There’s been speculation about possible links between the Dana Farber Institute, via Jay Bradner, with Myc, Novartis and immuno-oncology.
Perhaps Dana Farber’s work does link PYC’s phylomers to immuno-oncology – but not through Myc.
Though we’ve been told very little about the work of Dana Farber, what we have been told is that this collaboration is focused on the oncogene targets of STAT5 and YB-1. In the latest presentation it is suggested that both of these research programs are at functional validation stage and both are open to partnering.
From what I have read about STAT5 and YB-1, it seems to me that they may be targets of almost as much interest to pharma as Myc.
Some brief snippets from recent research…
STAT5
STAT5 proteins critically regulate vital cellular functions such as proliferation, differentiation, and survival. The physiological importance of STAT5 proteins is underscored by the plethora of primary human tumors that have aberrant constitutive activation of these proteins, which significantly contributes to tumor cell survival and malignant progression of disease.
https://www.ncbi.nlm.nih.gov/pubmed/26716518
STAT5 is a signal protein that is activated when certain cytokines bind to receptors on the cell surface. Consequently, it is an attractive target for drug therapies that seek to alter immune responses and there is keen interest in understanding how it works.
https://elifesciences.org/content/5/e08384
YB-1
…the multifunctionality of YB-1 renders it a true master-regulator of malignancy and therefore it deserves the status given to other multi-potent oncoproteins such as Myc and Ras.
YB-1 promotes the escape of tumour cells from the immune system …
Given that the position of YB-1 is upstream of the molecular pathways responsible for all nine hallmarks of cancer, YB-1 is a very attractive therapeutic target.
…(a) CPP (cell-permeable peptide) inhibited the proliferation of breast and prostate cancer cells in cell culture. Importantly, the CPP had no effect on the growth of normal mammary epithelial cells isolated from patients . Thus peptide-based delivery systems could be used to inhibit YB-1 therapeutically.
http://www.biochemj.org/content/449/1/11
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