Accession Number : ADA420325


Title :   Caspase Deficiency: Involvement in Breast Carcinogenesis and Resistance


Descriptive Note : Annual rept. 1 Jul 2002-30 Jun 2003


Corporate Author : OKLAHOMA UNIV HEALTH SCIENCES CENTER OKLAHOMA CITY


Personal Author(s) : Yang, Xiaohe


Full Text : http://www.dtic.mil/dtic/tr/fulltext/u2/a420325.pdf


Report Date : Jul 2003


Pagination or Media Count : 30


Abstract : In the past year, our work focused on defining the functional impact of specific caspase deficiency as proposed in aim 3. We demonstrated that caspase-3 had feedback action on cytochrome c release in TNF-(L treated cells, as it was observed in doxorubicin treated cells. We also found that functional caspase 3 contributed to the up regulation of Fas in the cells treated with chemotherapeutic agents. To study the interactions between caspase- 3 and bcl-2, we have established bcl-2 overexpression cell lines with or without caspase-3 expression, and found that high levels of caspase-3 and bcl-2 were not compatible. To study the specific role of caspase-3 and p53 dependent apoptosis, using SiRNA technology, we have established p53 knock out cell lines form MCF-7/pv, MCF-7/caspase 3 and MDA-MB-23l cells. We also studied the role of caspase 10 in chemotherapy responsiveness by examining the sensitivity of control and caspase-lO reconstituted MCF-7 cells to doxorubicin and etoposide. With our collaborators, we studied down regulation of caspase-3 in human breast cancers. The results and the cell lines generated in last year will facilitate the accomplishment of the proposed project.


Descriptors :   *BREAST CANCER , IMPACT , HUMANS , SENSITIVITY , FEEDBACK , DEFICIENCIES , THERAPY , RESPONSE(BIOLOGY) , CELLS(BIOLOGY) , CHEMOTHERAPY , MAMMARY GLANDS , BLOOD PROTEINS , CHEMOTHERAPEUTIC AGENTS , COLLABORATIVE TECHNIQUES , ONCOGENESIS


Subject Categories : Anatomy and Physiology
      Medicine and Medical Research


Distribution Statement : APPROVED FOR PUBLIC RELEASE