR = 0.15; 95%CI = 0.07, 0.34] to BC screening guidelines compared to women with a risk of < 20% due to low uptake of breast MRI, while at 8 years, high-risk women were also less adherent to mammography [multivariable adjusted OR = 0.42; 95%CI = 0.18, 0.95]. We observed similar associations among women at high-risk at 5- and 10-years. Adherence at 4 years predicted adherence at 8 years. Interestingly, women who did not uptake MRI complied with other health screening including for colorectal cancer. Conclusions: High-risk women were not adherent to risk-appropriate BC screening, and adherence did not improve over time. Low adherence appears specific to BC screening. New approaches to BC screening are urgently needed for this high-risk group.
Incidental atypical hyperplasia/LCIS in mammoplasty specimens and subsequent risk of breast cancer.
Authors: Acevedo Francisco , Armengol Victor Diego , Deng Zhengyi , Tang Rong , Coopey Suzanne , Mazzola Emanuele , Lanahan Conor , Braun Danielle , Yala Adam , Barzilay Regina , Li Clara , Santus Enrico , Colwell Amy , Guidi Anthony , Cetrulo Curt , Garber Judy Ellen , Smith Barbara L. , King Tari A. , Hughes Kevin S. 
Published: May 2019

1561 Background: Proliferative breast lesions with atypia (atypical hyperplasia and lobular carcinoma in-situ (LCIS)) increase the risk of breast cancer (BC). Most cases are diagnosed in the context of an abnormal mammogram. Little is known about BC risk for patients with these lesions who are asymptomatic. Mammoplasty specimens allow us to study breast tissue in asymptomatic healthy women. We previously published the rate of atypia in the largest reported mammoplasty cohort. The aim of this study is to examine the risk of BC in the atypia cohort. Methods: Breast pathology reports were retrospectively reviewed for evidence of atypical ductal hyperplasia (ADH), atypical lobular hyperplasia (ALH) or LCIS in bilateral reduction mammoplasty specimens from five institutions within a single healthcare system between 1990 to 2017. Patients with prior or concurrent BC or prior atypia were excluded. Data was extracted from electronic medical records using natural language processing and manual review to assess subsequent risk of BC. Results: From our mammoplasty cohort of 4771 patients, 295 patients were found to have atypia (6.2%) at baseline. 40 of these patients were lost to follow-up and excluded from the study. For the remaining 255 patients, 13 had severe ADH bordering on ductal carcinoma in situ, 52 had LCIS, 119 had ALH, and 71 had ADH at baseline. The median age at baseline was 52.1 (range 17.9 – 74.3). With a median follow-up of 7.7 years, of the 255 patients 9 patients developed BC (8 invasive carcinomas, 1 ductal carcinoma in situ). 81.3% of the cohort did not receive chemoprevention. Only one patient out of the nine who developed BC received chemoprevention. The risk of developing BC among women with atypia at baseline was 0.5%, 2.9% and 4.1%, at 3, 5 and 10 years respectively. Conclusions: Patients with asymptomatic atypias found in reduction mammoplasty specimens appear to be at lower risk of developing BC than those diagnosed with atypia in the context of an abnormal mammogram. These results may provide guidance on how to manage this group of patients related to future screening and/or chemoprevention.
A real-world evidence study of CDK4/6 inhibitor treatment patterns and outcomes in metastatic breast cancer by gBRCA mutation status.
Authors: McLaurin Kimmie , Dalvi Tapashi , Collins Jenna M , Nordstrom Beth L , McCutcheon Susan , Bennett James C , Murphy Brian R , Singhal Puneet K , Briceno Josefa Maria 
Published: May 2019

1563 Background: Limited data exist on the real-world treatment patterns and effectiveness of cyclin-dependent kinases 4 and 6 (CDK4/6) inhibitors in the germline BRCA (g BRCA) mutated breast cancer population. Methods: Adults with human epidermal growth factor receptor 2 negative (HER2-), hormone receptor positive (HR+) metastatic breast cancer (mBC) treated with a CDK4/6 inhibitor from 01Jan2013–31Jan2018 were retrospectively selected from the Flatiron Health Oncology electronic medical record database. Patients with known g BRCA status were classified as having g BRCA mutated (g BRCAm) or wild type (g BRCAwt) disease. Time to first subsequent therapy or death (TFST) and overall survival (OS) were calculated from start of the earliest line of therapy with a CDK4/6 inhibitor. Kaplan-Meier (KM) medians were estimated, and TFST and OS compared between g BRCA groups with Cox models stratified by line of therapy and adjusting for demographic and clinical characteristics that modified hazard ratios (HRs) for g BRCA status by > 10%. Results: Of 2968 HER2- HR+ patients with mBC receiving a CDK4/6 inhibitor, g BRCA status was known for 859 (28.9%). Patients with g BRCAm and g BRCAwt received letrozole plus palbociclib (42.4 and 39.8%, respectively), fulvestrant plus palbociclib (32.9 and 30.7%), or other CDK4/6 regimens (24.7 and 29.5%) across all lines. The g BRCAm group had a non-significant, shorter TFST than g BRCAwt (stratified HR 1.24; 95% CI 0.96–1.59). OS was significantly shorter in g BRCAm than g BRCAwt patients (stratified HR 1.50; 95% CI 1.06–2.14). Conclusions: The results of this real-world study suggest that treatment outcomes with CDK4/6 inhibitors may be poorer in patients with g BRCAm compared with g BRCAwt disease. These findings indicate a higher unmet need among patients with g BRCAm, potentially requiring alternative treatment options. [Table: see text]
Unselected germline screening in pancreatic adenocarcinoma yields high rates of pathogenic and likely pathogenic variants (PV) in hereditary cancer susceptibility genes.
Authors: Cremin Carol , Lee Michael , Hong Quan , Hoeschen Carolyn , Kalloger Steve , Karasinska Joanna , Mackenzie Anna , McCullum Mary , Nuk Jennifer E , Topham James Thomas , Sun Sophie , Schaeffer David F. , Renouf Daniel John , Schrader Kasmintan A 
Published: May 2019

1582 Background: Recent literature cites a germline mutation rate of 3.9-15.1% in patients diagnosed with pancreatic ductal adenocarcinoma (PDAC) depending on breadth of genes tested, pre-selection of high-risk history and population substructure. True incidence of germline mutations in PDAC is unknown in unselected population. Methods: All patients (pts) diagnosed with PDAC in the province of British Columbia, Canada and referred to the Hereditary Cancer Program, were eligible to undergo 30 gene Color saliva kit testing under a research protocol, or clinical multigene testing if they met existing local criteria regardless of whether they signed on to the protocol. Any healthcare provider or patients themselves could refer. Results: 243 pts were referred between August 2016 and October 2018 but 25.1% (61) declined and 9.1% (22) died before testing. Of the 141 pts who consented to research protocol and completed germline testing, median age was 64 (46.1-81.0), 68.8% were European, 1.4% Ashkenazi Jewish heritage, 42% male, 61% non-smoker, 24.1% had personal history of a second cancer and 39% had metastatic disease. Baseline characteristics were similar between the PV positive and uninformative group. 20/25 PV were in known PDAC susceptibility genes with cascade screening implications (ATM (9), BRCA2 (4), BRCA2/ATM (1), CDKN2A (4), and MSH2 (2)). Excluding the 3 PV identified through carrier testing (1) and prior research identification (2), the rate of PV in unselected, unrelated PDAC cohort is 22/138 (15.9%). Utilizing previous NCCN criteria for BRCA1/BRCA2 testing or for familial pancreatic cancer did not appear to select for patients with higher risk of PV positive (12/65 (18.4%) PV positive rate versus 13/76 (17.1%) in those that didn’t meet criteria). Previous criteria would have missed 52% (13/25) PV in ATM (6), BRCA2/ATM (1), BRCA2 (2), MSH2 (2), NBN (1), CHEK2 (1). To date, a third of families with PV identified have accessed cascade testing in 38 relatives. Conclusions: Given the high incidence of 15.9% PV in hereditary cancer susceptibility genes, our data support recommendations for universal germline genetic testing of PDAC pts.
Germline mutation profile among Hispanic women with epithelial ovarian cancer (EOC).
Authors: Chavarri Guerra Yanin , Weitzel Jeffrey N. , Blazer Kathleen Reilly , Slavin Thomas Paul , Mejia Rosa , Sand Sharon , Castillo Danielle , Herzog Josef , Villarreal-Garza Cynthia , Mohar Alejandro , Rodriguez Yeny , Mora Alferez Analí Pamela , Hake Christopher R. , Cescon Terrence , Bobolis Kristie , Kerlin Deborah , Komenaka Ian K. , Rice Patricia , Horcasitas Darling J ,   Clinical Cancer Genomics Community Research Network Consortium
Published: May 2019

1584 Background: Hospital-based studies have reported a 15% prevalence of BRCA1/ BRCA2( BRCA) mutations, with a slightly higher yield of other predisposition genes on multigene panel testing (MGPT) among women with EOC, and National Comprehensive Cancer Network guidelines recommend genetic cancer risk assessment for women with EOC. However, there is limited data about the genetic epidemiology of EOC among underrepresented populations, such as Hispanics. Consequently, we determined the germline mutation profile of Hispanics with EOC, and compared them with non-Hispanics. Methods: We included all women with a personal history of EOC from the U.S. and Latin America (LatAm; Mexico, Colombia, and Peru), enrolled in the Clinical Cancer Genomics Community Research Network registry. We assessed the prevalence of pathogenic variants (PV) in BRCA1/ BRCA2( BRCA) and other genes, contrasting the germline mutation profile between Hispanics living in LatAm, U.S. Hispanics, women of Ashkenazi Jewish (AJ) ancestry in the US, and other U.S. non-Hispanics. Results: Among 1186 women with EOC (209 from LatAm, 254 U.S. Hispanics l, 78 AJ, and 645 other non-Hispanic), 262 (22%) had a PV in BRCAgenes. Hispanics from LatAm and the U.S. had a similar frequency of BRCAmutations to AJ (30.6%, 29.9%, and 38.4%, respectively; p = 0.14); while non-Hispanics showed a significantly lower frequency of BRCAmutations (14.2%, p = 0.03). The most frequently mutated gene was BRCA1(n = 197, 74.6%), followed by BRCA2(n = 67, 25.3%). Among BRCA-negative cases (n = 924), 59% (n = 545) were evaluated by MGPT and PVs were identified in 2.9% [6 Hispanics (1.2%), 3 AJ (3.8%) and 26 Non-Hispanics (4%)]), of which 66% (n = 23) were in mismatch repair genes ( MSH2, MLH1, MSH6, PMS2), and 34% (n = 12) in other EOC-associated genes ( BRIP1, NBN, PALB2, RAD51C, and RAD51D). Clinically actionable PVs in ATM (n = 4; 0.3% ) and CHEK2 (n = 6; 0.5% ) were also observed. Conclusions: Hispanics with EOC have an elevated frequency of PV, similar to that of classic founder populations such as AJ, and significantly higher than other non-Hispanics. This is partially explained by a high prevalence of recurrent LatAm-specific PV, highlighting the importance of conducting genetic studies in underrepresented populations. There was modest incremental benefit of MGPT.
Updated predictive analysis of the WHO-defined molecular subgroups of low-grade gliomas within the high-risk treatment arms of NRG Oncology/RTOG 9802.
Authors: Bell Erica Hlavin , Won Minhee , Fleming Jessica L. , Becker Aline P. , McElroy Joseph P. , Shaw Edward G. , Mehta Minesh P. , Brachman David G. , Gertler Stanley Z. , Murtha Albert D. , Schultz Christopher J. , Johnson David B. , Laack Nadia N. , Hunter Grant Kirton , Crocker Ian R. , Chakravarti Arnab 
Published: May 2019

2002 Background: This study sought to update the predictive significance of the three WHO-defined molecular glioma subgroups ( IDHwt, IDHmt/noncodel, and IDHmt/codel) in the subset of specimens available for analysis in NRG Oncology/RTOG 9802, a phase III trial of high-risk low-grade gliomas (LGGs) treated with radiation (RT) with and without PCV after biopsy/surgical resection. Notably, this is the first phase III study to evaluate the predictive value of the WHO subgroups in LGGs using prospectively-collected, well-annotated long-term overall survival data, in a post-hoc analysis. Methods: IDH1/2 mutation status was determined by immunohistochemistry and/or next-generation sequencing. 1p/19q status was determined by Oncoscan and/or 450K methylation data. Treatment effects on overall survival (OS) and progression-free survival (PFS) by marker status were determined by the Cox proportional hazard model and tested using the log-rank test in a secondary and exploratory analysis. Results: Of all the randomized eligible high-risk G2 patients (N = 251) in NRG Oncology/RTOG 9802, 106(42%) patients had tissue available with sufficient quality DNA for profiling. Of these, 80(75%) were IDHmut; 43(41%) were IDHmut/non-co-deleted, 37(35%) were IDHmut/co-deleted, and 26(24%) were IDHwt. Upon univariate analyses, no significant difference in either PFS or OS was observed with the addition of PCV in the IDHwt subgroup. Both the IDHmut/non-co-deleted and IDHmut/co-deleted subgroups were significantly correlated with longer PFS (HR = 0.32; p = 0.003; HR = 0.13; p < 0.001) and OS (HR = 0.38; p = 0.013; HR = 0.21; p = 0.029) in the RT plus PCV arm, respectively. Conclusions: Our analyses suggest that both IDHmut/non-co-deleted and IDHmut/co-deleted subgroups received benefit from treatment with PCV although sample size is limited and analyses are post-hoc. Our results also support the notion that IDHwt high-risk LGG patients do not benefit from the addition of PCV to RT. Funding: U10CA180868, U10CA180822, and U24CA196067. Also, R01CA108633, R01CA169368, RC2CA148190, U10CA180850-01, BTFC, OSU-CCC (all to AC). Clinical trial information: NCT00003375.
Efficacy and safety of selinexor in recurrent glioblastoma.
Authors: Lassman Andrew B. , Wen Patrick Y. , Van Den Bent Martin J. , Plotkin Scott Randall , Walenkamp Anna Maria Elisabeth , Huang Xiu , Rodriguez-Lopez Karla , Kauffman Michael G. , Shacham Sharon , Mau-Sørensen Morten 
Published: May 2019

2005 Background: New treatment modalities are needed for recurrent glioblastoma (rGBM). Selinexor (SEL) is a novel, oral selective inhibitor of nuclear export which forces nuclear retention of tumor suppressor proteins including p53 and p27, leading to apoptosis. We previously reported interim results showing tolerability, preliminary efficacy, and blood-brain barrier penetration in a surgical cohort (N = 8). We now report updated results following completion of accrual to non-surgical cohorts (N = 68). Methods: This is an open-label, multicenter, phase 2 study of SEL monotherapy. Patients (pts) not undergoing surgery for measurable rGBM (per RANO) were enrolled in one of 3 arms encompassing different dosing schedules. Treatment was continuous, although cycles were defined as 28 days and response was assessed every other cycle by MRI. Prior treatment with radiotherapy and temozolomide was required and prior bevacizumab was exclusionary. The primary endpoint was 6-month progression free survival (6mPFS) rate, calculated by the Kaplan Meier method. Results: A total of 76 pts were enrolled. Median age was 56 years (range 21-78). Median number of prior treatments was 2 (range 1-7). At the end of the 6 cycles, 30.2% patients on 80 mg QW were free from progression. The 6mPFS rate on 80 mg QW was 15.1%. Best RANO-defined responses (assessed locally) among 26 evaluable pts on 80 mg QW included 1 complete response, 2 partial responses, 7 stable disease, and 16 with progressive disease. Median duration of response was 10.8 months. The most common related adverse events in pts on ~85 mg BIW/60 mg BIW/80 mg QW were nausea (42%/64%/60%), leukopenia (38%/7%/43%), fatigue (71%/71%/43%), neutropenia (29%/14%/33%), decreased appetite (46%/71%/27%), and thrombocytopenia (67%/29%/23%). Conclusions: SEL demonstrated efficacy, with durable responses and disease stabilization in rGBM. Based on the favorable efficacy and safety profile, SEL at a dose of 80 mg QW is recommended for further development in rGBM. Clinical trial information: NCT01986348. [Table: see text]