Evidence map›Paper›PMID 38151294›Full record

ArticleCancer genomics & proteomics

Impact of Mutations in Subunit Genes of the Mammalian SWI/SNF Complex on Immunological Tumor Microenvironment.

Chikako Hozumi, Akira Iizuka, Tomoatsu Ikeya, Haruo Miyata, Chie Maeda, Tadashi Ashizawa, Takeshi Nagashima, Kenichi Urakami, Yuji Shimoda, Keiichi Ohshima and 18 more

Open access · diamondAbstract read
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
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

28 authors at 2 institutions in 1 country.

Chikako HozumiImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Akira IizukaImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Tomoatsu IkeyaImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Haruo MiyataImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Chie MaedaImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Tadashi AshizawaImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Takeshi NagashimaCancer Diagnostic Research Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Kenichi UrakamiCancer Diagnostic Research Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Yuji ShimodaCancer Diagnostic Research Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Keiichi OhshimaMedical Genetics Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Koji MuramatsuDivision of Pathology, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Takashi SuginoDivision of Pathology, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Akio ShiomiDivision of Colon and Rectal Surgery, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Yasuhisa OhdeDivision of Thoracic Surgery, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Etsuro BandoDivision of Gastric Surgery, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Kenichiro FurukawaDivision of Gastric Surgery, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Teiichi SugiuraDivision of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Takashi MukaigawaDivision of Head and Neck Surgery, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Seiichiro NishimuraDivision of Breast Surgery, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Yasuyuki HirashimaDivision of Gynecology, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Koichi MitsuyaDivision of Neurosurgery, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Shusuke YoshikawaDivision of Dermatology, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Yasuhiro TsubosaDivision of Esophageal Surgery, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Hirohisa KatagiriDivision of Orthopedic Oncology, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Masashi NiwakawaDivision of Urology, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Ken YamaguchiOffice of the president, Shizuoka Cancer Center, Shizuoka, Japan.
Hirotsugu KenmotsuDivision of Thoracic Oncology, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Yasuto AkiyamaImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan; y.akiyama@scchr.jp.
Shizuoka Cancer Center · JPSRL (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimRecently, inactivating somatic mutations of SWI/SNF chromatin-remodeling genes in cancers have been reported. However, few studies have been performed regarding the immunological analysis of the tumor microenvironment (TME) in chromatin remodeling complex gene-mutated tumors. In the present study, we identified cancer patients harboring various mammalian SWI/SNF complex mutations and investigated the immunological features in those mutated cancers. PATIENTS AND

methodsCancer patients harboring any type of chromatin remodeling complex gene mutation were selected and clinicopathological features were compared between chromatin remodeling complex gene expression-low and expression-high groups. Specifically, expression levels of immune response-associated genes and cancer-associated genes were compared between the SMARCA4 expression-low and expression-high groups using volcano plot analysis.

resultsAmong cancers harboring PBRM1, SAMRACA4 and ARID2 gene mutations, T-cell marker and mature B-cell marker genes were up-regulated in the tumor. Specifically, T-cell effector genes (CD8B, CD40LG), central memory marker genes (CD27, CCR7) and mature B-cell marker genes (CD20, CD38, CD79 and IRF4) were up-regulated, and cancer-associated genes including MYB, MYC and AURKB genes were down-regulated in the SMARCA4 expression-low group. Remarkably, heatmap of gene expression and immunohistochemistry (IHC) data demonstrated that the tertiary lymphoid structure (TLS) gene signature of mature B cells was up-regulated in SMACA4 gene-mutated stomach cancers.

conclusionThese results suggest that immune tumor microenvironment status, such as mature B cell recruitment featuring the TLS gene signature and immune activation mediated by cancer signal down-regulation, might contribute to the classification of SMARCA4 gene-mutated tumors as immune checkpoint blockade therapy-sensitive target tumors.

Indexed as

NeoplasmsTumor MicroenvironmentAnimalsDNA HelicasesHumansMammalsMutationNuclear ProteinsTranscription FactorsDNA HelicasesNuclear ProteinsSMARCA4 protein, humanTranscription Factorschromatin remodeling geneImmunological tumor microenvironmentiTMEmammalian SWI/SNF complexSMARCA4 mutationTILstumor-infiltrating lymphocytes

Identifiers

PMID38151294
PMCPMC10756348
OpenAlexW4390267591

What OpenQuestion holds

Textmetadata
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.