A collaboration between scientists from The Memorial Sloan-Kettering Cancer Center in New York, Dana-Farber Cancer Institute in Boston and The Johns Hopkins Hospital in Baltimore reveals a new therapeutic target in Alveolar Soft Part Sarcoma.
The results of that collaboration were recently published in the scientific Journal Cancer Research volume 67 pages 919-929, 2007.
The new study demonstrates that ASPL-TFE3 (the specific fusion protein of ASPS) upregulates the expression of the active form of the MET gene product. MET activation leads to increased cell proliferation, survival, motility, and to the degradation of extracellular matrix. All of those MET-dependent activities contribute to tumor growth, invasiveness, and metastasis.
The new study from the laboratories of Marc Ladanyi, David Fisher and Ian Davis demonstrates that the elimination of MET or its inactivation by a new drug, PHA665752, inhibit cancer cell proliferation, adhesion, motility, and invasion. These important findings show a role for MET in human cancers that contain the specific TFE3 fusion protein. “MET inhibitors” are therefore a new hope for a line of therapies that may cure ASPS.
Here is a partial list of a few “MET inhibitors” that are currently in different phases of clinical development:
1. XL880
2. AMG 102
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4. SU11274
5. PHA6657524
6. AV299
__________________________
Yosef Landesman, Ph.D.
President & Cancer Research Director
Cure Alveolar Soft Part Sarcoma International (iCureASPS)
e-mail: landesmany@yahoo.com