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Dr. Mohamed Hassanfarah

Prof. Assistant
Biotechnoly Dept., Faculty of Science, PSU
23th Dec. St., 42521

Brief Biography:

I ha graduated from the Faculty of Science, Biology Dept., Assuit University, Egypt. I got Master degree in Physiology and Biochemistry and PhD., in Molecular cancer biology from Graduate School of Medicine, Hokkaido University, Japan. Now I am working as a Prof. assistant for biotechnology dept. Faculty of Science, PSU. My research area is the molecular cancer biology. We are interested in studying the molecular mechanism involved in carcinogenesis more precisely, the mechanisms responsible for the resistance of different cancer cells to chemotherapeutic agents as a standard therapy for many kinds of cancers. Also we are searching for possible mechanism to disturb, block or inhibit these resistance mechanisms and increase the efficacy of the therapeutic reagents as final targets. Our first point of interest was studying the genes involved in the resistance of some human ovarian cancer cells to a standard chemotherapy used widely for treating the ovarian cancer patients, paclitaxel (Taxane; TX), which was derived originally from the plant. We compared the genomic products (mRNA and miRNA) from chemo-responsive cells with these from TX-resistant cells in a DNA microarray experiment and get some candidate genes might be a candidate genes involved in the resistant mechanism. We focused our study on one of these genes which is Apolipoprotein J (cluterin), a putative tumor suppressor gene and also a stresses-responsive gene. We then verified the relationship, for the first time, between this gene and resistance for Paclitaxel by cloning this gene and over-expressing it in the responsive cells on one hand, and then knocking down this gene in the resistance cells by small interference RNA technique on the other hand. Importantly we introduced this gene as a candidate target when we block its expression, the response for chemotherapy should be significantly improved. Now, we are designing small molecule to target the clusterin protein and study its applicability in the experimental animals to improve the efficacy of pacitaxel as a standard chemotherapeutic reagent. Moreover, we realized this gene is secretable into media. We then tried to study the effect of another isoform of this gene, which is truncated and of course not secretable, just kept inside cells. Importantly, we found that this truncated isoform, unlike the full-length isoform, is doing opposite effect and sensitizes the ovarian cancer cells to TX. Furthermore, we compare the micoRNA content in both resistant versus responsive ovarian cancer cells in another microarray experiment to get another candidate molecules involved in the resistant mechanism to paclitaxel, thus we can detect which microRNAs are involved in the resistant mechanism and find their downstream molecules. Another research issue is the resistance mechanism of cancer cells to thermal therapy. We tried to map out the mechanism which inhibit the activation of pro-apoptotic Bax under thermal stress and we found that Ku70 is involved. We performed a study in which we knocked out Ku70 in the non small lung cancer cells. We found that Ku70 KD sensitizes lung cancer cells to thermal stress through two different mechanism. First, by allowing Bax activation. Second, by inhibiting the G2/M arrest after hyperthermia which cause cytotoxic arrest instead of cytostatic arrest.

What I think of the idea behind WebmedCentral:

Because we noticed it is an interesting growing publishing area in the field.