Meredith Stevers
University of California, San Francisco
7 Papers
Meredith Stevers is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Germline mutation & Cohesin. The author has an hindex of 7, co-authored 7 publications.
Chat about Author
Papers
A requirement for STAG2 in replication fork progression creates a targetable synthetic lethality in cohesin-mutant cancers.
TL;DR: It is shown that STAG2 is essential for DNA replication fork progression, wherebySTAG2 inactivation in non-transformed cells leads to replication fork stalling and collapse with disruption of interaction between the cohesin ring and the replication machinery as well as failure to establish SMC3 acetylation.
Cell of origin and mutation pattern define three clinically distinct classes of sebaceous carcinoma.
Jeffrey P. North,Justin Golovato,Charles J. Vaske,J. Zachary Sanborn,Andrew Anh Nguyen,Wei Wu,Benjamin Goode,Meredith Stevers,Kevin McMullen,Bethany E. Perez White,Eric A. Collisson,Michele M. Bloomer,David A. Solomon,Stephen C. Benz,Raymond J. Cho +14 more
TL;DR: In this paper, the authors report whole-exome sequencing on 32 SeC, revealing distinct mutational classes that explain both cancer ontogeny and clinical course, and exemplify how different mutational processes convergently drive histopathologically related but clinically distinct cancers.
Next-Generation Sequencing of Retinoblastoma Identifies Pathogenic Alterations beyond RB1 Inactivation That Correlate with Aggressive Histopathologic Features.
Armin R. Afshar,Melike Pekmezci,Michele M. Bloomer,Nicola J. Cadenas,Meredith Stevers,Anuradha Banerjee,Ritu Roy,Adam B. Olshen,Jessica Van Ziffle,Courtney Onodera,W. Patrick Devine,James P. Grenert,Boris C. Bastian,David A. Solomon,Bertil Damato +14 more
TL;DR: Comprehensive NGS analysis reliably detects relevant mutations, amplifications, and chromosomal copy number changes in retinoblastoma and correlates with aggressive histopathologic features.
58
Deep sequencing of WNT-activated medulloblastomas reveals secondary SHH pathway activation.
J. Bryan Iorgulescu,J. Bryan Iorgulescu,Jessica Van Ziffle,Jessica Van Ziffle,Meredith Stevers,James P. Grenert,James P. Grenert,Boris C. Bastian,Boris C. Bastian,Lukas Chavez,Damian Stichel,Damian Stichel,Ivo Buchhalter,Ivo Buchhalter,David Samuel,Theodore Nicolaides,Anuradha Banerjee,Sabine Mueller,Nalin Gupta,Tarik Tihan,Andrew W. Bollen,Paul A. Northcott,Marcel Kool,Stefan M. Pfister,Stefan M. Pfister,Andrey Korshunov,Andrey Korshunov,Arie Perry,Arie Perry,David A. Solomon,David A. Solomon +30 more
TL;DR: Author(s): Iorgulescu, J Bryan; Van Ziffle, Jessica; Stevers, Meredith; Grenert, James P; Bastian, Boris C; Chavez, Lukas; Stichel, Damian; Buchhalter, Ivo; Samuel, David; Nicolaides, Theodore; Banerjee, Anuradha; Mueller, Sabine; Gupta, Nalin; Tihan, Tarik; Bollen, Andrew W.
Well-differentiated papillary mesothelioma of the peritoneum is genetically defined by mutually exclusive mutations in TRAF7 and CDC42.
Meredith Stevers,Joseph T. Rabban,Karuna Garg,Jessica Van Ziffle,Courtney Onodera,James P. Grenert,Iwei Yeh,Boris C. Bastian,Charles Zaloudek,David A. Solomon +9 more
TL;DR: In this article, the authors performed genomic profiling on a cohort of ten well-differentiated papillary mesothelioma of the peritoneum and found that all tumors harbored somatic missense mutations in either the TRAF7 or CDC42 genes, and lacked alterations involving BAP1, NF2, CDKN2A, DDX3X, SETD2, and ALK that are frequent in malignant mesothelial tumor.