I am looking for Ph.D. position in USA.
Here are my resume, M.Sc. thesis summary and conference presentation :
RESUME
Igor Entin
108 Stryker Street, 2 fl.,
Brooklyn NY 11223 USA.
Phone: 1-718-3368678
1-718-3824629 (for messages)
E-mail: googol at nyct.net
Purpose:
Admission to Ph.D. program
Personal data:
I was born in 1966 in Gomel, Belarus (former USSR). In 1990 I immigrated to Israel. I
completed all academic degrees (B.Sc. & M.Sc.) not in my native language (!) within four
years.
Education:
Nov. 95 - M.Sc. in microbiology from Tel-Aviv University, Israel.
Oct. 93 - Nov. 95 - graduate student towards M.Sc. at Tel-Aviv University, Department of
Cell Research & Immunology under supervision of professor Ilan Friedberg.
Oct. 93 - B.Sc. in biology from Tel-Aviv University, Israel.
Oct. 91-Oct. 93 - undergraduate student towards B.Sc. in biology (Tel-Aviv University,
Israel).
Sept. 87-Jan. 90 - medical student in Grodno medical institute (Belarus, former USSR).
Honors/activities:
TEL-AVIV UNIVERSITY - full fellowship, assistantship.
GRODNO MEDICAL INSTITUTE - academic competition winner in biology and chemistry.
M.Sc. thesis:
Correlation between cell tumorigenicity and exogenous ATP-induced growth inhibition in
malignant cells.
Conference Presentation:
Massas R., Entin I., Oged-Plesz O., Friedberg I. Correlation between cell tumorigenicity
and cell susceptibility to ATP-induced cell growth inhibition. The International
Conference on tumor microenviroment progression, therapy & prevention. (14-18 May 1995 -
Tiberias and Beit Gabriel, Israel). Abstracts.
Research project:
Entin I., Sagi-Asif O., Witz I. IL-6 secretion by spleen cells of plasmacytoma regressor
mice.
Skills:
ELISA, protein purification, cell cultures, protein radiolabeling, enzyme assay, growing
of transformed cells in soft agar, working with laboratory animals.
Computers:
Knowledge of the PC (Windows and DOS), Macintosh Apple. Microsoft applications: Word,
Excel, Power Point. On-line Database Search. Sigma Plot, EndNote, InterNet software.
Word processing using WordPerfect and Microsoft Word.
Languages:
Hebrew, English, Russian (native).
REFERENCES:
1. Ilan Friedberg, Ph.D., professor.
2. Asher Frensdorff, Ph.D., professor.
3. Isaac P. Witz, Ph.D., professor.
Address for all of the references:
Department of Cell Research & Immunology
Tel-Aviv University,
Ramat Aviv, 69978 Israel.
FAX. 972-3-642-2046
M.Sc. THESIS SUMMARY.
The effect of cell tumorigenicity on ATP-induced cell growth inhibition has been studied
in cell cultures. Mouse fibroblasts, Balb/c-3T3 (B-3T3), the polyoma virus-transformed
derivatives (C-cells, or Culture-cells) and C-cells that were injected into mice to form
tumor and re-cultured from the tumor (CTC-cells, or Culture-Tumor-Culture cells) have been
used in this study. The level of tumorigenicity was found to be: CTC>C>B-3T3.
The results obtained in this study have shown that exogenous ATP considerably inhibited
the growth of CTC-cells, the growth inhibition of C-cells was less pronounced, whereas the
growth of B-3T3 cells was only slightly affected. In parallel, the activity of
ecto-protein kinase (ecto-PK) in these cells was found to be in the order CTC>C>>B-3T3.
These data show that ecto-PK has a pivotal role in the ATP-induced growth inhibition, as
well as in the selectivity of the inhibition for tumorigenic cells. Furthermore, the data
support our previous studies, in which we have shown that a latent growth inhibitor is
activated by its phosphorylation, mediated by ecto-PK. The growth inhibitor has been found
in conditioned media of ATP-treated cultures (CM+). In this study the effect of CM+ from
B-3T3, C and CTC cell cultures on the growth of these cells was studied. It has been
found that the efficiency of the growth inhibition is dependent not only on the activity
of ecto-PK, but also on the response of the cells to the growth inhibitor: the growth of
CTC cells was inhibited by CM+ from the three cell types, the growth of C cells was
inhibited by two types of CM+, whereas the growth of B-3T3 cells was inhibited by CM+ from
B-3T3 cells. Thus, the selectivity of the growth inhibition decreased with increase of the
cell tumorigenicity.
The correlation between the three parameters: cell tumorigenicity, ecto-PK activity and
ATP-induced growth inhibition, as well as reduction of the selectivity to the growth
inhibitor with the increase of cell tumorigenicity - indicate the chemotherapeutic
potential of the ATP-induced cell growth inhibition.
CORRELATION BETWEEN CELL TUMORIGENICITY AND CELL SUSCEPTIBILITY TO ATP-INDUCED CELL GROWTH
INHIBITION
R. Massas, I. Entin, O. Oged-Plesz and I. Friedberg.
Dept. of Cell Research and Immunology, Tel Aviv University, Israel.
Previous studies in our laboratory have shown that extracellular ATP inhibits the growth
of transformed murine fibroblasts in a concentration-dependent manner, whereas the growth
of their non-transformed counterparts is only slightly affected. Similarly, exogenous ATP
has been found to exert cell growth inhibition of various cancerous cells of human origin.
Furthermore, ATP inhibits cancer development in experimental animals, as was shown in our
laboratory, and in others'. We found that ecto-protein kinase (ecto-PK) plays a major
role in the inhibition process, by phospho-activation of a latent inhibitor. In this
research project we examined the possibility of a correlation between the level of cell
tumorigenicity and the efficiency of exogenous ATP as an inducer of cell growth
inhibition. For this purpose we used lines of murine fibroblasts, Balb/C-3T3 cells
(B-3T3), and their virally transformed derivatives: C-cells (culture cells) and CTC-cells
(culture-tumor-culture cells). (The cells were gratefully obtained from the laboratory of
Prof. I. P. Witz, in which the cell tumorigenicity was found to be in the order
CTC>C>B-3T3). Studies on the effects of exogenous ATP on these cells have shown that the
growth of CTC cells is markedly inhibited, the growth inhibition of C cells is less
pronounced, whereas the growth of B-3T3 cells is only insignificantly affected. The
activity of ecto-PK was found to increase with the increase of cell tumorigenicity. These
data suggest that the correlation between cell tumorigenicity and the efficiency of
ATP-induced growth inhibition is due, at least in part, to the increase of ecto-PK
activity with the increase of cell tumorigenicity.
Supported by the Ela Kodesz institute for Research on Cancer Development and Prevention,
and by TAU.
