M. Ahmad Chaudhry, Ph.D.

Assistant Professor, Medical Laboratory and Radiation Sciences
Academic Director, Radiation Therapy Program
Director, DNA Microarray Facility

Research Program: Genome Stability & Expression
VCC Membership Level: Full Member

Contact Information

302 Rowell Building
University of Vermont
Burlington, VT 05405

ph: (802) 656-0569
f: (802) 656-8749
Muhammad.Chaudhry@uvm.edu

Biography

Dr. Chaudhry received his Ph.D. in Molecular Biology from the University of Manchester, UK. He did postdoctoral research work at University of Alberta, Canada with Dr. Michael Weinfeld, before joining University of Pennsylvania as a Senior Research Investigator. His research interests are DNA microarrays, radiation-induced bystander effect, radiation-induced cell cycle arrest and the enzymatic processing of clustered DNA damage. Dr. Chaudhry joined the faculty of the University of Vermont in 2002. In 2004 he joined the faculty of the Department of Medical Laboratory and Radiation Sciences where he serves as the Academic Director of the Radiation Therapy Program. He also serves as the Director of DNA Microarray Facility at the University of Vermont.

Research

Dr. Chaudhry's research interests are DNA microarrays, radiation-induced cell cycle arrest and the enzymatic processing of clustered DNA damage.

Molecular basis of the radiation-induced bystander effect
The health effects of occupational and environmental ionizing radiation exposure to humans have not been completely understood. Recent advances in radiobiology have established that in cell populations exposed to ionizing radiation, the biological effects occur in a much larger proportion of cells than are estimated to be traversed by radiation. This phenomenon is termed as the “bystander effect”. The manifestation of radiation-induced genetic effects requires that DNA must be hit and damaged directly by the radiation. The irradiated cells are capable of providing signals to the neighboring cells and that signal results in damage to nearby unirradiated cells. Direct evidence of the bystander effect was provided in studies where the transfer of medium from irradiated cells was shown to reduce the plating efficiency of unirradiated bystander cells. The mechanisms underlying the bystander effects remain unknown. It has been suggested that the production of reactive oxygen species and direct cell-to-cell signaling via gap junctional intercellular communication may be involved. It is suggested that either 1) a damage signal(s) is passed through gap junctions to neighboring cells, which in turn exhibit enhanced or decreased survival after irradiation, or 2) a soluble factor(s) is released into the medium surrounding irradiated cells and affects cells that have not been irradiated through a receptor-mediated mechanism. The nature of the bystander effect signal and how it impacts unirradiated cells remains to be elucidated. Examination of the changes in gene expression could lead to the identification of the molecular pathways underlying the bystander effect. We are examining the global gene expression alterations in bystander cells with DNA microarray technology to gain insight into the molecular pathways responsible for the bystander effect.

DNA Microarrays
The availability of complete human genomic DNA sequence has prompted the need to develop technologies that permit to define the function of these genes. To this end DNA microarray technology has been developed in order to assess global gene expression alterations. Thousands of cDNAs are printed on membranes or glass slides using robotics. The oligonucleotides corresponding to thousands of genes are synthesized on a miniaturized surface, the so-called Gene Chip. DNA Microarrays are used to compare patterns of gene expression in which thousands of genes can be examined simultaneously. My laboratory is interested in applying the DNA microarray technology to investigate the bystander effect and perturbation of cell cycle in human cells exposed to ionizing radiation.

Recent Publications

Chaudhry, MA. (2008). Analysis of gene expression in normal and cancer cells exposed to g-radiation. J Biomed. Biotech. 2008: 541678.

Chaudhry, MA. (2008). Biomarkers for human radiation exposure. J Biomed Sci.

Chaudhry, MA. (2007). Base excision repair of ionizing radiation-induced DNA damage in G1 and G2 cell cycle phases. Cancer Cell Int. 7: 15.

Chaudhry, MA. (2006). Bystander effect: Biological endpoints and microarray analysis. Mutation Research 597: 98-112.

Chaudhry MA. (2006). Radiation-Induced Gene Expression Profile of Human Cells Deficient in 8-hydroxy-2'-deoxyguanine glycosylase. Int J Cancer 118: 633-642.

Yang N, Chaudhry MA, Wallace SS. Base Excision Repair by hNTH1 and hOGG1: A Two Edged Sword in the Processing of DNA Damage in g-irradiated Human Cells. DNA Repair 5: 43-51.

Inoue M, Shen GP, Chaudhry MA, Galick H, Blaisdell JO, Wallace SS. Expression of the oxidative base excision repair enzymes is not induced in TK6 human lymphoblastoid cells after low doses of ionizing radiation. Radiat Res 2004 Apr 161(4), 409-17.

Chaudhry, MA, Chodosh, LA, McKenna, WG, Muschel, RJ. Gene expression profile of human cells irradiated in G1 and G2 phases of cell cycle. Cancer Lett. 10;195(2):221-233, 2003.

Chaudhry MA, Chodosh LA, McKenna WG, Muschel RJ. Gene expression profiling of HeLa cells in G1 or G2 phases. Oncogene 2002 21:1934-1942.