Infertility Clinical Trial
Official title:
Human MATER and Idiopathic Infertility
Approximately 15 percent of couples experience infertility, yet no abnormalities can be
detected in the man or the woman. In a number of couples, their embryos unexpectedly slow
down growth or stop growth completely. Some of these situations may be genetically
determined. For instance, a portion of cases may be caused by poor egg quality related to
genetic or functional deficiencies in heretofore unidentified human maternal effect genes. A
model has been developed of such unexplained fertility by creating a mouse line lacking a
critical maternal effect gene. (Maternal effect genes produce mRNA or proteins that
accumulate in the egg and are required for normal early embryonic development.) This pilot
project will test the hypothesis that a similar defect may be a cause of human infertility.
Thirty cubic centimeters of blood will be collected from 40 women who have a clinical history
consistent with a defective maternal effect gene. DNA from these blood cells will be examined
and stored. Some of the blood cells will be treated so that they can be frozen and grown in
the laboratory to produce more DNA in the future. If certain mutations are not found, that
means that the prevalence of such mutations is less than 10 percent, and investigators may
initiate another study with 100 women. If a common mutation is found in at least four
patients, the investigators will seek to collect DNA from 150 normal fertile control women
for comparison.
This project is purely investigational; therefore, findings will not be shared with
participants.
The pilot investigation will examine the hypothesis that human infertility may be caused by mutations in the human MATER gene. We will determine the prevalence of these mutations in a select group of women who have a clinical infertility history consistent with a possible defect in a maternal effect gene. After obtaining informed consent and DNA from 100 women, relevant mutations in the MATER gene will be searched for by single strand conformation polymorphism analysis. ;
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