Evidence map›Paper›PMID 27956380›Full record

ArticleCancer immunology research2017

Somatic Mutations and Neoepitope Homology in Melanomas Treated with CTLA-4 Blockade.

Tavi Nathanson, Arun Ahuja, Alexander Rubinsteyn, Bulent Arman Aksoy, Matthew D Hellmann, Diana Miao, Eliezer Van Allen, Taha Merghoub, Jedd D Wolchok, Alexandra Snyder and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 3 pooled it
5.8field-weighted citation impact, top 3% 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

134 citing papers in PubMed, 3 syntheses or guidelines pooled it, 238 citations in OpenAlex.

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74 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

11 authors at 1 institution in 1 country.

Tavi NathansonGenetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York.
Arun AhujaGenetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York.
Alexander RubinsteynGenetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York.
Bulent Arman AksoyGenetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York.
Matthew D HellmannDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.
Diana MiaoDepartment of Medical Oncology, Dana-Farber Cancer Institute, Broad Institute of MIT and Harvard, Boston, Massachusetts.
Eliezer Van AllenDepartment of Medical Oncology, Dana-Farber Cancer Institute, Broad Institute of MIT and Harvard, Boston, Massachusetts.
Taha MerghoubDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.
Jedd D WolchokDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.
Alexandra SnyderDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York. snyderca@mskcc.org.
Jeff HammerbacherGenetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York.
Cornell University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Tumor Genetics and Response to Checkpoint Blockade in Melanoma and Ovarian CancerK08CA201544 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SNYDER CHAREN, ALEXANDRA · 2016 to 2016
$180k
NCI NIH HHS K08 CA201544NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Immune checkpoint inhibitors are promising treatments for patients with a variety of malignancies. Toward understanding the determinants of response to immune checkpoint inhibitors, it was previously demonstrated that the presence of somatic mutations is associated with benefit from checkpoint inhibition. A hypothesis was posited that neoantigen homology to pathogens may in part explain the link between somatic mutations and response. To further examine this hypothesis, we reanalyzed cancer exome data obtained from our previously published study of 64 melanoma patients treated with CTLA-4 blockade and a new dataset of RNA-Seq data from 24 of these patients. We found that the ability to accurately predict patient benefit did not increase as the analysis narrowed from somatic mutation burden, to inclusion of only those mutations predicted to be MHC class I neoantigens, to only including those neoantigens that were expressed or that had homology to pathogens. The only association between somatic mutation burden and response was found when examining samples obtained prior to treatment. Neoantigen and expressed neoantigen burden were also associated with response, but neither was more predictive than somatic mutation burden. Neither the previously described tetrapeptide signature nor an updated method to evaluate neoepitope homology to pathogens was more predictive than mutation burden. Cancer Immunol Res; 5(1); 84-91. ©2016 AACR.

Indexed as

MutationAdultAgedAged, 80 and overAmino Acid SequenceAntigens, NeoplasmAntineoplastic Agents, ImmunologicalCTLA-4 AntigenEpitopesFemaleHumansMaleMelanomaMiddle AgedPrognosisSequence Homology, Amino AcidAntigens, NeoplasmAntineoplastic Agents, ImmunologicalCTLA-4 AntigenEpitopes

Identifiers

PMID27956380
PMCPMC5253347
OpenAlexW2949453788

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.