Evidence map›Paper›PMID 20228134›Full record

ReviewEndocrine-related cancer2010

Familial testicular germ cell tumors in adults: 2010 summary of genetic risk factors and clinical phenotype.

Mark H Greene, Christian P Kratz, Phuong L Mai, Christine Mueller, June A Peters, Gennady Bratslavsky, Alex Ling, Peter M Choyke, Ahalya Premkumar, Janet Bracci and 3 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrine-related cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

  1. Guideline
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  16. Review
  17. PeerJ · 2020
    Article
  18. Contemporary management of early stage testicular seminoma.Translational andrology and urology · 2020
    Review
  19. Article
  20. Article
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

13 authors at 5 institutions in 1 country.

Mark H GreeneClinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland 20852, USA. greenem@mail.nih.gov
Christian P Kratz
Phuong L Mai
Christine Mueller
June A Peters
Gennady Bratslavsky
Alex Ling
Peter M Choyke
Ahalya Premkumar
Janet Bracci
Rissah J Watkins
Mary Lou McMaster
Larissa A Korde
National Cancer Institute · USDivision of Cancer Epidemiology and GeneticsNational Institutes of Health · USWestat (United States) · USCancer Genetics (United States) · US

Funding

Clinical Genetic Studies of Familial and Hereditary Cancer SyndromesZIACP010144 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI SAVAGE, SHARON A. · 2009 to 2025
$111.8M
CASE-CONTROL STUDY OF BRAIN CANCER AND OCCUPATIONN01CP011019 · CP · ABT ASSOCIATES, INC. · PI STONER, DIANE · 1985 to 1986
–
Intramural NIH HHS ZIA CP010144NCI NIH HHS N02 CP011019NCI NIH HHS N02 CP065504NCI NIH HHS N02-CP-11019-50
6 · The paper itself

Abstract

Familial aggregations of testicular germ cell tumor (FTGCT) have been well described, suggesting the existence of a hereditary TGCT subset. Approximately 1.4% of newly diagnosed TGCT patients report a positive family history of TGCT. Sons and siblings of TGCT patients have four- to sixfold and eight- to tenfold increases in TGCT risk respectively. Segregation analyses suggest an autosomal recessive mode of inheritance. Linkage analyses have identified several genomic regions of modest interest, although no high-penetrance cancer susceptibility gene has been mapped yet. These data suggest that the combined effects of multiple common alleles, each conferring modest risk, might underlie familial testicular cancer. Families display a mild phenotype: the most common number of affected families is 2. Age at diagnosis is 2-3 years younger for familial versus sporadic cases. The ratio of familial seminoma to nonseminoma is 1.0. FTGCT is more likely to be bilateral than sporadic TGCT. This syndrome is cancer site specific. Testicular microlithiasis is a newly recognized FTGCT component. Candidate gene-association studies have implicated the Y chromosome gr/gr deletion and PDE11A gene mutations as genetic modifiers of FTGCT risk. Two genomewide association studies of predominantly sporadic but also familial cases of TGCT have implicated the KIT-ligand, SPRY4, and BAK1 genes as TGCT risk modifiers. All five loci are involved in normal testicular development and/or male infertility. These genetic data provide a novel insight into the genetic basis of FTGCT, and an invaluable guide to future TGCT research.

Indexed as

Genes, NeoplasmGenetic Association StudiesAdultAge of OnsetChromosomes, Human, YGenes, Tumor SuppressorGenetic LinkageHumansMaleNeoplasms, Germ Cell and EmbryonalPedigreePenetranceRisk FactorsSeminomaTesticular Neoplasms

Identifiers

PMID20228134
PMCPMC3101798
OpenAlexW2172279582

What OpenQuestion holds

Textmetadata
LicenceTDM
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.