Analysis of Molecular Markers of Drug Resistance in Tumor Biopsies From Previously Untreated Aggressive Non-Hodgkin's Lymphoma

National Cancer Institute (NCI)

Status: Completed

Conditions: Non-Hodgkin Lymphoma

Study type: Observational

Funder types: NIH

Identifiers

NCT00026910

980136

98-C-0136

Details and patient eligibility

About

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 [including but not restricted to bcl-2, BAX, bcl-6, MIB-1, p53, p21, p27, p16, cyclin D(1), 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.

Full description

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.

Sex: All

Volunteers: No Healthy Volunteers

Inclusion and exclusion criteria

Prior enrollment on the clinical trial of ProMACE-CytaBOM versus ProMACE-MOPP (81-C-0166) or Short Course ProMACE-CytaBOM (87-C-0180) for the treatment of previously untreated aggressive lymphomas.

Informed consent for participation in the above clinical trials.

Adequate biopsy material from initial biopsy and/or biopsies at relapse of disease.