JNCI: Journal of the National Cancer Institute

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ISSN / EISSN : 00278874 / 14602105
Current Publisher: Oxford University Press (OUP) (10.1093)
Total articles ≅ 30,400
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Xiao Chang, Marina Bakay, Yichuan Liu, Joseph Glessner, Komal S Rathi, Cuiping Hou, Huiqi Qu, Zalman Vaksman, Kenny Nguyen, Patrick M A Sleiman, et al.
JNCI: Journal of the National Cancer Institute; doi:10.1093/jnci/djaa024

The publisher has not yet granted permission to display this abstract.
Aimée R Kreimer, Joshua N Sampson, Carolina Porras, John T Schiller, Troy Kemp, Rolando Herrero, Sarah Wagner, Joseph Boland, John Schussler, Douglas R Lowy, et al.
Journal of the National Cancer Institute; doi:10.1093/jnci/djaa011

The publisher has not yet granted permission to display this abstract.
Sabrina H Tsang, Joshua N Sampson, John Schussler, Carolina Porras, Sarah Wagner, Joseph Boland, Bernal Cortes, Douglas R Lowy, John T Schiller, Mark Schiffman, et al.
Journal of the National Cancer Institute; doi:10.1093/jnci/djaa010

The publisher has not yet granted permission to display this abstract.
Chunling Hu, Eric C Polley, Siddhartha Yadav, Jenna Lilyquist, Hermela Shimelis, Jie Na, Steven N Hart, David E Goldgar, Swati Shah, Tina Pesaran, et al.
Journal of the National Cancer Institute; doi:10.1093/jnci/djaa023

Abstract:The germline cancer predisposition genes associated with increased risk of each clinical subtype of breast cancer, defined by estrogen receptor (ER), progesterone receptor (PR), and HER2, are not well defined. A total of 54,555 invasive breast cancer patients with 56,480 breast tumors were subjected to clinical hereditary cancer multigene panel testing. Heterogeneity for predisposition genes across clinical breast cancer subtypes was assessed by comparing mutation frequencies by gene among tumor subtypes and by association studies between each tumor subtype and reference controls. Mutations in 15 cancer predisposition genes were detected in 8.6% of patients with ER+/HER2-; 8.9% with ER+/HER2+; 7.7% with ER-/HER2+; and 14.4% of ER-/PR-/HER2- tumors. BRCA1, BRCA2, BARD1 and PALB2 mutations were enriched in ER- and HER2- tumors, RAD51C and RAD51D mutations were enriched in ER- tumors only, TP53 mutations were enriched in HER2+ tumors, and ATM and CHEK2 mutations were enriched in both ER+ and/or HER2+ tumors. All genes were associated with moderate (odds ratio (OR)>2.00) or strong (OR > 5.00) risks of at least one subtype of breast cancer in case-control analyses. Mutations in ATM, BARD1, BRCA1, BRCA2, CHEK2, PALB2, RAD51C, RAD51D, and TP53 had predicted lifetime absolute risks of ≥ 20.0% for breast cancer. Germline mutations in hereditary cancer panel genes confer subtype-specific risks of breast cancer. Combined tumor subtype, age at breast cancer diagnosis, and family history of breast and/or ovarian cancer information provides refined categorical estimates of mutation prevalence for women considering genetic testing.
Gillian Gresham, Márcio A Diniz, Zahra S Razaee, Michael Luu, Sungjin Kim, Ron D Hays, Steven Piantadosi, Mourad Tighiouart, Greg Yothers, Patricia A Ganz, et al.
Journal of the National Cancer Institute; doi:10.1093/jnci/djaa028

Abstract:The National Cancer Institute Moonshot℠ research initiative calls for improvements in the analysis and reporting of treatment toxicity to advise key stakeholders on treatment tolerability and inform regulatory and clinical decision-making. This study illustrates alternative approaches to toxicity evaluation using the National Surgical Adjuvant Breast and Bowel Project (NSABP-R04) clinical trial as an example. NSABP-R04 was a neoadjuvant chemo-radiation trial in stage II-III rectal cancer patients. A 2x2 factorial design was used to evaluate whether the addition of oxaliplatin (Oxa) to 5-fluorouracil (5FU) or capecitabine (Cape) with radiation therapy improved local-regional tumor control. The toxicity index (TI), which accounts for the frequency and severity of toxicities, was compared across treatments using multivariable probabilistic index models (PIMs), where Pr A < B indicates the probability that higher values of TI were observed for A when compared to B. Baseline age, gender, performance status (PS), body mass index (BMI), surgery type and stage were evaluated as independent risk factors. A total of 4,560 toxicities from 1,558 patients were analyzed. Results from adjusted PIMs indicate that oxaliplatin-containing regimens had statistically significant (p < 0.001) probability for higher TI compared to regimens without oxaliplatin: Pr 5FU < 5FU + Oxa = 0.619 (95% CI 0.560-0.674); Pr 5FU< Cape + Oxa = 0.627 (95% CI 0.568-0.682); Pr Cape < 5FU + Oxa =0.587 (95% 0.527-0.644); and Pr Cape < Cape+ Oxa = 0.596 (95% 0.536-0.653).When compared to other existing toxicity analysis methods, TI provided greater power to detect differences between treatments. This paper uses standard data collected in a cancer clinical trial to introduce descriptive and analytic methods that account for the additional burden of multiple toxicities. These methods may provide a more accurate description of a patient's treatment experience that could lead to individualized dosing for better toxicity control. Future research will evaluate the generalizability of these findings in trials with similar drugs.
Emily Z Keung, Jeffrey E Gershenwald
JNCI: Journal of the National Cancer Institute; doi:10.1093/jnci/djaa012

The publisher has not yet granted permission to display this abstract.
Martin J Yaffe, James G Mainprize
JNCI: Journal of the National Cancer Institute; doi:10.1093/jnci/djaa025

Abstract:While screening mammography has been demonstrated to contribute to reducing mortality due to breast cancer, some have suggested that reduced all-cause mortality should constitute the burden of proof for effectiveness. Using a microsimulation model of the development, detection and treatment of breast cancer it is straightforward to demonstrate that this is an unrealistic expectation for trials of practical size and period of observation, even where the reduction of breast cancer mortality is substantial. Estimates of all-cause mortality will depend not only on the efficacy of the screening intervention, but also on the alignment between the age distribution of the effect of screening on reduction of deaths and that of the other major causes of death. The size of a randomized trial required to demonstrate a reduction in all-cause mortality will, therefore, depend on the length and timing of the observation period and will be typically at least ten times larger than the size of a trial powered to test for a reduction in deaths due to breast cancer. For breast cancer, which represents a small fraction of overall deaths, all-cause mortality is not a practical, nor informative metric for assessing the effectiveness of screening.
F Lennie Wong, Jennifer Berano, Liezl Atencio, Tracey Stiller, Heeyoung Kim, Dayana Chanson, Stephen J Forman, Ryotaro Nakamura, Saro H Armenian
JNCI: Journal of the National Cancer Institute; doi:10.1093/jnci/djaa022

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Summer S Han, Eric Chow, Kevin Ten Haaf, Iakovos Toumazis, Pianpian Cao, Mehrad Bastani, Martin Tammemagi, Jihyoun Jeon, Eric Feuer, Rafael Meza, et al.
JNCI: Journal of the National Cancer Institute; doi:10.1093/jnci/djaa013

The publisher has not yet granted permission to display this abstract.
George J Chang, Y Nancy Y You, Christy A Russell, Marni B Tierno, Michelle Turner, John P Bennett, Anna Lau, Howard S Hochster
JNCI: Journal of the National Cancer Institute; doi:10.1093/jnci/djaa019

Abstract:The incidence and mortality from colorectal cancer in younger adults (<55 years) is increasing. We reviewed the complete database of a gene-expression test, Oncotype DX Colon Recurrence Score® test, to determine age-related differences in Recurrence Score® (RS) and single-gene results (7 cancer-related of the 12-gene assay). We included 20,478 Stage II & III A/B colon cancer patients submitted to Genomic Health. RS results were grouped by low, intermediate, and high risk groups. Single-gene scores were described using median and interquartile range. Seventy-two and a half percent of all patients and 72.6% of those <40 years had low risk RS. Comparing older versus younger patients, RS or single-gene expression did not differ by age group or stage. Young-onset colon cancer does not differ by expression of the RS component genes. Most patients with stage II/III colon cancer have low-risk disease as measured by the 12-gene assay, regardless of age.