The Pathophysiology of Bortezomib Induced Peripheral Neuropathy (BIPN)
Recruitment status was Not yet recruiting
|Study Design:||Observational Model: Case-Only
Time Perspective: Prospective
|Official Title:||Is There a Role of Oxidative Stress in the Pathophysiology of Bortezomib Induced Peripheral Neuropathy (BIPN) in Multiple Myeloma Patients?|
|Study Start Date:||August 2010|
|Estimated Study Completion Date:||August 2011|
|Estimated Primary Completion Date:||August 2011 (Final data collection date for primary outcome measure)|
The proteasome inhibitor bortezomib has shown impressive clinical activity alone and in combination with other novel agents for the treatment of multiple myeloma (MM).
Peripheral neuropathy is a significant dose limiting toxicity of bortezomib, which typically occurs within the first treatment cycles with bortezomib, reaching plateau around cycle 5, and does not appear to increase thereafter.
Although bortezomib is known to be selective proteasome inhibitor, the mechanisms of cytotoxicity are poorly understood.
It has been theoretically hypothesized that bortezomib abrogates the degradation of I-kB, which blocks the transcriptional activity of NF-kB, however, recent studies demonstrated that bortezomib elicits activation of multiple pathways in cancer cells, such as reactive oxygen species (ROS) pathway.
The involvement of oxidative stress is supported by emerging studies showing that ROS generation plays a critical role in the initiation of the bortezomib induced apoptotic cascade.
Oxidative stress is a complex and dynamic situation characterized by an imbalance between the productions of ROS and the availability and action of antioxidants.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01171443
|Contact: Ghoti Hossamfirstname.lastname@example.org|
|Wolfsson Medical Center||Not yet recruiting|
|Contact: GHOTI HOSSAM 970-35028110 email@example.com|
|Principal Investigator:||GHOTI HOSSAM||HEMATOLOGY DEPARTMENT ON WOLFSSON MEDICAL CENTER|