Analysis of Molecular Markers of Drug Resistance in Tumor Biopsies From Previously Untreated Aggressive Non-Hodgkin's Lymphoma
Although the cause(s) of clinical drug resistance in non-Hodgkin's lymphomas (NHL) are
unknown, in vitro studies suggest that abnormalities of the cell cycle and mechanisms of
apoptosis may play an important role. Clinical studies have now shown that p53, bcl-2 and
tumor proliferation all have significant effects on clinical drug resistance. To further
investigate the role of genes that control the cell cycle and apoptosis, we wish to
correlate the expression of multiple molecular targets using immunohistochemistry and cDNA
microarray expression profiling (including but not restricted to bcl-2, BAX, bcl-6, MIB-1,
p53, p21, p27, p16, cyclin D1, cyclin A, cyclin E, mdm-2, cpp 32, mcl-1, EBER-1, ALK, and a
panel of B, T and other cell lineage markers), involving these pathways, with clinical
outcome following treatment with combination chemotherapy. All clinical data and tissue
samples for this study will come from patients who have been previously enrolled on two
protocols for the initial treatment of aggressive lymphomas. No new patients will be
enrolled for this study.
Observational
N/A
United States: Federal Government
980136
NCT00026910
July 1998
May 2002
Name | Location |
---|---|
National Cancer Institute (NCI) | Bethesda, Maryland 20892 |