Author

V. L. Cannataro

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Cancer Biology· 5

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Organism:human· 5 Approach:statistical model· 5 Research Focus:cancer & tumor microenvironment· 3 Research Focus:variant effect prediction· 3 Assay:whole-exome sequencing· 3 Assay:whole-genome sequencing· 2 Research Focus:clustering· 1 Approach:deep learning· 1

Frequent Co-Authors

J. P. Townsend· 5 shared J. D. Mandell· 2 shared S. G. Gaffney· 2 shared A. Greenstein· 1 shared C. Stender· 1 shared D. F. Stern· 1 shared H. Zhao· 1 shared K. A. Glasmacher· 1 shared

Activity by Year

2017-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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5 shared papersCancer Biology

J. P. Townsend

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5 papers

Recent·Most cited

Early NOTCH1 mutation is positively selected but epistatically suppresses evolution of later esophageal squamous-cell carcinoma drivers

K. A. Glasmacher, J. D. Mandell, M. Jackson, N. Fisk, V. L. Cannataro, J. P. Townsend

The paper shows early NOTCH1 mutations are selected in normal tissue but suppress later cancer driver mutations through epistasis, highlighting stage-specific mutation effects in esophageal cancer.

bioRxiv · Nov 3, 2023 · PreprintCancer Biology

Attribution of Cancer Origins to Endogenous, Exogenous, and Actionable Mutational Processes

V. L. Cannataro, J. D. Mandell, J. P. Townsend

The paper attributes cancer origins to endogenous, exogenous, and actionable mutational processes across 23 cancer types, highlighting preventable factors like UV light and tobacco.

bioRxiv · Oct 24, 2020Cancer Biology

Identifying Modules of Cooperating Cancer Drivers

M. I. Klein, V. L. Cannataro, S. Newman, J. P. Townsend, D. F. Stern, H. Zhao

The paper introduces CRSO to identify cooperating driver combinations in cancer, finding 11 core combinations per cancer type with clinical relevance.

bioRxiv · Jun 29, 2020Cancer Biology

Effect sizes of somatic mutations in cancer

V. L. Cannataro, S. G. Gaffney, J. P. Townsend

The paper estimates effect sizes of recurrent single nucleotide variants in 23 cancer types to quantify their relative importance in cancer growth and therapeutic response.

bioRxiv · Feb 27, 2018Cancer Biology

The likelihood of heterogeneity or additional mutation in KRAS or associated oncogenes to compromise targeting of oncogenic KRAS G12C

V. L. Cannataro, S. G. Gaffney, C. Stender, Z.-M. Zhao, M. Philips, A. Greenstein, J. P. Townsend

The study finds no evidence of resistance-conferring mutations in KRAS or downstream genes in KRAS G12C positive tumors at treatment time, and predicts BRAF mutations as likely resistance mechanisms with existing therapies.

bioRxiv · Jun 13, 2017Cancer Biology