Evidence map›Paper›PMID 38848470›Full record

ArticleJNCI cancer spectrum2024

The genomic landscape of breast and non-breast cancers from individuals with germline CHEK2 deficiency.

Snežana Hinić, Rachel S van der Post, Lilian Vreede, Janneke Schuurs-Hoeijmakers, Saskia Koene, Erik A M Jansen, Franziska Bervoets-Metge, Arjen R Mensenkamp, Nicoline Hoogerbrugge, Marjolijn J L Ligtenberg and 1 more

Abstract read
In one paragraph

Article in JNCI cancer spectrum, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, BRCA2, PALB2, and CHEK2.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Trial
  2. Review
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Snežana HinićDepartment of Human Genetics, Radboud University Medical Center, Research Institute for Medical Innovation, Nijmegen, The Netherlands.
Rachel S van der PostDepartment of Pathology, Radboud University Medical Center, Research Institute for Medical Innovation, Nijmegen, The Netherlands.
Lilian VreedeDepartment of Human Genetics, Radboud University Medical Center, Research Institute for Medical Innovation, Nijmegen, The Netherlands.
Janneke Schuurs-HoeijmakersDepartment of Human Genetics, Radboud University Medical Center, Research Institute for Medical Innovation, Nijmegen, The Netherlands.
Saskia KoeneDepartment of Human Genetics, Radboud University Medical Center, Research Institute for Medical Innovation, Nijmegen, The Netherlands.
Erik A M JansenDepartment of Human Genetics, Radboud University Medical Center, Research Institute for Medical Innovation, Nijmegen, The Netherlands.
Franziska Bervoets-MetgeDepartment of Pathology, Radboud University Medical Center, Research Institute for Medical Innovation, Nijmegen, The Netherlands.
Arjen R MensenkampDepartment of Human Genetics, Radboud University Medical Center, Research Institute for Medical Innovation, Nijmegen, The Netherlands.ORCID 0000-0003-3805-877X
Nicoline HoogerbruggeDepartment of Human Genetics, Radboud University Medical Center, Research Institute for Medical Innovation, Nijmegen, The Netherlands.ORCID 0000-0003-2393-8141
Marjolijn J L LigtenbergDepartment of Human Genetics, Radboud University Medical Center, Research Institute for Medical Innovation, Nijmegen, The Netherlands.
Richarda M de VoerDepartment of Human Genetics, Radboud University Medical Center, Research Institute for Medical Innovation, Nijmegen, The Netherlands.ORCID 0000-0002-8222-0343

Funding

Dutch Cancer Society KWF 12174
6 · The paper itself

Abstract

CHEK2 is considered to be involved in homologous recombination repair (HRR). Individuals who have germline pathogenic variants (gPVs) in CHEK2 are at increased risk to develop breast cancer and likely other primary cancers. PARP inhibitors (PARPi) have been shown to be effective in the treatment of cancers that present with HRR deficiency-for example, caused by inactivation of BRCA1/2. However, clinical trials have shown little to no efficacy of PARPi in patients with CHEK2 gPVs. Here, we show that both breast and non-breast cancers from individuals who have biallelic gPVs in CHEK2 (germline CHEK2 deficiency) do not present with molecular profiles that fit with HRR deficiency. This finding provides a likely explanation why PARPi therapy is not successful in the treatment of CHEK2-deficient cancers.

Indexed as

Breast NeoplasmsCheckpoint Kinase 2Germ-Line MutationPoly(ADP-ribose) Polymerase InhibitorsAdultBreast Neoplasms, MaleFemaleHumansMaleMiddle AgedNeoplasmsOvarian NeoplasmsRecombinational DNA RepairCheckpoint Kinase 2CHEK2 protein, humanPoly(ADP-ribose) Polymerase Inhibitors

Identifiers

PMID38848470
PMCPMC11216722

What OpenQuestion 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 OpenQuestion graph.