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

2014-08-27 03:56:28 | BioPortfolio

Summary

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.

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.

Study Design

N/A

Conditions

Non-Hodgkin Lymphoma

Location

National Cancer Institute (NCI)
Bethesda
Maryland
United States
20892

Status

Completed

Source

National Institutes of Health Clinical Center (CC)

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:56:28-0400

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Medical and Biotech [MESH] Definitions

Two or more distinct types of malignant lymphoid tumors occurring within a single organ or tissue at the same time. It may contain different types of non-Hodgkin lymphoma cells or both Hodgkin and non-Hodgkin lymphoma cells.

A form of non-Hodgkin lymphoma having a usually diffuse pattern with both small and medium lymphocytes and small cleaved cells. It accounts for about 5% of adult non-Hodgkin lymphomas in the United States and Europe. The majority of mantle-cell lymphomas are associated with a t(11;14) translocation resulting in overexpression of the CYCLIN D1 gene (GENES, BCL-1).

Any of a group of malignant tumors of lymphoid tissue that differ from HODGKIN DISEASE, being more heterogeneous with respect to malignant cell lineage, clinical course, prognosis, and therapy. The only common feature among these tumors is the absence of giant REED-STERNBERG CELLS, a characteristic of Hodgkin's disease.

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A systemic, large-cell, non-Hodgkin, malignant lymphoma characterized by cells with pleomorphic appearance and expressing the CD30 ANTIGEN. These so-called "hallmark" cells have lobulated and indented nuclei. This lymphoma is often mistaken for metastatic carcinoma and MALIGNANT HISTIOCYTOSIS.

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