Evidence map›Paper›PMID 20833340›Full record

ReviewBest practice & research. Clinical endocrinology & metabolism2010

Familial testicular germ cell tumours.

Christian P Kratz, Phuong L Mai, Mark H Greene

Open access · greenAbstract readReview
In one paragraph

Review in Best practice & research. Clinical endocrinology & metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Sacrococcygeal Teratoma : A Tumor at the Center of Embryogenesis.Journal of Korean Neurosurgical Society · 2021
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Prospectively Identified Incident Testicular Cancer Risk in a Familial Testicular Cancer Cohort.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2015
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Cyclic AMP and c-KIT signaling in familial testicular germ cell tumor predisposition.The Journal of clinical endocrinology and metabolism · 2013
    Article
  17. Review
  18. Article
  19. Molecular genetics of testicular germ cell tumors.American journal of cancer research · 2012
    Article
  20. 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

3 authors at 2 institutions in 1 country.

Christian P KratzClinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20852, USA.
Phuong L Mai
Mark H Greene
National Cancer Institute · USDivision of Cancer Epidemiology and Genetics

Funding

CASE-CONTROL STUDY OF BRAIN CANCER AND OCCUPATIONN01CP011019 · CP · ABT ASSOCIATES, INC. · PI STONER, DIANE · 1985 to 1986
–
Intramural NIH HHS Z99 CA999999NCI NIH HHS N02 CP011019NCI NIH HHS N02 CP065504
6 · The paper itself

Abstract

This article defines familial testicular germ cell tumours (FTGCTs) as testicular germ cell tumours (TGCTs) diagnosed in at least two blood relatives, a situation which occurs in 1-2% of all cases of TGCT. Brothers and fathers of TGCT patients have an 8-10- and 4-6-fold increased risk of TGCT, respectively, and an even higher elevated risk of TGCT in twin brothers of men with TGCT has been observed, suggesting that genetic elements play an important role in these tumours. Nevertheless, previous linkage studies with multiple FTGCT families did not uncover any high-penetrance genes and it has been concluded that the combined effects of multiple common alleles, each conferring a modest risk, might underlie FTGCT. In agreement with this assumption, recent candidate gene-association analyses have identified the chromosome Y gr/gr deletion and mutations in the PDE11A gene as genetic modifiers of FTGCT risk. Moreover, two genome-wide association studies of predominantly sporadic but also familial cases of TGCT have identified three additional susceptibility loci, KITLG, SPRY4 and BAK1. Notably, all five loci are involved in the biology of primordial germ cells, representing the cell of origin of TGCT, suggesting that the tumours arise as a result of disturbed testicular development.

Indexed as

3',5'-Cyclic-GMP PhosphodiesterasesAnimalsbcl-2 Homologous Antagonist-Killer ProteinChromosome DeletionChromosome MappingChromosomes, Human, YGenetic VariationGenome-Wide Association StudyHumansIntracellular Signaling Peptides and ProteinsMaleNeoplasms, Germ Cell and EmbryonalNerve Tissue ProteinsPhosphoric Diester HydrolasesTesticular Neoplasms3',5'-Cyclic-GMP PhosphodiesterasesBAK1 protein, humanbcl-2 Homologous Antagonist-Killer ProteinIntracellular Signaling Peptides and ProteinsNerve Tissue ProteinsPDE11A protein, humanPhosphoric Diester HydrolasesSPRY4 protein, human

Identifiers

PMID20833340
PMCPMC2939736
OpenAlexW2102443531

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.