Evidence map›Paper›PMID 36088508›Full record

ArticleBritish journal of cancer2022

Somatic hits in mismatch repair genes in colorectal cancer among non-seminoma testicular cancer survivors.

Berbel L M Ykema, Emilie C H Breekveldt, Beatriz Carvalho, Tom van Wezel, Gerrit A Meijer, Martijn Kerst, Michael Schaapveld, Flora E van Leeuwen, Petur Snaebjornsson, Monique E van Leerdam

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In one paragraph

Article in British journal of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

10 authors at 2 institutions in 1 country.

Berbel L M YkemaDepartment of Gastrointestinal Oncology, Netherlands Cancer Institute, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0002-0314-7986
Emilie C H BreekveldtDepartment of Gastrointestinal Oncology, Netherlands Cancer Institute, Amsterdam, the Netherlands.
Beatriz CarvalhoDepartment of Pathology, Netherlands Cancer Institute, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0003-4903-399X
Tom van WezelDepartment of Pathology, Netherlands Cancer Institute, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0001-5773-7730
Gerrit A MeijerDepartment of Pathology, Netherlands Cancer Institute, Amsterdam, the Netherlands.
Martijn KerstDepartment of Medical Oncology, Netherlands Cancer Institute, Amsterdam, the Netherlands.
Michael SchaapveldDepartment of Epidemiology, Netherlands Cancer Institute, Amsterdam, the Netherlands.
Flora E van LeeuwenDepartment of Epidemiology, Netherlands Cancer Institute, Amsterdam, the Netherlands.
Petur SnaebjornssonDepartment of Pathology, Netherlands Cancer Institute, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0002-1086-8108
Monique E van LeerdamDepartment of Gastrointestinal Oncology, Netherlands Cancer Institute, Amsterdam, the Netherlands. m.v.leerdam@nki.nl.ORCID http://orcid.org/0000-0002-5719-3208
The Netherlands Cancer Institute · NLLeiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-seminoma testicular cancer survivors (TCS) have an increased risk of developing colorectal cancer (CRC) when they have been treated with platinum-based chemotherapy. Previously we demonstrated that among Hodgkin lymphoma survivors (HLS) there is enrichment of rare mismatch repair (MMR) deficient (MMRd) CRCs with somatic hits in MMR genes. We speculate that this phenomenon could also occur among other cancer survivors. We therefore aim to determine the MMR status and its underlying mechanism in CRC among TCS (TCS-CRC).

methodsThirty TCS-CRC, identified through the Dutch pathology registry, were analysed for MMR proteins by immunohistochemistry. Next-generation sequencing was performed in MMRd CRCs without MLH1 promoter hypermethylation (n = 4). Data were compared with a male cohort with primary CRC (P-CRC, n = 629).

resultsMMRd was found in 17% of TCS-CRCs vs. 9% in P-CRC (p = 0.13). MMRd was more often caused by somatic double or single hit in MMR genes by mutation or loss of heterozygosity in TCS-CRCs (3/30 (10%) vs. 11/629 (2%) in P-CRCs (p < 0.01)).

conclusionsMMRd CRCs with somatic double or single hit are more frequent in this small cohort of TCS compared with P-CRC. Exposure to anticancer treatments appears to be associated with the development of these rare MMRd CRC among cancer survivors.

Indexed as

Colorectal NeoplasmsTesticular NeoplasmsDNA Mismatch RepairHumansMaleMutationMutL Protein Homolog 1SurvivorsMutL Protein Homolog 1

Identifiers

PMID36088508
PMCPMC9681876
OpenAlexW4296276655

What Socratic holds

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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 Socratic graph.