Her name is Estela Medrano, and she was a scientist at Baylor who focused on melanoma. I have pasted a synopsis of her work below for those who are interested, but must confess that I have trouble finding it.
Her name is Estela Medrano, and she was a scientist at Baylor who focused on melanoma. I have pasted a synopsis of her work below for those who are interested, but must confess that I have trouble finding it.
There exists a network of dedicated, brilliant scientists who work long hours for not a lot of pay, trying to gain further understanding into what causes melanoma. These researchers lay the groundwork for all the clinical development that takes place, and every clinical trial had its origin in their work. Their names will not be on the news, and they will not be interviewed for their view on melanoma. But without them drugs that are all the rage now–ipi, PLX, etc.–wouldn't exist.
I have been impressed with the collegiality and cooperation that is evident among this group. We heard this evening about Estela's untimely death and my inbox is full of people expressing sympathy and a sense of loss.
She did not have melanoma, but she was a melanoma warrior, and the fight is a bit poorer for her passing.
Tim–MRF
Estela's work at Baylor:
The second project is focused on the role of the protein SKI in melanoma tumor progression. Ski encodes a nuclear protein that binds DNA in association with other proteins and can act as either an activator or repressor of transcription. Using the yeast two-hybrid system, we have demonstrated that SKI physically associates with Smad2 and Smad3, two transcriptional activators that mediate the TGF-beta response. SKI suppresses TGF-beta signaling by binding the MH2 domains of Smad2 and Smad3, and repressing promoters bound by these proteins and the common mediator Smad4. We propose that SKI functions as a potent oncogene in melanoma cells by counteracting the effect of the TGF-beta pathway that usually functions to suppress cellular transformation. We are analyzing additional SKI-protein interactions to determine their contribution to melanoma progression. Also, we have recently cloned the ski promoter to determine, by DNase foot-printing, electrophoretic mobility-band shift assays (EMSA), chromatin immunoprecipitation (ChIP), and reporter analysis, regulatory elements and factors involved in its activation during the malignant transformation of human melanocytes.
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