Abstract
Derangement of the nuclear factor κB (NF-κB) pathway initiates and/or sustains many types of human cancer. B-cell malignancies are particularly affected by oncogenic mutations, translocations, and copy number alterations affecting key components the NF-κB pathway, most likely owing to the pervasive role of this pathway in normal B cells. These genetic aberrations cause tumors to be 'addicted' to NF-κB, which can be exploited therapeutically. Since each subtype of lymphoid cancer utilizes different mechanisms to activate NF-κB, several different therapeutic strategies are needed to address this pathogenetic heterogeneity. Fortunately, a number of drugs that block signaling cascades leading to NF-κB are in early phase clinical trials, several of which are already showing activity in lymphoid malignancies.
Original language | English |
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Pages (from-to) | 359-378 |
Number of pages | 20 |
Journal | Immunological Reviews |
Volume | 246 |
Issue number | 1 |
DOIs | |
State | Published - Mar 2012 |
Externally published | Yes |
Keywords
- ABC DLBCL
- B-cell receptor
- CARD11
- Lymphoma
- Multiple myeloma
- MyD88