Invited Speakers: see below
Program:
Morning session
Invited participants: Kiran Chada, Nils Mandahl, Cynthia C. Morton, Kevin
Lee, David Ron, Eric Schoenmakers, Wim Van De Ven (chair)
One part of the symposium will be devoted to solid tumors in which cancer
genes mapping to chromosome 12 are implicated. Cytogenetics of chromosome
12 aberrations in solid tumors will be reviewed whereas recent progress
in the identification and functional characterisation of chromosome 12
cancer genes will be discussed by others; i.e. the EWS/ATF1 oncogene in
malignant melanoma of the soft parts, the CHOP gene in myxoid liposarcoma,
and the high mobility group protein gene HMGI-C in a variety of benign
mesenchymal tumors. A poster session will also be part of the symposium.
Afternoon session
Invited participants: Roland Berger, Stefan K. Bohlander, D. Gary
Gilliland, Todd R. Golub, Anne Hagemeijer (chair), Leanne M. Wiedemann,
Gerard Grosfeld
In myeloid and lymphoid leukemias recurrent chromosomal aberrations can be
detected of chromosome region 12p13. In this region the TEL and KIP1
genes are found.
Fusion of the amino-terminal HLH-domain of TEL to the PDGF-beta receptor
in chronic myelomonocytic leukemia with t(5;12) was first described.
Cloning of the t(12;22), involving MN1 on 22q11, suggested that the
involvement of TEL in leukemogenesis could be dual; both the isolated
protein-dimerisation and DNA-binding domains may be involved in oncogenic
activation.
The activation of ABL by fusion to TEL appears to be a rare event in cALL.
The fusion of TEL to AML1 in childhood ALL with t(12;21) , also with the
expression of two fusion proteins, appears to be frequent in childhood
ALL. Both events remain mostly undetected by cytogenetic analysis. The
t(12;21) appears associated with the deletion of the region with the TEL
and KIP1 genes on the normal 12. This can be detected as LOH at the TEL
and KIP1 loci.
Deletions are perhaps the most freqent chromosomal anomaly involving 12p
in leukemia. The commonly deleted region in these cases also contains TEL
and KIP1.
The biology of TEL and its different fusion proteins, and of KIP1 will be
the main topic of the afternoon session.
Registration :
Deadline for Abstracts:
Email for Requests and Registration: siska.waelkens@med.kuleuven.ac.be