ArticleOncogene2001
Chk2 tumour suppressor protein in human spermatogenesis and testicular germ-cell tumours.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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.
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.
Who cites it
21 citing papers in PubMed, 71 citations in OpenAlex.
- ILP-2: A New Bane and Therapeutic Target for Human Cancers.Frontiers in oncology · 2022Review
- Role of HP1β during spermatogenesis and DNA replication.Chromosoma · 2020Article
- Spermatogonial Stem Cells for In Vitro Spermatogenesis and In Vivo Restoration of Fertility.Cells · 2020Review
- Germline genome protection: implications for gamete quality and germ cell tumorigenesis.Andrology · 2019Review
- Association of Inherited Pathogenic Variants in Checkpoint Kinase 2 (CHEK2) With Susceptibility to Testicular Germ Cell Tumors.JAMA oncology · 2019Article
- Patterns of DNA damage response in intracranial germ cell tumors versus glioblastomas reflect cell of origin rather than brain environment: implications for the anti-tumor barrier concept and treatment.Molecular oncology · 2014Article
- Retinoblastoma protein (RB1) controls fate determination in stem cells and progenitors of the mouse male germline.Biology of reproduction · 2013Article
- The E3 ligase PIRH2 polyubiquitylates CHK2 and regulates its turnover.Cell death and differentiation · 2013Article
- Article
- Human spermatogonial stem cells: a possible origin for spermatocytic seminoma.International journal of andrology · 2011Review
- Loss of heterozygosity of CDKN2A (p16INK4a) and RB1 tumor suppressor genes in testicular germ cell tumors.Radiology and oncology · 2010Article
- Levonorgestrel enhances spermatogenesis suppression by testosterone with greater alteration in testicular gene expression in men.Biology of reproduction · 2009Article
- Alterations of Chk1 and Chk2 expression in colon cancer.International journal of colorectal disease · 2008Article
- Regulation of Chk2 ubiquitination and signaling through autophosphorylation of serine 379.Molecular and cellular biology · 2008Article
- P53 expression between 13-27 weeks old human male fetus gonads.Journal of molecular histology · 2007Article
- Article
- Article
- Article
- The CHEK2(*)1100delC mutation has no major contribution in oesophageal carcinogenesis.British journal of cancer · 2004Article
- A CHEK2 genetic variant contributing to a substantial fraction of familial breast cancer.American journal of human genetics · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chk2 is a transducer of DNA damage signals and a tumour suppressor whose germ-line mutations predispose to diverse tumour types. Unlike its downstream targets such as the p53 tumour suppressor, the expression patterns of Chk2 in tissues and tumours remain unknown. As DNA breaks occur commonly during gametogenesis, and p53 is wild-type and overexpressed in testicular cancer, we examined abundance and localisation of the Chk2 protein during normal development of human testes, and at various stages of germ-cell tumour (GCT) pathogenesis. Our results show that Chk2 is abundant in foetal germ cells and adult spermatogonia, yet only weakly expressed or lacking during the meiotic and later stages of spermatogenesis. High levels of Chk2 are detected in the majority of GCTs including all pre-invasive carcinoma-in-situ lesions, contrary to variable expression and even lack of Chk2 in subsets of invasive GCTs and some teratoma structures, respectively. Together with our analyses of cell culture models, these results indicate that downmodulation or lack of Chk2 is not simply attributable to quiescence or differentiation, they suggest a role for Chk2 in mitotic rather than meiotic divisions, support the concept of foetal origin of GCTs, and have implications for protein-based screening for tumour-associated aberrations of Chk2.
Indexed as
Identifiers
What OpenQuestion holds
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.