Now as it seems to be suggested the mechanism of Cancer development seems to be multiple but one recognize that stimulation of the Myc or one of its variations seem to still the center piece of many neoplastic transformations. From Burkitt to Small cell cancer, the most aggressive cancer seem to act through this gene. Even Watson the DNA man went after the Myc as a potential drive for neoplasm. Myc can increase proliferation by acting through general proliferation factors (transcription factors) but in specific diseases, it can act specifically on downstream genes to drive the neoplastic transformation by using the Leucine unzipping prong (opening the nuclear machine to proliferation) or by opening the Ribosome to protein production needed in the neoplastic transformation.
Our interest in this area stems from our involvement with one family of 4 members that we suspect have Neurofibromatosis. NF1 has not been established yet but all members have development issues and lipomatous lesions and imaging has suggested diffuse Neurofibromas. One member developed Breast cancer, a BRCA was negative, One member has gait disturbances and speech impairement, and the member with several lipomatous lesions, came to our attention for cough. CT chest suggested a new peripheral nerve sheath tumor that we are following. NF1 is a tumor suppressor of the Ras of which amplification will reach the Myc. The Myc has interactions with BRCA but also several other genes
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