ArticleCancer research2008
Loss of the transmembrane but not the soluble kit ligand isoform increases testicular germ cell tumor susceptibility in mice.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 71 citations in OpenAlex.
- Driving precision medicine in testicular germ cell tumors: from preclinical models to clinical applications.Therapeutic advances in medical oncology · 2026Review
- Germline stem cells in human.Signal transduction and targeted therapy · 2022Review
- Identification of 22 susceptibility loci associated with testicular germ cell tumors.Nature communications · 2021Article
- Mammalian germ cells are determined after PGC colonization of the nascent gonad.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Testicular germ cell tumor: a comprehensive review.Cellular and molecular life sciences : CMLS · 2019Review
- The virtuous cycle of human genetics and mouse models in drug discovery.Nature reviews. Drug discovery · 2019Review
- Testicular cancer.Nature reviews. Disease primers · 2018Review
- Delayed male germ cell sex-specification permits transition into embryonal carcinoma cells with features of primed pluripotency.Development (Cambridge, England) · 2018Article
- Exploring the molecular aspects associated with testicular germ cell tumors: a review.Oncotarget · 2018Review
- Review
- Variants in BAK1, SPRY4, and GAB2 are associated with pediatric germ cell tumors: A report from the children's oncology group.Genes, chromosomes & cancer · 2017Article
- Germ cell tumors: Insights from the Drosophila ovary and the mouse testis.Molecular reproduction and development · 2017Review
- Genetic changes associated with testicular cancer susceptibility.Seminars in oncology · 2016Review
- Parent-of-origin effects of A1CF and AGO2 on testicular germ-cell tumors, testicular abnormalities, and fertilization bias.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The genomic landscape of testicular germ cell tumours: from susceptibility to treatment.Nature reviews. Urology · 2016Review
- Misexpression of cyclin D1 in embryonic germ cells promotes testicular teratoma initiation.Cell cycle (Georgetown, Tex.) · 2016Article
- Multi-stage genome-wide association study identifies new susceptibility locus for testicular germ cell tumour on chromosome 3q25.Human molecular genetics · 2015Article
- Tumor loci and their interactions on mouse chromosome 19 that contribute to testicular germ cell tumors.BMC genetics · 2014Article
- Testicular cancer: biology and biomarkers.Virchows Archiv : an international journal of pathology · 2014Review
- Fetal cyclophosphamide exposure induces testicular cancer and reduced spermatogenesis and ovarian follicle numbers in mice.PloS one · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Several genetic variants act as modifiers of testicular germ cell tumor (TGCT) susceptibility in the 129/Sv mouse model of human pediatric TGCTs. One such modifier, the Steel locus, encodes the transmembrane-bound and soluble ligand of the kit receptor. Some (Sl and SlJ) but not all (Sld) mutations of the Steel locus increase TGCT incidence in heterozygous mutant mice. Because Sl and SlJ are large deletions that affect multiple transcripts and Sld is an intragenic deletion of the kit ligand (Kitl) from which only the soluble protein is produced, it was uncertain whether Kitl or a neighboring gene is a modifier of TGCT susceptibility. We tested the effect of the small Steel grizzle-belly (Slgb) deletion on TGCT susceptibility to determine whether Kitl is a TGCT modifier gene. An increase in TGCT incidence was observed in Slgb/+ heterozygotes, and fine mapping of the deletion breakpoints revealed that Kitl is the only conventional gene deleted by the mutation, suggesting that Kitl is the TGCT modifier gene at the Steel locus. Additionally, we propose that soluble KITL in Sld/+ heterozygous mutant mice complements a dosage effect of transmembrane-associated kit ligand on TGCT susceptibility and that the kit receptor (Kit) is haplosufficient for primordial germ cell development.
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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.