Approximately 33% of all human cancers are directly influenced by hormone receptors or their ligands. Moreover, a usual characteristic of these malignant tumors is a disregulation in signal transduction pathways or a dysfunction of genes normally regulated by growth factors, cytokines or hormonal signals. The wealth of information generated by the powerful techniques of molecular biology is rapidly showing a much clearer picture of the chain of cellular events which lead to disregulation of normal gene expression and malignant transformation. At the same time, the unavoidable degree of specialization reached in various sectors of endocrine research makes it increasingly important for endocrinologists on one hand, and cell biologists, on the other hand, to integrate key developments in an interdisciplinary approach. It is the purpose of this conference to gather leading researchers in both the fundamental and clinical aspects of oncology, endocrinology and cell biology and thus stimulate interactions between various specialists concerned with the problem of cancer, endocrinology and therapy of hormone-sensitive cancers. The proposed symposia at this conference will encompass 3 general themes, namely (1) the basic developments in cell biology which have general and direct relevance to cancer in general, (2) recent progress in the use of antihormones and enzyme inhibitors in hormone-sensitive cancer therapy, and (3) a coverage of the most significant developments in the understanding of the 2 main hormone-related human malignancies, namely breast and prostate cancer.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Conference (R13)
Project #
1R13CA069117-01
Application #
2113190
Study Section
Special Emphasis Panel (SRC (X3))
Project Start
1995-09-30
Project End
1996-09-29
Budget Start
1995-09-30
Budget End
1996-09-29
Support Year
1
Fiscal Year
1995
Total Cost
Indirect Cost
Name
Laval University
Department
Type
DUNS #
208704593
City
Quebec
State
PQ
Country
Canada
Zip Code
G1 0-A6