Evidence map›Paper›PMID 33476333›Full record

ArticlePLoS genetics2021

Impaired tumor immune response in metastatic tumors is a selective pressure for neutral evolution in CRC cases.

Shotaro Sakimura, Satoshi Nagayama, Mitsuko Fukunaga, Qingjiang Hu, Akihiro Kitagawa, Yuta Kobayashi, Takanori Hasegawa, Miwa Noda, Yuta Kouyama, Dai Shimizu and 19 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 38% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
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  7. Modeling colorectal cancer evolution.Journal of human genetics · 2021
    Review
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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

29 authors at 7 institutions in 1 country.

Shotaro SakimuraDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID 0000-0003-2913-8313
Satoshi NagayamaGastroenterological Center, Department of Gastroenterological Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID 0000-0001-9632-914X
Mitsuko FukunagaDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Qingjiang HuDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID 0000-0002-8313-5861
Akihiro KitagawaDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Yuta KobayashiDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID 0000-0002-2029-8292
Takanori HasegawaDivision of Health Medical Data Science, Health Intelligence Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID 0000-0001-7251-9950
Miwa NodaDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID 0000-0001-9502-9700
Yuta KouyamaDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Dai ShimizuDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Tomoko SaitoDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Atsushi NiidaLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID 0000-0002-6851-8004
Yusuke TsurudaDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Hajime OtsuDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID 0000-0002-0774-6150
Yoshihiro MatsumotoDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Hiroki UchidaDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID 0000-0002-2744-0917
Takaaki MasudaDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID 0000-0002-6341-2438
Keishi SugimachiDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID 0000-0001-8768-5388
Shin SasakiDepartment of Surgery, Omori Red Cross Hospital, Tokyo, Japan.
Kazutaka YamadaDepartment of Surgery, Takano Hospital, Kumamoto, Japan.ORCID 0000-0003-1385-3347
Kazuki TakahashiDepartment of Evolutionary Studies of Biosystems, SOKENDAI, The Graduate University for Advanced Studies, Tokyo, Japan.ORCID 0000-0001-5924-1376
Hideki InnanDepartment of Evolutionary Studies of Biosystems, SOKENDAI, The Graduate University for Advanced Studies, Tokyo, Japan.ORCID 0000-0001-6375-9231
Yutaka SuzukiMedical Genome Sciences, Graduate School of Frontier Sciences, University of Tokyo, Chiba, Japan.
Hiromi NakamuraDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
Yasushi TotokiDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0003-1876-6859
Shinichi MizunoCenter for Advanced Medical Innovation, Kyushu University, Fukuoka, Japan.ORCID 0000-0002-0960-5036
Masanobu OhshimaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Tatsuhiro ShibataDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0002-0477-210X
Koshi MimoriDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID 0000-0003-3897-9974
Kyushu University Beppu Hospital · JPKyushu University · JPThe Graduate University for Advanced Studies, SOKENDAI · JPChiba University · JPJapanese Foundation For Cancer Research · JPKanazawa University · JPTakano Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A Darwinian evolutionary shift occurs early in the neutral evolution of advanced colorectal carcinoma (CRC), and copy number aberrations (CNA) are essential in the transition from adenoma to carcinoma. In light of this primary evolution, we investigated the evolutionary principles of the genome that foster postoperative recurrence of CRC. CNA and neoantigens (NAG) were compared between early primary tumors with recurrence (CRCR) and early primary tumors without recurrence (precancerous and early; PCRC). We compared CNA, single nucleotide variance (SNV), RNA sequences, and T-cell receptor (TCR) repertoire between 9 primary and 10 metastatic sites from 10 CRCR cases. We found that NAG in primary sites were fewer in CRCR than in PCRC, while the arm level CNA were significantly higher in primary sites in CRCR than in PCRC. Further, a comparison of genomic aberrations of primary and metastatic conditions revealed no significant differences in CNA. The driver mutations in recurrence were the trunk of the evolutionary phylogenic tree from primary sites to recurrence sites. Notably, PD-1 and TIM3, T cell exhaustion-related molecules of the tumor immune response, were abundantly expressed in metastatic sites compared to primary sites along with the increased number of CD8 expressing cells. The postoperative recurrence-free survival period was only significantly associated with the NAG levels and TCR repertoire diversity in metastatic sites. Therefore, CNA with diminished NAG and diverse TCR repertoire in pre-metastatic sites may determine postoperative recurrence of CRC.

Indexed as

AdenomaAdultAgedAged, 80 and overCD8-Positive T-LymphocytesColorectal NeoplasmsDNA Copy Number VariationsFemaleGenetic DriftGenome, HumanHepatitis A Virus Cellular Receptor 2HumansImmunityMaleMiddle AgedNeoplasm Recurrence, LocalHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2PDCD1 protein, humanProgrammed Cell Death 1 ReceptorReceptors, Antigen, T-Cell

Identifiers

PMID33476333
PMCPMC7864431
OpenAlexW3121448410

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Registered trials

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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.