Evidence map›Paper›PMID 31064401›Full record

ArticleJournal for immunotherapy of cancer2019

Tumor genomic alterations in severe-combined immunodeficiency bare-lymphocyte syndrome genes are associated with high mutational burden and disproportional neo-antigen rates.

Yu Wang, Douglas B Johnson, Steve Lu, Luis A Diaz, Yaomin Xu, Justin M Balko

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 55% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Article
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

6 authors at 5 institutions in 1 country.

Yu WangDepartment of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, 37232, USA.
Douglas B JohnsonDivision of Hematology and Oncology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, 37232, USA.
Steve LuJohns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
Luis A DiazMemorial Sloan Kettering Cancer Center, New York, NY, 10065, USA.
Yaomin XuDepartment of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, 37232, USA. yaomin.xu@vumc.org.
Justin M BalkoDivision of Hematology and Oncology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, 37232, USA. justin.balko@vumc.org.ORCID 0000-0002-4263-5974
Quantitative BioSciences · USBreast Cancer Research Foundation · USJohns Hopkins University · USMemorial Sloan Kettering Cancer Center · USVanderbilt University Medical Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STACIE B DUSETZINA · 1995 to 2026
$172.8M
Vanderbilt Clinical Oncology Research Career Development ProgramK12CA090625 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Debra L. Friedman, Paula Jill Hurley · 2001 to 2026
$16.9M
Predicting and profiling long-term survival after immune checkpoint inhibitionK23CA204726 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI JOHNSON, DOUGLAS B · 2016 to 2020
$756k
Dusp4 in breast cancer: tumor suppressor biology and therapeutic strategiesR00CA181491 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BALKO, JUSTIN M · 2015 to 2017
$750k
NCI NIH HHS K12 CA090625NCI NIH HHS K23CA204726NCI NIH HHS P30 CA008748NCI NIH HHS P30CA68485NCI NIH HHS R00CA181491
6 · The paper itself

Abstract

The progression of cancer requires mutational adaptation to permit unrestrained proliferation. A fraction of cancer mutations are oncogenic drivers, while others are putative 'passengers' that do not contribute to oncogenesis. However, altered peptides arising from passenger mutations may bind MHCs and activate non-self immunologic signals (i.e. neoantigens), thus requiring immunoediting for cancer persistence. Disruption of antigen processing machinery in tumor cells may diminish this requirement. Here, we show that rare mutations in antigen processing machinery are associated with high mutational burden and increased predicted neoantigen load, providing insights into the mechanisms of high mutation burden in some patients.

Indexed as

Antigen PresentationAntigens, NeoplasmComputational BiologyDatasets as TopicDNA Mutational AnalysisExome SequencingGene Expression ProfilingHistocompatibility Antigens Class IHumansMutation RateNeoplasmsSevere Combined ImmunodeficiencyAntigens, NeoplasmHistocompatibility Antigens Class IAntigen presentationBare lymphocyte syndromeCancerImmunotherapyNeoantigensSevere combined immunodeficiency syndrome

Identifiers

PMID31064401
PMCPMC6503546
OpenAlexW2947847094

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.