Rebecca A Betensky

Chair of the Department of Biostatistics

Professor of Biostatistics

Professional overview

Prior to NYU, Dr. Betensky was Professor of Biostatistics at the Harvard T.H. Chan School of Public Health. She was director of the Harvard Catalyst (Clinical and Translational Science Award) Biostatistics Program; director of the Data and Statistics Core for the Massachusetts Alzheimer’s Disease Research Center; and director of the Biostatistics Neurology Core at Massachusetts General Hospital. Previously, she was the Biostatistics Program Leader for the Dana-Farber/Harvard Cancer Center.

Dr. Betensky’s research focuses on methods for the analysis of censored and truncated outcomes and covariates, which frequently arise from the subsampling of cohort studies. She has a long-time interest in clinical trials, and has written on the evaluation of biomarkers and the use and interpretation of p-values. She has collaborated extensively in studies in neurologic diseases, and serves as statistical editor for Annals of Neurology.

Dr. Betensky was awarded, and directed for 15 years, an NIH T32 training program in neurostatistics and neuroepidemiology for pre- and post-doctoral students in biostatistics and epidemiology and for clinician-scientists. She previously directed Harvard’s Biostatistics programs to promote and support diversity at all levels in the field of quantitative public health. She was also a member of the BMRD Study Section for review of NIH statistical methodology grants; on committees for the Institute of Medicine; and a co-chair of the technical advisory committee for the scientific registry of transplant recipients.

Dr. Betensky an elected Fellow of the American Statistical Association and of the International Statistical Institute, and is a past recipient of the Spiegelman Award from the American Public Health Association. She currently serves as a member of the Board of Scientific Counselors for Clinical Science and Epidemiology at the National Cancer Institute.

Education

AB, Mathematics, Harvard University, Cambridge, MA

PhD, Statistics, Stanford University, Stanford, CA

Areas of research and study

Biology

Biostatistics

Neuroepidemiology

Neurology

Neurostatistics

Translational science

Publications

Publications

An O'Brien-Fleming sequential trial for comparing three treatments

Betensky, R. A. (n.d.).

Publication year

1996

Journal title

Annals of Statistics

Volume

24

Issue

4

Page(s)

1765-1791

10.1214/aos/1032298294

Abstract

Abstract

We consider a sequential procedure for comparing three treatments with the goal of ultimately selecting the best treatment. This procedure starts with a sequential test to detect an overall treatment difference and eliminates the apparently inferior treatment if this test rejects the equality of the treatments. It then proceeds with a sequential test of the remaining two treatments. We base these sequential tests on the stopping boundaries popularized by O'Brien and Fleming. Our procedure is similar in structure to that used by Siegmund in conjunction with modified repeated significance tests. We compare the performances of the two procedures via a simulation experiment. We derive analytic approximations for an error probability, the power and the expected sample size of our procedure, which we compare to simulated values. Furthermore, we propose a modification of the procedure for the comparison of a standard treatment with experimental treatments.

Low-grade, latent prostate cancer volume: Predictor of clinical cancer incidence?

Whittemore, A. S., Keller, J. B., & Betensky, R. (n.d.).

Publication year

1991

Journal title

Journal of the National Cancer Institute

Volume

83

Issue

17

Page(s)

1231-1235

10.1093/jnci/83.17.1231

Abstract

Abstract

We hypothesize that each cell in lowgrade (Gleason grade 1-3) prostate cancer tissue is at risk of transformation into a cell which produces a highgrade (Gleason grade 4-5) clinical cancer after a short period of growth. As a consequence, the volume of low-grade, latent cancer tissue in the prostate glands of men at any age determines their incidence rate for high-grade, clinical cancer a few years later. Autopsy and incidence data for both white men and black men support this conclusion, with a tumor growth period of about 7 years. The transformation rate is similar for black men and for white men, about 0.024 high-grade cancers per year per cm3 of lowgrade latent cancer volume. Our hypothesis explains the infrequent occurrence of clinical cancer despite the high prevalence of latent cancer, the steep rise of clinical cancer incidence with age despite the slow rise of latent cancer prevalence with age, and the disparities in clinical cancer incidence among some populations despite their similar latent cancer prevalence. This hypothesis suggests that low-grade cancer volume is a critical determinant of clinical cancer risk. [J Natl Cancer Inst 83:1231-1235, 1991]

Actual versus ideal weight in the calculation of surface area: Effects on dose of 11 chemotherapy agents

Gelman, R. S., Tormey, D. C., Betensky, R., Mansour, E. G., Falkson, H. C., Falkson, G., Creech, R. H., & Haller, D. G. (n.d.).

Publication year

1987

Journal title

Cancer Treatment Reports

Volume

71

Issue

10

Page(s)

907-911

Abstract

Abstract

This study of 2382 breast, 182 rectal, 817 colon, and 351 lung cancer patients treated with combination chemotherapy on eight phase III Eastern Cooperative Oncology Group protocols indicates that 69% would receive a higher dose of at least one drug if surface area were calculated from actual weight rather than from the minimum of actual and ideal weight. Forty-eight percent of the patients would have at least a 10% increase in drug dose based on actual weight and only 8% would have at least a 25% increase in drug dose based on actual weight. Only on the premenopausal adjuvant breast cancer protocol and among women on the rectal adjuvant study do the differences in dose based on actual rather than ideal weight increase significantly with age. On the postmenopausal adjuvant breast study and on the lung cancer study, the differences in dose decrease significantly with age. For all age decades and both sexes within each protocol, the mean differences between dose based on actual and dose based on ideal weights were on the same order as the rounding factors for the 11 drugs studied. From the literature on the effects of doses of common chemotherapies on leukopenia, it appears that the percent of hematologic toxicity would not be raised to unacceptable levels by using actual weight to set doses.