Pawel K. Mazur, Ph.D.
Welcome to the Mazur Laboratory at MD Anderson Cancer Center. Our work focuses on the identification of drug target combinations that can efficiently treat pancreatic cancer. Our goal is to guide clinical drug development for precision medicine clinical trials.
Pancreatic cancer is one of the deadliest and most aggressive forms of cancer. There is an urgent need to develop new drugs and drug combinations to treat this disease.
- Over 46,400 Americans will be diagnosed this year and over 95% will die from this deadly disease.
- More than 75% of patients die within the first twelve months of diagnosis
- Pancreatic cancer is one of the few cancers for which survival has not substantially improved over the past 25 years
- Pancreatic cancer is projected to surpass breast, prostate, and colorectal cancers to become the 2nd leading cause of cancer-related death by 2020
Our work is dedicated to translating cancer discovery into cancer cures.
Our aim is to define upfront polytherapy approaches based upon deep systematic interrogation of the aberrant signal transduction operating in Kras-driven pancreatic cancer to combat or eliminate targeted therapy resistance, and transform pancreatic cancer from lethal disease into a chronic or curable condition.
Our vision is to To build a comprehensive disease modeling platform to study novel signaling networks and generate accurate animal models to better understand human pancreatic cancer biology. Our ultimate goal is to guide clinical drug development for precision medicine clinical trials.
Translating cancer discoveries into cancer cures
Research in the Mazur Lab is dedicated to identifying therapeutic targets in pancreatic cancer cells to guide clinical drug development and treatment approaches.
NATURE MEDICINE, 2015
Dual inhibition of BET proteins and HDACs synergistically suppresses PDAC development and maintenance.
JQ1 inhibits MYC and inflammatory cytokines, and synergizes with SAHA to activate p57 and induce death.
PDAC is sensitive to epigenetic-based therapies, which may be quickly implemented for patient use or clinical drug development.
SMYD3-mediated MAP3K2methylation activates RAS signaling and drives carcinogenesis in vivo.
Methylation of MAP3K2 by SMYD3 disrupts binding to PP2A and activates MEK1/2 signaling.
Those results reveal an unexpected role for lysine methylation in a kinase signalling pathway and establish SMYD3 as a potential therapeutic target for clinical drug development.
NATURE MEDICINE, 2013
Disruption of IQGAP1 scaffold function inhibits oncogenic ERK signaling without toxicity.
An IQGAP1 peptide reduces RAS/RAF–driven tumor growth and bypasses vemurafenib resistance.
Blockade of scaffold-kinase interactions can complement direct kinase inhibition for pancreatic cancer treatment and clinical drug development.
GENES & DEVELOPMENT, 2016
Loss of SMYD2 function reduces the growth of various tumor cell populations while its overexpression is pro-tumorigenic.
SMYD2 methylation of MK3 stress kinase promotes the proliferation and the survival of pancreas and lung cancer cells.
Inhibition of SMYD2 cooperates with standard chemotherapy to treat pancreatic cancer cells and reduces growth of patient derived tumors.