Evidence map›Paper›PMID 27197066›Full record

ArticleCancer immunology research2016

Immunogenic Subtypes of Breast Cancer Delineated by Gene Classifiers of Immune Responsiveness.

Lance D Miller, Jeff A Chou, Michael A Black, Cristin Print, Julia Chifman, Angela Alistar, Thomas Putti, Xiaobo Zhou, Davide Bedognetti, Wouter Hendrickx and 6 more

Abstract read
In one paragraph

Article in Cancer immunology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

72 citing papers in PubMed, 1 synthesis or guideline pooled it.

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12 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

16 authors.

Lance D MillerDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, North Carolina. The Comprehensive Cancer Center of Wake Forest University, Winston Salem, North Carolina. ldmiller@wfubmc.edu.
Jeff A ChouDepartment of Biostatistical Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Michael A BlackDepartment of Biochemistry, Otago School of Medical Sciences, University of Otago, Dunedin, New Zealand.
Cristin PrintDepartment of Molecular Medicine and Pathology and Maurice Wilkins Institute, Faculty of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand.
Julia ChifmanDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Angela AlistarThe Comprehensive Cancer Center of Wake Forest University, Winston Salem, North Carolina. Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Thomas PuttiDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, National University Hospital, Singapore.
Xiaobo ZhouDepartment of Radiology, Center for Bioinformatics and Systems Biology, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Davide BedognettiDivision of Translational Medicine, Sidra Medical and Research Center, Doha, Qatar.
Wouter HendrickxDivision of Translational Medicine, Sidra Medical and Research Center, Doha, Qatar.
Ashok PullikuthDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Jonathan RennhackDepartment of Physiology, Michigan State University, East Lansing, Michigan.
Eran R AndrechekDepartment of Physiology, Michigan State University, East Lansing, Michigan.
Sandra DemariaDepartment of Radiation Oncology and Pathology, Weill Cornell Medical College, New York, New York.
Ena WangDivision of Translational Medicine, Sidra Medical and Research Center, Doha, Qatar.
Francesco M MarincolaOffice of the Chief Research Officer, Research Branch, Sidra Medical and Research Center, Doha, Qatar.

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
Dissecting Tumor Heterogeneity by Analyzing Signaling Pathway Requirements.R01CA160514 · NCI · MICHIGAN STATE UNIVERSITY · PI ANDRECHEK, ERAN ROBERT · 2012 to 2016
$1.5M
The Role of E2F2 in HER2 Positive Breast CancerF99CA212221 · NCI · MICHIGAN STATE UNIVERSITY · PI RENNHACK, JONATHAN · 2016 to 2017
$85k
NCI NIH HHS P30 CA012197NCI NIH HHS R01 CA160514
6 · The paper itself

Abstract

The abundance and functional orientation of tumor-infiltrating lymphocytes in breast cancer is associated with distant metastasis-free survival, yet how this association is influenced by tumor phenotypic heterogeneity is poorly understood. Here, a bioinformatics approach defined tumor biologic attributes that influence this association and delineated tumor subtypes that may differ in their ability to sustain durable antitumor immune responses. A large database of breast tumor expression profiles and associated clinical data was compiled, from which the ability of phenotypic markers to significantly influence the prognostic performance of a classification model that incorporates immune cell-specific gene signatures was ascertained. Markers of cell proliferation and intrinsic molecular subtype reproducibly distinguished two breast cancer subtypes that we refer to as immune benefit-enabled (IBE) and immune benefit-disabled (IBD). The IBE tumors, comprised mostly of highly proliferative tumors of the basal-like, HER2-enriched, and luminal B subtypes, could be stratified by the immune classifier into significantly different prognostic groups, while IBD tumors could not, indicating the potential for productive engagement of metastasis-protective immunity in IBE tumors, but not in IBD tumors. The prognostic stratification in IBE was independent of conventional variables. Gene network analysis predicted the activation of TNFα/IFNγ signaling pathways in IBE tumors and the activation of the transforming growth factor-β pathway in IBD tumors. This prediction supports a model in which breast tumors can be distinguished on the basis of their potential for metastasis-protective immune responsiveness. Whether IBE and IBD represent clinically relevant contexts for evaluating sensitivity to immunotherapeutic agents warrants further investigation. Cancer Immunol Res; 4(7); 600-10. ©2016 AACR.

Indexed as

Breast NeoplasmsCluster AnalysisFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansImmunomodulationLeukocytesLymphocytes, Tumor-InfiltratingNeoplasm MetastasisNeoplasm StagingPhenotypePrognosisProportional Hazards Models

Identifiers

PMID27197066
PMCPMC4930674

What OpenQuestion holds

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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.