Analysis of Molecular Markers of Drug Resistance in Tumor Biopsies From Previously Untreated Aggressive Non-Hodgkin's Lymphoma
2 other identifiers
observational
200
1 country
1
Brief 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.
Trial Health
Trial Health Score
Automated assessment based on enrollment pace, timeline, and geographic reach
participants targeted
Target at P75+ for all trials
Started Jul 1998
Longer than P75 for all trials
1 active site
Health score is calculated from publicly available data and should be used for screening purposes only.
Trial Relationships
Click on a node to explore related trials.
Study Timeline
Key milestones and dates
Study Start
First participant enrolled
July 1, 1998
CompletedFirst Submitted
Initial submission to the registry
November 14, 2001
CompletedFirst Posted
Study publicly available on registry
November 15, 2001
CompletedStudy Completion
Last participant's last visit for all outcomes
May 1, 2002
CompletedMarch 4, 2008
May 1, 2002
November 14, 2001
March 3, 2008
Conditions
Keywords
Eligibility Criteria
Contact the study team to discuss eligibility requirements. They can help determine if this study is right for you.
Sponsors & Collaborators
Study Sites (1)
National Cancer Institute (NCI)
Bethesda, Maryland, 20892, United States
Related Publications (3)
Harris CC, Hollstein M. Clinical implications of the p53 tumor-suppressor gene. N Engl J Med. 1993 Oct 28;329(18):1318-27. doi: 10.1056/NEJM199310283291807. No abstract available.
PMID: 8413413BACKGROUNDWilson WH, Teruya-Feldstein J, Fest T, Harris C, Steinberg SM, Jaffe ES, Raffeld M. Relationship of p53, bcl-2, and tumor proliferation to clinical drug resistance in non-Hodgkin's lymphomas. Blood. 1997 Jan 15;89(2):601-9.
PMID: 9002964BACKGROUNDSachs L, Lotem J. Control of programmed cell death in normal and leukemic cells: new implications for therapy. Blood. 1993 Jul 1;82(1):15-21.
PMID: 8324219BACKGROUND
MeSH Terms
Conditions
Condition Hierarchy (Ancestors)
Study Design
- Study Type
- observational
- Sponsor Type
- NIH
Study Record Dates
First Submitted
November 14, 2001
First Posted
November 15, 2001
Study Start
July 1, 1998
Study Completion
May 1, 2002
Last Updated
March 4, 2008
Record last verified: 2002-05