ReviewFrontiers in genetics2022
Meiotic Genes and DNA Double Strand Break Repair in Cancer.
Review in Frontiers in genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Proteomic analysis of cisplatin-induced spermatogenesis defects in mice.Annals of medicine · 2026Article
- Epigenetic dynamics of human spermatogenesis and their dysregulation in non-obstructive azoospermia.Protein & cell · 2026Article
- High-throughput mapping of spontaneous mitotic crossover and genome instability events with sci-L3-Strand-seq.Nucleic acids research · 2026Article
- ATRX safeguards cellular identity duringbioRxiv : the preprint server for biology · 2026Article
- Double jeopardy: howFrontiers in cell and developmental biology · 2026Review
- On the potential origin of the zygote-like cancer stem cell with a focus on fusion for cell rescue.Frontiers in cell and developmental biology · 2026Article
- Identification of Novel Susceptibility Genes for Early-Onset Colorectal Cancer Through Germline Rare Variant Burden Testing.Cancers · 2025Article
- Article
- ABL1-mediated tyrosine phosphorylation of SYCP2 contributes to transcription-coupled homologous recombination and platinum resistance in ovarian cancer.NAR cancer · 2025Article
- Parallel and convergent dynamics in the evolution of primary breast and lung adenocarcinomas.Communications biology · 2025Article
- Identification of prognostic hub genes and functional role of BAIAP2L2 in prostate cancer progression: a transcriptomic and experimental study.Frontiers in immunology · 2025Article
- MAX controls meiotic entry in sexually undifferentiated germ cells.Scientific reports · 2024Article
- Article
- The transcriptional regulator Ume6 is a major driver of early gene expression during gametogenesis.Genetics · 2023Article
- DNA double-strand break genetic variants in patients with premature ovarian insufficiency.Journal of ovarian research · 2023Review
- Review
- Importance of Germline and Somatic Alterations in HumanInternational journal of molecular sciences · 2023Review
- Challenges in next generation sequencing of homology recombination repair genomic variants in prostate cancer: A nationwide survey and calibration project in China.Prostate international · 2022Article
- Clinically relevant fusion oncogenes: detection and practical implications.Therapeutic advances in medical oncology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells show widespread genetic alterations that change the expression of genes driving tumor progression, including genes that maintain genomic integrity. In recent years, it has become clear that tumors frequently reactivate genes whose expression is typically restricted to germ cells. As germ cells have specialized pathways to facilitate the exchange of genetic information between homologous chromosomes, their aberrant regulation influences how cancer cells repair DNA double strand breaks (DSB). This drives genomic instability and affects the response of tumor cells to anticancer therapies. Since meiotic genes are usually transcriptionally repressed in somatic cells of healthy tissues, targeting aberrantly expressed meiotic genes may provide a unique opportunity to specifically kill cancer cells whilst sparing the non-transformed somatic cells. In this review, we highlight meiotic genes that have been reported to affect DSB repair in cancers derived from somatic cells. A better understanding of their mechanistic role in the context of homology-directed DNA repair in somatic cancers may provide useful insights to find novel vulnerabilities that can be targeted.
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Registered trials
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.