Marcelo C. Aldaz, M.D.
1980, University of Buenos Aires
UT M. D. Anderson Cancer Center
Science Park/Research Division
My laboratory is located in Smithville, Texas, at UT Science Park -- Research Division.
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Marcelo C. Aldaz, M.D. 1980, University of Buenos Aires UT M. D. Anderson Cancer Center My laboratory is located in Smithville, Texas, at UT Science Park -- Research Division. |
Research Interests: Carcinogenesis; molecular cytogenetics; oncogenes; tumor suppressor genes; mammary gland cancer; tumor progression
The overall objective of Dr.Aldaz research progam is to contribute information of relevance for a better understanding of early human breast carcinogenesis. A major goal of this research is to identify novel molecular tools of use in diagnosis and/or prognosis of human breast cancer (i.e. breast cancer biomarkers). To this end his laboratory is engaged in a comprehensive approach using human breast cancer samples and cells and breast carcinogenesis models. Numerous recently developed molecular approaches are employed in Dr.Aldaz's research in order to elucidate the role of key abnormalities which affect the genome and transcriptome of breast cells leading to cancer development. These studies are aimed at dissecting the multiple stages of breast cancer development and studying specific genetic, and molecular alterations within a dynamic and sequential interpretation of the carcinogenesis process. In one of the on-going major projects, recently this laboratory cloned a novel gene of interest in breast carcinogenesis (WWOX) since it maps to a specific region in chromosome 16 frequently affected by genomic abnormalities.
In a second area of research, Dr.Aldaz's laboratory is employing state of the art methodologies for characterizing global changes in gene expression in breast carcinogenesis particularly focusing on the effects of sex-steroid hormones, the effects of anti-hormonal therapies and the development of clinical resistance to such therapies. The development of resistance to anti-estrogen therapy constitutes a major clinical problem in the treatment of breast cancer. Recently as a result of this work several novel estrogen regulated genes (E2IG1-5) have been cloned at this laboratory. The role of these various genes as targets of estrogen action and as potential breast cancer biomarkers is currently being investigated.
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Aldaz CM, Hu Y, Daniel R, Gaddis S, Kittrell F, Medina D (2002) Serial analysis of gene expression in normal p53 null mammary epithelium. Oncogene 21(41):6366-76.
Bednarek AK, Keck-Waggoner CL, Daniel RL, Laflin KJ, Bergsagel PL, Kiguchi K, Brenner AJ, Aldaz CM (2001) WWOX, the FRA16D gene, behaves as a suppressor of tumor growth. Cancer Res 61(22):8068-73.
Charpentier AH, Bednarek AK, Daniel RL, Hawkins KA, Laflin KJ, Gaddis S, MacLeod MC, Aldaz CM (2000) Effects of estrogen on global gene expression: identification of novel targets of estrogen action. Cancer Res 60(21):5977-83.
Bednarek AK, Laflin KJ, Daniel RL, Liao Q, Hawkins KA, Aldaz CM (2000) WWOX, a novel WW domain-containing protein mapping to human chromosome 16q23.3-24.1, a region frequently affected in breast cancer. Cancer Res 60(8):2140-5.
Brenner AJ, Paladugu A, Wang H, Olopaole OI, Dreyling MH, Aldaz CM (1996) Preferential loss of expression of p16INR4a rather than p19ARF in breast cancer. Clin Cancer Res 2:1993-1998.
Chen T, Sahin A, Aldaz CM (1996) Deletion map of chromosome 16q in ductal carcinoma in situ of the breast: refining a putative tumor suppressor gene region. Cancer Res 56:5605-5609.
Program Affiliation:
Program in Molecular
Carcinogenesis