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Mixed lineage leukemia: roles in human malignancies and potential therapy
Author(s) -
Marschalek Rolf
Publication year - 2010
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2010.07608.x
Subject(s) - biology , leukemia , fusion gene , chromosomal translocation , lineage (genetic) , gene , cancer research , genetics , fusion protein , cancer , computational biology , recombinant dna
The increasing number of chromosomal rearrangements involving the human MLL gene, in combination with differences in clinical behavior and outcome for MLL ‐rearranged leukemia patients, makes it necessary to reflect on the cancer mechanism and to discuss potential therapeutic strategies. To date, 64 different translocations have been identified at the molecular level. With very few exceptions, most of the identified fusion partner genes encode proteins that display no homologies or functional equivalence. Only the most frequent fusion partners ( AF4 family members, AF9 , ENL , AF10 and ELL ) are involved in the positive transcription elongation factor b‐dependent activation cycle of RNA polymerase II. Biological functions remain to be elucidated for the other fusion partners. This minireview tries to sum up some of the available data and mechanisms identified in leukemic stem and leukemic tumor cells and link this information with the known functions of mixed lineage leukemia and certain mixed lineage leukemia fusion partners.