Boris C. Bastian

UCSF Helen Diller Family Comprehensive Cancer Center

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Iwei Yeh

University of California, San Francisco

A. Hunter Shain

University of California, San Francisco

Philip E. LeBoit

University of California, San Francisco

Nancy M. Joseph

University of California, San Francisco

Trever G. Bivona

UCSF Helen Diller Family Comprehensive Cancer Center

Reinhard Dummer

University Hospital of Zurich

Victor Olivas

University of California, San Francisco

Nicholas K. Hayward

QIMR Berghofer Medical Research Institute

Eric A. Collisson

Cape Town HVTN Immunology Laboratory / Hutchinson Centre Research Institute of South Africa

Jessica Van Ziffle

University of California, San Francisco

Cooperative Institutions

University of California, San Francisco

378

National Institutes of Health

300

Harvard University

179

UCSF Helen Diller Family Comprehensive Cancer Center

173

The University of Texas MD Anderson Cancer Center

147

Heidelberg University

145

Memorial Sloan Kettering Cancer Center

130

Inserm

118

National Cancer Institute

116

Massachusetts General Hospital

101

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Mutations in the promoter of the telomerase gene TERT contribute to tumorigenesis by a two-step mechanism

Science (2017)

Kunitoshi Chiba Franziska K. Lorbeer A. Hunter Shain David T. McSwiggen Eva Schruf

Two-step role for mutant TERT promoters Telomeres preserve genomic stability by preventing chromosomal fusions. The recent discovery that human tumors harbor mutations in the promoter region of the telomerase gene ( TERT ) produced a flurry of research aimed at elucidating the role of these mutations in cancer development. Chiba et al. present data that reconcile many of the conflicting results reported to date (see the Perspective by Shay). In human melanoma samples and a fibroblast model, TERT promoter mutations acted in two steps. First, the mutations allowed cells to proliferate with short telomeres. This fueled genomic instability and up-regulation of telomerase expression, leading to uncontrolled cell proliferation. Science , this issue p. 1416 ; see also p. 1358

10.1126/science.aao0535

Cite

Citations (249)

Improving Melanoma Classification by Integrating Genetic and Morphologic Features

PLoS Medicine (2008)

Amaya Virós Jane Fridlyand Jürgen Bauer Konstantin Lasithiotakis Claus Garbe

In melanoma, morphology-based classification systems have not been able to provide relevant information for selecting treatments for patients whose tumors have metastasized. The recent identification of causative genetic alterations has revealed mutations in signaling pathways that offer targets for therapy. Identifying morphologic surrogates that can identify patients whose tumors express such alterations (or functionally equivalent alterations) would be clinically useful for therapy stratification and for retrospective analysis of clinical trial data.

10.1371/journal.pmed.0050120

Cite

Citations (374)

Chromosomal gains and losses in primary cutaneous melanomas detected by comparative genomic hybridization.

PubMed (1998)

Boris C. Bastian Philip E. LeBoit Henning Hamm E.-B. Bröcker Daniel Pinkel

The analysis of genetic changes in primary cutaneous melanoma has been limited by the need for fixation for diagnostic purposes. However, comparative genomic hybridization is able to analyze such specimens. We have applied comparative genomic hybridization to 32 primary melanomas to discover and map genomic regions with aberrant DNA copy numbers. The analysis was performed on native, nonamplified DNA extracted from manually dissected tumor sections. Loss of chromosome 9 was detected in 81% of the tumors, most commonly affecting the p arm. Additional common losses occurred on chromosomes 10 (63%), 6q (28%), and 8p (22%). Gains in copy number involved chromosomes 7 (50%), 8 (34%), 6p (28%), 1q (25%), 20 (13%), 17 (13%), and 2 (13%). Amplifications indicating areas harboring potential oncogenes were seen at 4q12, 5p14.3-pter, 7q33-qter, 8q12-13, 11q13.3-14.2, and 17q25. Correlations among the regions with copy number changes indicate that losses of chromosomes 9 and 10 occur early on in melanoma progression, whereas gains of chromosome 7 occur later. This sequence of events was further substantiated by an intratumoral comparison of copy number changes in areas with radial and vertical growth phase patterns. The overall pattern of regions affected by copy number changes is consistent with cytogenetic data from metastatic melanoma; however, the frequencies of involvement differ, providing further insight into the course of genetic events.

Comparative genomic hybridization

Copy number analysis

Source

Cite

Citations (515)

Myxoid glioneuronal tumor of the septum pellucidum and lateral ventricle is defined by a recurrent PDGFRA p.K385 mutation and DNT-like methylation profile

Acta Neuropathologica (2018)

David A. Solomon Andrey Korshunov Martin Sill David Jones Marcel Kool

PDGFRA

Septum pellucidum

10.1007/s00401-018-1883-2

Cite

Citations (50)

Mutations inGNA11in Uveal Melanoma

New England Journal of Medicine (2010)

Catherine D. Van Raamsdonk Klaus Griewank Michelle B. Crosby María C. Garrido Swapna S. Vemula

Uveal melanoma is the most common intraocular cancer. There are no effective therapies for metastatic disease. Mutations in GNAQ, the gene encoding an alpha subunit of heterotrimeric G proteins, are found in 40% of uveal melanomas.

GNAQ

10.1056/nejmoa1000584

Cite

Citations (1,372)

Data from Co-occurring Alterations in the RAS–MAPK Pathway Limit Response to MET Inhibitor Treatment in MET Exon 14 Skipping Mutation-Positive Lung Cancer

Julia Rotow Philippe Gui Wei Wu Victoria M. Raymond Richard B. Lanman

<div>AbstractPurpose:Although patients with advanced-stage non–small cell lung cancers (NSCLC) harboring MET exon 14 skipping mutations (METex14) often benefit from MET tyrosine kinase inhibitor (TKI) treatment, clinical benefit is limited by primary and acquired drug resistance. The molecular basis for this resistance remains incompletely understood.Experimental Design:Targeted sequencing analysis was performed on cell-free circulating tumor DNA obtained from 289 patients with advanced-stage METex14-mutated NSCLC.Results:Prominent co-occurring RAS–MAPK pathway gene alterations (e.g., in KRAS, NF1) were detected in NSCLCs with METex14 skipping alterations as compared with EGFR-mutated NSCLCs. There was an association between decreased MET TKI treatment response and RAS–MAPK pathway co-occurring alterations. In a preclinical model expressing a canonical METex14 mutation, KRAS overexpression or NF1 downregulation hyperactivated MAPK signaling to promote MET TKI resistance. This resistance was overcome by cotreatment with crizotinib and the MEK inhibitor trametinib.Conclusions:Our study provides a genomic landscape of co-occurring alterations in advanced-stage METex14-mutated NSCLC and suggests a potential combination therapy strategy targeting MAPK pathway signaling to enhance clinical outcomes.</div>

T790M

10.1158/1078-0432.c.6528503

Cite

Citations (0)

Supplemental Figure S3 from Co-occurring Alterations in the RAS–MAPK Pathway Limit Response to MET Inhibitor Treatment in MET Exon 14 Skipping Mutation-Positive Lung Cancer

Julia Rotow Philippe Gui Wei Wu Victoria M. Raymond Richard B. Lanman

MET tyrosine kinase domain modeling location of the F1200 residue

Protein kinase domain

Residue (chemistry)

10.1158/1078-0432.22473419.v1

Cite

Citations (0)

Supplementary Figure 1 from SOX10 Ablation Arrests Cell Cycle, Induces Senescence, and Suppresses Melanomagenesis

Julia C. Cronin Dawn E. Watkins‐Chow Art Incao Joanne H. Hasskamp Nicola Schönewolf

PDF file, 122K, Senescence associated heterochromatin foci (SAHF) are more pronounced in melanoma cells when SOX10shRNA is expressed compared to non-silencing (NS) control.

Senescence

10.1158/0008-5472.22398242.v1

Cite

Citations (0)

Supplementary Figure 3 from SOX10 Ablation Arrests Cell Cycle, Induces Senescence, and Suppresses Melanomagenesis

Julia C. Cronin Dawn E. Watkins‐Chow Art Incao Joanne H. Hasskamp Nicola Schönewolf

PDF file, 173K, Transient transfection of SOX10-specific siRNAs in 0380-MMU and UACC 1022 cells.

Senescence

10.1158/0008-5472.22398236

Cite

Citations (0)

Author Correction: From melanocytes to melanomas

Nature reviews. Cancer (2020)

A. Hunter Shain Boris C. Bastian

10.1038/s41568-020-0269-7

Cite

Citations (3)