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Arthur B. Pardee, Ph.D.

Professor, Department of Emeritus, Harvard Medical School

Chief, Cell Growth and Regulation, Dana-Farber Cancer Institute

Contact Info

Arthur Pardee
Dana-Farber Cancer Institute
450 Brookline Avenue
Boston, MA, 02215
Mailstop: Dana Bldg, D 610D
Phone: 617-632-3372
Fax: 617-632-4680


Not Available.

Research Abstract

A major focus of research activities in this laboratory is to identify and characterize clinically useful breast cancer markers by using differential RNA-display technique. We have identified several genes by this approach and large-scale hybridization array studies have identified gene clusters whose patterns of expression in human breast tumor biopsy specimens are linked with clinical parameters including estrogen receptor status and tumor stage. Similar analysis revealed differential expression of HSIX-1, a homeobox gene in human breast cancer cells and HLM gene that shows homology with oxysterol binding protein in human lung cancers. Both of these genes showed significantly increased expression in metastatic cells. In addition, HSIX1 was shown to play a role in the DNA-damage-induced G2 cell cycle checkpoint. Our results demonstrate that HSIX1 overexpression leads to more aggressive tumors. Futhermore, a novel gene identified by differential display technique and designated as 055 is suppressed in metastatic colon cancer tissues and metastatic colon cancer cell line SW620. The working hypothesis is that overexpression of 055 gene suppresses metastasis by inducing colon cancer cell differentiation and reversing the malignant phenotype.

Another research focus of this laboratory is to identify alternative target-directed therapy for human breast cancers, more specifically for anti-hormone resistant breast cancers. This is based on targeting downstream site or sites of hormone dependent and hormone independent pathways of enhanced proliferation of breast cancer cells. An approach which is also currently investigated in this laboratory is differentiation therapy. Compounds that are found to induce terminal cellular differentiation, cell cycle arrest and apoptosis are proposed to be potential therapeutic agents for human breast cancers. One of our therapeutic studies revealed that when cancer cells, more specifically protstate cancer cells, are treated simultaneously with compounds activating more than one cell cycle check points, the conflicting regulatory signals induce apoptosis of cancer cells, thus providing a new avenue for developing anti-cancer therapy.


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