DESCRIPTION: (Adapted from investigator's abstract) The etiology of germ
cell tumors (GCT) is poorly understood. Previous studies, mainly focused on
testicular cancer and conducted among adult populations, have suggested that
certain pre-natal exposures, such a maternal exogenous hormone use and high
endogenous hormone level during pregnancy, and parental occupational
exposures, may be associated with an increased risk of GCT. These adult
studies, however, were limited because: a) the time between pre-natal
exposures and GCT diagnosis is long and validation of pre-natal exposure was
not feasible; b) post-natal exposures, particularly hormone-related factors
and occupational exposures were usually not adjusted; c) only one type of
GCT was studied in virtually all previous studies, which precluded a
comparison of the risk factors for different types of GCT.
This proposed study is designed to investigate specific and shared risk
factors for three types of GCT (testicular, ovarian, and non-gonadal) and to
test the following hypotheses: (1) Maternal exogenous hormone use and high
endogenous estrogen level are associated with an increase risk of GCT; (2)
Parental occupational exposures are related to the risk of GCT in offspring;
(3) Expression of human long repetitive elements (L1Hs) defines a sub-group
of GCT cases with specific etiologic, histologic and prognostic features;
(4) Male GCT cases have a high frequency of constitutional chromosome
abnormalities, and risk factors for GCT are different between GCTs with and
without constitutional chromosome abnormalities.
Utilizing the unique resources available through the Children's Cancer
Group, this study aims to (1) recruit 615 childhood GCT cases and 836
frequency matched controls, (2) interview parents of all study subjects
using a comprehensive questionnaire eliciting information on exposures of
index child in pre-conception, pre-natal and post-natal periods, and
validate maternal exposures during 6 months prior to and during index
pregnancy through review of medical records, (3) collect tumor tissue of GCT
cases for measuring L1Hs expression and tumor karyotype, and (4) examine the
constitutional chromosome abnormalities for all GCT cases.
This study represents the first large epidemiologic investigation to study
risk factors of childhood GCT and to examine the interaction between genetic
and environmental factors in the development of GCT. The relatively short
interval between exposures and GCT diagnosis will facilitate recall of
pre-natal exposures and allow for validation of exposures. The relatively
large sample size will provide sufficient statistical power to address the
hypotheses being investigated.
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