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Testicular Dysgenesis, Testis Cancer and the Environment

Hosted by:
Harvard University, School of Public Health
Speaker:
Niels Skakkebaek, University Department of Growth and Reproduction, Rigshospitalet, Copenhagen, Denmark
Starts:
June 26, 2006 at 12:00 pm
Ends:
June 26, 2006 at 01:00 pm
Location:
Harvard School of Public Health, Building Name, Snyder Auditorium, 655 Huntington Avenue, Boston, MA. 2115
Maps:

Description

There is evidence that testicular cancer originates from early primitive fetal germ cells, which fail to differentiate normally into spermatogonia. These carcinoma in situ germ cells express pluripotency markers (e.g.Oct-4, Nanog, AP2 gamma) and we consider them “hybrids” between stem cells and germ cells. There is epidemiological evidence that the prenatal environment is associated with risk of germ cell cancer. Thus testis cancer seems to be a developmental disease, which shares fetal risk factors with other reproductive health problems, e.g. cryptorchidism, hypospadias and infertility. Endocrine disrupters are among the possible candidates causing the several fold rise in testis cancer in Denmark and other developed countries. Testis cancer is also becoming more common among young US men.

Registration required:
No
Free:
Yes

Additional information

Lunch and drinks will be available.

For more information

Contact person:
Russ Hauser
Email:
Website:
Testicular Dysgenesis, Testis Cancer and the Environment
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