Molecular Biology of Anaplastic Lymphoma Kinase–Positive Anaplastic Large-Cell Lymphoma

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摘要：

Anaplastic large-cell lymphoma (ALCL) provides an excellent example of how molecular insights into tumor pathogenesis are influencing and improving tumor classification. ALCL was described initially as a subtype of T-cell/null-cell lymphoma characterized by unusual tumor cell morphology and the expression of CD30. However, it was soon recognized that a subset of ALCLs contained chromosomal translocations involving anaplastic lymphoma kinase (), a novel receptor tyrosine kinase gene. These rearrangements create chimeric genes encoding self-associating, constitutively active ALK fusion proteins that activate a number of downstream effectors, including phospholipase C-gamma, phosphoinositol 3'-kinase, RAS, and signal transducer and activator of transcription proteins, all of which seem potentially important in cellular transformation. Not all tumors classified as ALCLs have rearrangements and, conversely, rearrangements occur in lymphomas of widely varying morphology. Hence, only molecular markers can reliably identify ALKALCL. The importance of doing so is reflected by clinical studies suggesting that ALKALCLs have a significantly better prognosis than other aggressive peripheral T-cell or B-cell lymphomas, including ALKALCLs. The unique molecular pathogenesis of ALKALCL is likely to lead to novel therapeutic approaches directed at specific inhibition of ALK or downstream effectors.

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chronotherapy colorectal cancer oxaliplatin irinotecan sodium folinate

DOI：

10.1200/JCO.2002.12.033

被引量：

4229

年份：

2002