Evidence map›Paper›PMID 37597185›Full record

ArticleCell reports2023

Distinct mutational processes shape selection of MHC class I and class II mutations across primary and metastatic tumors.

Michael B Mumphrey, Noshad Hosseini, Abhijit Parolia, Jie Geng, Weiping Zou, Malini Raghavan, Arul Chinnaiyan, Marcin Cieslik

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Michael B MumphreyDepartment of Computational Medicine & Bioinformatics, University of Michigan, Ann Arbor, MI 48109, USA.
Noshad HosseiniDepartment of Computational Medicine & Bioinformatics, University of Michigan, Ann Arbor, MI 48109, USA.
Abhijit ParoliaDepartment of Pathology, University of Michigan, Ann Arbor, MI 48109, USA; Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI 48109, USA.
Jie GengDepartment of Microbiology & Immunology, University of Michigan, Ann Arbor, MI 48109, USA.
Weiping ZouDepartment of Microbiology & Immunology, University of Michigan, Ann Arbor, MI 48109, USA; Center of Excellence for Cancer Immunology and Immunotherapy, University of Michigan, Ann Arbor, MI 48109, USA; University of Michigan Rogel Cancer Center, Ann Arbor, MI 48109, USA.
Malini RaghavanDepartment of Microbiology & Immunology, University of Michigan, Ann Arbor, MI 48109, USA.
Arul ChinnaiyanDepartment of Pathology, University of Michigan, Ann Arbor, MI 48109, USA; Department of Computational Medicine & Bioinformatics, University of Michigan, Ann Arbor, MI 48109, USA; Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI 48109, USA; Department of Urology, University of Michigan, Ann Arbor, MI 48109, USA; Howard Hughes Medical Institute, Ann Arbor, MI 48109, USA; University of Michigan Rogel Cancer Center, Ann Arbor, MI 48109, USA.
Marcin CieslikDepartment of Pathology, University of Michigan, Ann Arbor, MI 48109, USA; Department of Computational Medicine & Bioinformatics, University of Michigan, Ann Arbor, MI 48109, USA; Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI 48109, USA; University of Michigan Rogel Cancer Center, Ann Arbor, MI 48109, USA. Electronic address: mcieslik@med.umich.edu.
University of Michigan · USHoward Hughes Medical Institute · US

Funding

INTERACTIONS &MECHANISMS OF FUNCTION OF THE TAP COMPLEXR01AI044115 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MALINI RAGHAVAN · 1999 to 2026
$9.3M
Proteogenomics of Cancer Training ProgramT32CA140044 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RAO, ARVIND, SARTOR, MAUREEN AGNES · 2010 to 2024
$3.9M
Howard Hughes Medical InstituteNCI NIH HHS T32 CA140044NIAID NIH HHS R01 AI044115
6 · The paper itself

Abstract

Disruption of antigen presentation via loss of major histocompatibility complex (MHC) expression is a strategy whereby cancer cells escape immune surveillance and develop resistance to immunotherapy. Here, we develop the personalized genomics algorithm Hapster and accurately call somatic mutations within the MHC genes of 10,001 primary and 2,199 metastatic tumors, creating a catalog of 1,663 non-synonymous mutations that provide key insights into MHC mutagenesis. We find that MHC class I genes are among the most frequently mutated genes in both primary and metastatic tumors, while MHC class II mutations are more restricted. Recurrent deleterious mutations are found within haplotype- and cancer-type-specific hotspots associated with distinct mutational processes. Functional classification of MHC residues reveals significant positive selection for mutations disruptive to the B2M, peptide, and T cell binding interfaces, as well as to MHC chaperones.

Indexed as

Histocompatibility Antigens Class INeoplasmsHistocompatibility Antigens Class IIHLA AntigensHumansMutationT-LymphocytesHistocompatibility Antigens Class IHistocompatibility Antigens Class IIHLA AntigenscancerCP: CancerCP: ImmunologyevolutiongenomicsHLAimmunogeneticsMHCselectionsomatic mutations

Identifiers

PMID37597185
PMCPMC11847572
OpenAlexW4386009541

What OpenQuestion holds

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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.