scispace - formally typeset
W

William C. Hahn

Researcher at Harvard University

Publications -  515
Citations -  85047

William C. Hahn is an academic researcher from Harvard University. The author has contributed to research in topics: Cancer & Medicine. The author has an hindex of 130, co-authored 448 publications receiving 72191 citations. Previous affiliations of William C. Hahn include Brigham and Women's Hospital & University of Washington.

Papers
More filters
Journal ArticleDOI

Signaling and Transcriptional Changes Critical for Transformation of Human Cells by Simian Virus 40 Small Tumor Antigen or Protein Phosphatase 2A B56γ Knockdown

TL;DR: The data support a model in which ST promotes survival through constitutive integrin signaling, src phosphorylation, and nuclear factor κB activation, while inhibiting cell-cell adhesion pathways.
Journal ArticleDOI

Oncogenic transformation and experimental models of human cancer.

TL;DR: Experimental models derived from the manipulation of oncogenes, tumor suppressor genes and telomerase provide useful platforms to delineate pathways involved in cell transformation, to connect specific cancer-associated mutations with particular cancer phenotypes and to discover and validate new targets for therapeutic development.
Journal ArticleDOI

Nek4 Regulates Entry into Replicative Senescence and the Response to DNA Damage in Human Fibroblasts

TL;DR: Observations implicate Nek4 as a novel regulator of replicative senescence and the response to double-stranded DNA damage.
Journal ArticleDOI

RMRP Is a Non-Coding RNA Essential for Early Murine Development

TL;DR: It is found that insertion of this cassette suppressed RMRP expression, and it was unable to obtain viable mice homozygous for the R MRP conditional allele, indicating that RMRp is essential for early embryonic development.
Journal ArticleDOI

ATM Loss Confers Greater Sensitivity to ATR Inhibition than PARP Inhibition in Prostate Cancer

TL;DR: The results have important implications for planned and ongoing prostate cancer clinical trials and suggest that patients with tumor ATM alterations may be more likely to benefit from ATR inhibitor than PARP inhibitor therapy.