Name: Dr. James W DuMond
Title: Dean-School of Science
Office Location: Donnelly 228
Extension: (845) 575-3228
Degrees Held:

Doctor of Philosophy (1999) University of Alabama at Birmingham, Birmingham, AL. Major: Environmental Health Sciences/Environmental Toxicology Program

Masters of Science (1995) Montana College of Mineral Science and Technology, Butte, MT. Major: Industrial Hygiene

Bachelor of Science (1993) Eastern Montana College, Billings, MT. Major: Biology-Extended Major, Minor: Geology

  • Singh KP, Kumari R, Treas J, and DuMond JW, Chronic Exposure to Arsenic Causes Increased Cell Survival, DNA Damage, and Increased Expression of Mitochondrial Transcription Factor A (mtTFA) in Human Prostate Epithelial Cells. Chemical Research in Toxicology, 2011 Mar 21;24(3):340-9.
  • Singh KP, Kumari R, DuMond JW. Simulated microgravity-induced epigenetic changes in human lymphocytes. Journal of Cellular Biochemistry 2010 Sep 1;111(1):123-9
  • Ragini Kumari, Kamaleshwar Singh, James DuMond. Simulated microgravity decreases DNA repair capacity and induces DNA damage in human lymphocytes. Journal of Cellular Biochemistry 2009 Jul 1;107(4):723-31
  • Kamaleshwar P Singh, Ragini Kumari, Christina Pevey, Desiree Jackson, James W. DuMond. Long duration exposure to cadmium leads to increased cell survival, decreased DNA repair capacity, and genomic instability in mouse testicular Leydig cells. Cancer Letters. 2009 Jun 28;279(1):84-92
  • DuMond JW, Singh KP. Gene expression changes and induction of cell proliferation by chronic exposure to arsenic of mouse testicular Leydig cells. J. Tox. Env. Health, Part A, 70:13, 1150-1154, 2007
  • Singh KP, DuMond JW. Genetic and epigenetic changes induced by chronic low-dose exposure to arsenic of mouse testicular Leydig cells Int. J of Oncology, Jan;30(1):253-60, 2007
  • DuMond JW, Singh KP. Gene expression changes and induction of cell proliferation by chronic exposure to arsenic of mouse testicular Leydig cells. J. Tox. Env. Health, In press Accepted June 3, 2006
  • DuMond JW, Singh KP and Roy D. Development of a self-proliferating Leydig cell line; a hyper-sensitive E-screening model. Oncology Reports 16: 73-77, 2006.
  • DuMond JW and Roy D. “The inhibition of DNA Repair Capacity by Stilbene Estrogen in Leydig cells: its implications in the induction of instability in the testicular genome. Mutation Research, 483(1-2): 27-33, 2001
  • DuMond JW, Singh, KP, and Roy D. The Biphasic Stimulation of Proliferation of Leydig Cells by Estrogen Exposure. International Journal of Oncology, 18:3, 623-628, 2001
  • DuMond JW, Singh, KP, and Roy D “Regulation of the growth of mouse Leydig cells by the inactive stereoisomer, 17a-estradiol: Lack of correlation between the elevated expression of ERa and difference in sensitivity to estradiol isomers.” Oncology Reports 8:4, 899-902, 2001
  • Spear TM, DuMond JW, Lloyd C, and Vincent JH. An Effective Protection Factor Study of Respirators Used By Primary Lead Smelter Workers. Applied Occupational Safety and Environmental Hygiene, 15(2):235-44, 2000
Research Interests:

For the last two decades, my research focus has been on how environmental conditions and contaminates are able to perturb the process of DNA repair, which can lead to genomic instability. To date, my research has examined the effects of various chemicals such as environmental estrogens, nicotine, alcohol and heavy metals on genomic stability in addition to examining the effect of simulated microgravity for the same end point.

Fundamentally, the process of DNA repair is time dependent and has a distinct preference to repair areas of active transcription over areas that are not being actively transcribed. Hence it is reasonable to conclude that actively dividing cells are more susceptible to genotoxic agents then cells that are at rest.  Based on this deduction, it can be further postulated that any condition that “temporarily” perturbs the process of DNA repair during cell division could result in an increased rate of mutation and that inactive areas of DNA will be the most susceptible for mutations. This increase rate of mutation could ultimately lead to the loss of genomic stability through perturbation of gene expression and eventually to the induction of cancer. This is of course a rather simplistic view of mechanisms the involved, which are inherently more complex. However, research to date is in support of this hypothesis.

For the future, my research will continue to identify additional chemicals and combination for their ability to perturb genomic stability and shall be expanded to focus on prevention through potential gene therapies whereby DNA repair is up regulated, which is postulated to increases a cell protection against potential mutations.