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Naim U. Rashid
Researcher at University of North Carolina at Chapel Hill
Publications - 70
Citations - 4182
Naim U. Rashid is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Medicine & Cancer. The author has an hindex of 20, co-authored 57 publications receiving 2873 citations. Previous affiliations of Naim U. Rashid include Brigham and Women's Hospital & Harvard University.
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Journal ArticleDOI
Virtual microdissection identifies distinct tumor- and stroma-specific subtypes of pancreatic ductal adenocarcinoma
Richard A. Moffitt,Raoud Marayati,Elizabeth L. Flate,Keith E. Volmar,S. Gabriela Herrera Loeza,Katherine A. Hoadley,Naim U. Rashid,Lindsay A. Williams,Samuel C. Eaton,Alexander H. Chung,Jadwiga K. Smyla,Judy M. Anderson,Hong Jin Kim,David J. Bentrem,Mark S. Talamonti,Christine A. Iacobuzio-Donahue,Michael A. Hollingsworth,Jen Jen Yeh +17 more
TL;DR: By digitally separating tumor, stromal and normal gene expression, two tumor subtypes are identified and validated, including a 'basal-like' subtype that has worse outcome and is molecularly similar to basal tumors in bladder and breast cancers.
Journal ArticleDOI
Heterogeneity of genomic evolution and mutational profiles in multiple myeloma
Niccolo Bolli,Hervé Avet-Loiseau,David C. Wedge,Peter Van Loo,Ludmil B. Alexandrov,Inigo Martincorena,Kevin J. Dawson,Francesco Iorio,Serena Nik-Zainal,Graham R. Bignell,Jonathan Hinton,Yang Li,Jose M. C. Tubio,Stuart McLaren,Sarah O' Meara,Adam Butler,Jon W. Teague,Laura Mudie,Elizabeth Anderson,Naim U. Rashid,Yu-Tzu Tai,Masood A. Shammas,Adam S. Sperling,Mariateresa Fulciniti,Paul G. Richardson,Giovanni Parmigiani,Florence Magrangeas,Stephane Minvielle,Philippe Moreau,Michel Attal,Thierry Facon,P. Andrew Futreal,Kenneth C. Anderson,Peter J. Campbell,Nikhil C. Munshi +34 more
TL;DR: The myeloma genome is heterogeneous across the cohort, and exhibits diversity in clonal admixture and in dynamics of evolution, which may impact prognostic stratification, therapeutic approaches and assessment of disease response to treatment.
Journal ArticleDOI
High tumor mutation burden fails to predict immune checkpoint blockade response across all cancer types.
Daniel J. McGrail,Patrick G. Pilie,Naim U. Rashid,Leonie Voorwerk,Maarten Slagter,Marleen Kok,Eric Jonasch,Mustafa Khasraw,Amy B. Heimberger,Bora Lim,NT Ueno,Jennifer K. Litton,Renata Ferrarotto,Jeffrey T. Chang,S. L. Moulder,Sy Lin +15 more
TL;DR: In this article, the authors compared approaches to determine TMB and identify the correlation between predicted neoantigen load and CD8 T cells, and found that TMB-H tumors exhibited a 39.8% ORR to ICB [95% confidence interval (CI) 34.9-44.8], which was significantly higher than that observed in low TMB (TMB-L) tumors.
Journal ArticleDOI
ZINBA integrates local covariates with DNA-seq data to identify broad and narrow regions of enrichment, even within amplified genomic regions
TL;DR: ZINBA (Zero-Inflated Negative Binomial Algorithm) identifies genomic regions enriched in a variety of ChIP-seq and related next-generation sequencing experiments (DNA-seq) by calling both broad and narrow modes of enrichment across a range of signal-to-noise ratios.
Journal ArticleDOI
Enhancer Remodeling during Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacologic Targeting of the P-TEFb Complex
Jon S. Zawistowski,Samantha M. Bevill,Daniel R. Goulet,Timothy J. Stuhlmiller,Adriana S. Beltran,Jose F. Olivares-Quintero,Darshan Singh,Noah Sciaky,Joel S. Parker,Naim U. Rashid,Xin Chen,James S. Duncan,Martin C. Whittle,Steven P. Angus,Sara H. Velarde,Brian T. Golitz,Xiaping He,Charlene M. Santos,David B. Darr,Kristalyn K. Gallagher,Lee M. Graves,Charles M. Perou,Lisa A. Carey,H. Shelton Earp,Gary L. Johnson +24 more
TL;DR: Widespread transcriptional adaptation to pharmacologic MEK inhibition was observed in TNBC patient tumors, and pharmacologic targeting of P-TEFb members in conjunction with MEK inhibited by trametinib is an effective strategy to durably inhibit epigenomic remodeling required for adaptive resistance.