Seminar

Seminar

Date:
8 September 2011 00:00 hrs.
Location:
Title:
TET2 Inactivation predisposes to the development of hematological malignancies.
Speaker(s):

Dr. Olivier Bernard, INSERM Institut Gustave Roussy, Villejuif, France

Host(s):

Prof. Henk Stunnenberg, Department of Molecular Biology, NCMLS, Nijmegen

08-09-2011 00:00:00Europe/AmsterdamTET2 Inactivation predisposes to the development of hematological malignancies. Rimlsrimls@radboudumc.nl

Remarks / more information:

Olivier-BernardThe Ten-Eleven-translocation (TET)2 gene belongs to a 3 genes-familly that codes for dioxygenases dependent on iron and 2 oxoglutarate. The TET proteins have been shown to be able to oxydate methylcytosine (mC) into hydroxymethylcytosine (hmC) and thereby participate to active DNA demethylation and epoigenetic control of transcription. Acquired mutations impairing TET2 function have been described in various human myeloid malignancies suggesting a tumor suppressor function of the gene. We have now shown that inactivation of Tet2 in mouse perturbs both early and late steps of hematopoiesis including myeloid and lymphoid differentiation in a cell-autonomous manner, endows the cells with competitive advantage and eventually to the development of malignancies. We also report TET2 mutations in human lymphoid disorders that could be detected in immature progenitors endowed with myeloid-colonies forming potential. Our results show that the mutations present in lymphoid tumor cells may occur at both early and later steps of lymphoid development and indicate that impairment of TET2 function or/and expression predisposes to the development of hematological malignancies.



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