Evidence map›Paper›PMID 26771497›Full record

ArticleCell2016

Functional Genomic Landscape of Human Breast Cancer Drivers, Vulnerabilities, and Resistance.

Richard Marcotte, Azin Sayad, Kevin R Brown, Felix Sanchez-Garcia, Jüri Reimand, Maliha Haider, Carl Virtanen, James E Bradner, Gary D Bader, Gordon B Mills and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 275 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
275citing papers in PubMed, 1 pooled it
34.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

275 citing papers in PubMed, 1 synthesis or guideline pooled it, 493 citations in OpenAlex.

  1. Pooled it
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  9. Synthetic lethality between RB-loss and E2F3 inhibition in small cell cancers targeted by pyrimidine synthesis blockade.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  14. Super-enhancer profiling reveals ThPOK/ZBTB7B, a CD4Cellular and molecular life sciences : CMLS · 2025
    Article
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  19. Review
  20. Enter sandman: how to tackle dormant breast cancer cells.Medical oncology (Northwood, London, England) · 2025
    Review

215 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 2 countries.

Richard MarcottePrincess Margaret Cancer Centre, University Health Network, Toronto, ON M5G 1L7, Canada.
Azin SayadPrincess Margaret Cancer Centre, University Health Network, Toronto, ON M5G 1L7, Canada.
Kevin R BrownThe Donnelly Centre, University of Toronto, ON M5S 3E1, Canada.
Felix Sanchez-GarciaColumbia University, New York, NY 10027, USA.
Jüri ReimandThe Donnelly Centre, University of Toronto, ON M5S 3E1, Canada.
Maliha HaiderPrincess Margaret Cancer Centre, University Health Network, Toronto, ON M5G 1L7, Canada.
Carl VirtanenPrincess Margaret Cancer Centre, University Health Network, Toronto, ON M5G 1L7, Canada.
James E BradnerDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA; Department of Medicine, Harvard Medical School, Boston, MA 02215, USA.
Gary D BaderThe Donnelly Centre, University of Toronto, ON M5S 3E1, Canada.
Gordon B MillsDepartment of Systems Biology, Sheikh Khalifa Al Nahyan Ben Zayed Institute for Personalized Cancer Therapy, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Dana Pe'erColumbia University, New York, NY 10027, USA.
Jason MoffatThe Donnelly Centre, University of Toronto, ON M5S 3E1, Canada; Department of Molecular Genetics, University of Toronto, ON M5S 3E1, Canada.
Benjamin G NeelPrincess Margaret Cancer Centre, University Health Network, Toronto, ON M5G 1L7, Canada; Laura and Isaac Perlmutter Cancer Centre, NYU-Langone Medical Center, NY 10016, USA. Electronic address: benjamin.neel@nyumc.org.
University Health Network · CAUniversity of Toronto · CAColumbia University · USHarvard University · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TR&D 3 - Network Guided Machine LearningP41GM103504 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI IDEKER, TREY · 2012 to 2024
$17.3M
Tyrosine Kinase-Dependant and - Independent Pathways of EGFR in Breast Cancer ProP01CA099031 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUNG, MIEN-CHIE · 2003 to 2014
$11.6M
Pathway Commons: Research Resource for Biological PathwaysU41HG006623 · NHGRI · SLOAN-KETTERING INST CAN RESEARCH · PI SANDER, CHRIS · 2012 to 2017
$5.7M
Cytoscape: A Modeling Platform for Biomolecular NetworksR01GM070743 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI IDEKER, TREY · 2004 to 2016
$5.7M
SIGNAL TRANSDUCTION BY NON-TRANSMEMBRANE PTPSR01CA049152 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NEEL, BENJAMIN G. · 1989 to 2020
$4.4M
Integrative Cancer Genomics: Drivers, Pathways and DrugsR01CA164729 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI PE'ER, DANA · 2012 to 2016
$1.9M
NCI NIH HHS CA16672NCI NIH HHS P01 CA099031NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA049152NCI NIH HHS R01 CA164729NCI NIH HHS R37 CA49132NHGRI NIH HHS U41 HG006623NIGMS NIH HHS P41 GM103504NIGMS NIH HHS R01 GM070743
6 · The paper itself

Abstract

Large-scale genomic studies have identified multiple somatic aberrations in breast cancer, including copy number alterations and point mutations. Still, identifying causal variants and emergent vulnerabilities that arise as a consequence of genetic alterations remain major challenges. We performed whole-genome small hairpin RNA (shRNA) "dropout screens" on 77 breast cancer cell lines. Using a hierarchical linear regression algorithm to score our screen results and integrate them with accompanying detailed genetic and proteomic information, we identify vulnerabilities in breast cancer, including candidate "drivers," and reveal general functional genomic properties of cancer cells. Comparisons of gene essentiality with drug sensitivity data suggest potential resistance mechanisms, effects of existing anti-cancer drugs, and opportunities for combination therapy. Finally, we demonstrate the utility of this large dataset by identifying BRD4 as a potential target in luminal breast cancer and PIK3CA mutations as a resistance determinant for BET-inhibitors.

Indexed as

AlgorithmsBreast NeoplasmsBromodomain Containing ProteinsCell Cycle ProteinsCell Line, TumorClass I Phosphatidylinositol 3-KinasesCluster AnalysisDrug Resistance, NeoplasmGene DosageGene Expression ProfilingGenome-Wide Association StudyHumansLinear ModelsNuclear ProteinsPhosphatidylinositol 3-KinasesTranscription FactorsBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsClass I Phosphatidylinositol 3-KinasesNuclear ProteinsPhosphatidylinositol 3-KinasesPIK3CA protein, humanTranscription Factors

Identifiers

PMID26771497
PMCPMC4724865
OpenAlexW2237475663

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.