School of Medicine


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  • Jason Wong

    Jason Wong

    Postdoctoral Research fellow, Endocrinology, Gerontology, and Metabolism

    Bio I am a graduate of the Harvard School of Public Health with a dual-doctorate in molecular/genetic epidemiology and environmental health. I have extensive expertise in quantitative analysis, epidemiological study design, and causal inference in observational studies. However, I am best described as a genomic trauma specialist focusing on the relationship between molecular markers, environmental factors, and risk of chronic diseases. My current research is multifaceted. I am currently investigating the relationship between sex hormone levels and risk of uterine fibroids in the Study of Women's Health Across the Nation (SWAN). Additionally, I am characterizing chromosomal copy-number variations in relation to risk of cardiovascular outcomes in the Cardiovascular Health Study (CHS). I am also exploring gene-environment interactions within the Epidemiology of Endometrial Cancer Consortium (E2C2).

    My career in biological research began at the British Columbia Cancer Agency under the guidance of Dr. Keith Humphries, a world renowned expert on the genetics of hematological disorders. It was in the Humphrie?s laboratory that I developed a strong foundation in molecular genetic techniques which served as a primer for the rest of my career. Subsequently, I became research laboratory manager for Dr. Immaculata De Vivo, a pioneer in molecular epidemiology at the Channing Division of Network Medicine at the Brigham and Women?s Hospital. Not only did I hone my expertise in molecular biology, but also received extensive training in the burgeoning field of molecular and genetic epidemiology.

    I used a three-pronged paradigm in my research to combat cancer; understanding genetic and biological susceptibility, prevention by attenuating modifiable risk factors, and treatment of underlying causative factors. With respect to genetic susceptibility, my projects focused on functional characterization of polymorphisms which predisposed women to endometrial cancer. With respect to attenuating modifiable risk factors, we studied how smoking and other lifestyle choices affect cancer risk. With respect to treatment of underlying disease, I studied how a novel therapeutic molecule called dichloroacetate induces cell death in a panel of endometrial cancer cells.

    My doctoral thesis focused on the effect of airborne particulate matter on telomere length, mediated through chronic inflammation and global DNA methylation. My interest in predictors of chronic disease is not limited to only to biological and environmental factors, but also social factors such as exposure to racism and early-life adversity in susceptible populations.

  • Michael Wosczyna

    Michael Wosczyna

    Postdoctoral Research fellow, Neurology and Neurological Sciences

    Current Research and Scholarly Interests Stem cell fate determination and microenvironment dynamics

  • Mark Wossidlo

    Mark Wossidlo

    Postdoctoral Research fellow, Stem Cell Biology and Regenerative Medicine

    Current Research and Scholarly Interests I am interested in the epigenetic reprogramming of DNA methylation during early mammalian preimplantation development. Early mammalian development is characterized by dramatic epigenetic changes. Upon fertilization of the oocyte with the sperm, the maternal and paternal genomes of the zygote are extensively reprogrammed to ensure the development of a totipotent potential. During this period of epigenetic reprogramming, DNA methylation (5-methyl-cytosine, 5mC) of paternal and maternal chromosomes is erased and reset during formation of the blastocyst. Interestingly, in mouse zygotes, the paternal genome becomes actively demethylated, as judged by immunofluorescence with antibodies against 5mC and bisulfite-sequencing data. Since the discovery of active DNA demethylation many scientists were trying to identify the putative ?DNA demethylase? and a lot of candidate enzymes and pathways have been suggested and disproven. The identification of the enzymatic conversion of 5mC to 5-hydroxymethyl-cytosine (5hmC), 5-formyl-cytosine (5fC) and 5-carboxyl-cytosine (5caC) by Tet1-3 enzymes sheds new light on this process.
    However, the analysis of epigenetic reprogramming in mammals is mainly focused on the mouse model and little is known about human embryonic development. Understanding the basic molecular mechanisms of human epigenetic reprogramming will impact human reproductive health and the generation of pluripotent stem cells

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