Dr. W Stratford May MD
Oncologist | Medical Oncology
1600 SW Archer Rd Gainesville FL, 32610About
Dr. W May is an oncologist practicing in Gainesville, FL. Dr. May specializes in the care and treatment of patients with cancer. As an oncologist, Dr. May manages and oversees the treatment of a cancer patient after he or she has been diagnosed with the disease. Oncologists will care for their patients throughout the course of the disease. Types of oncologists include medical oncologists, surgical oncologists, radiation oncologists, gynecologic oncologists, pediatric oncologists and hematologist oncologists.
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Expert Publications
Data provided by the National Library of Medicine- Novel triterpenoid CDDO-Me is a potent inducer of apoptosis and differentiation in acute myelogenous leukemia.
- A functional role for the B56 alpha-subunit of protein phosphatase 2A in ceramide-mediated regulation of Bcl2 phosphorylation status and function.
- A functional role for nicotine in Bcl2 phosphorylation and suppression of apoptosis.
- Bryostatin-I: an antineoplastic treasure from the deep?
- Protein kinase C-dependent phosphorylation and mitochondrial translocation of aldose reductase.
- Phosphorylation by aurora B converts MgcRacGAP to a RhoGAP during cytokinesis.
- Cleavage of Bax to p18 Bax accelerates stress-induced apoptosis, and a
- Bcl2 retards G1/S cell cycle transition by regulating intracellular ROS.
- A novel role for RAX, the cellular activator of PKR, in synergistically stimulating SV40 large T antigen-dependent gene expression.
- Mono- and multisite phosphorylation enhances Bcl2's antiapoptotic function and inhibition of cell cycle entry functions.
- Serine 18 phosphorylation of RAX, the PKR activator, is required for PKR activation and consequent translation inhibition.
- Bcl2 suppresses DNA repair by enhancing c-Myc transcriptional activity.
- Bcl2's flexible loop domain regulates p53 binding and survival.
- RAX, the PKR activator, sensitizes cells to inflammatory cytokines, serum withdrawal, chemotherapy, and viral infection.
- JAZ mediates G1 cell-cycle arrest and apoptosis by positively regulating p53 transcriptional activity.
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