Sanjay J. Chandriani

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BACKGROUND The MYC oncogene contributes to induction and growth of many cancers but the full spectrum of the MYC transcriptional response remains unclear. METHODOLOGY/PRINCIPAL FINDINGS Using microarrays, we conducted a detailed kinetic study of genes that respond to MYCN or MYCNDeltaMBII induction in primary human fibroblasts. In parallel, we determined(More)
Estrogen, progesterone, and HER2 receptor-negative triple-negative breast cancers encompass the most clinically challenging subtype for which targeted therapeutics are lacking. We find that triple-negative tumors exhibit elevated MYC expression, as well as altered expression of MYC regulatory genes, resulting in increased activity of the MYC pathway. In(More)
Lytic infection by Kaposi's sarcoma-associated herpesvirus (KSHV) is associated with an extensive shutoff of host gene expression, mediated chiefly by accelerated mRNA turnover due to expression of the viral SOX protein. We have previously identified a small number of host mRNAs that can escape SOX-mediated degradation. Here we present a detailed,(More)
Deregulated Myc expression can lead to profound physiological changes in cells, including increased cell proliferation, oncogenic transformation, apoptosis and inhibition of differentiation. Myc is a transcription factor that can both stimulate and inhibit transcription and is believed to affect the physiological changes by coordinate regulation of many Myc(More)
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