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Infant leukemia linked to MLL fusion genes
09-22-2006
According to recent research from England, "MLL fusion genes are a predominant feature of acute leukemias in infants and in secondary acute myeloid leukemia (AML) associated with prior chemotherapy with topo-II poisons. The former is considered to possibly arise in utero via transplacental chemical exposure."
"A striking feature of these leukemias is their malignancy and remarkably brief latencies implying the rapid acquisition of any necessary additional mutations," explained M. Eguchi and colleagues, Institute of Cancer Research. "We have suggested that these coupled features might be explained if MLL fusion gene encoded proteins rendered cells more vulnerable to further DNA damage and mutation in the presence of chronic exposure to the agent(s) that induced the MLL fusion itself.
"We have tested this idea by exploiting a hormone regulated MLL-ENL (MLLT1) activation system and show that MLL-ENL function in normal murine progenitor cells substantially increases the incidence of chromosomal abnormalities in proliferating cells that survive exposure to etoposide VP-16."
The researchers concluded, "This phenotype is associated with an altered pattern of cell cycle arrest and/or apoptosis."
Eguchi and colleagues published their study in Genes Chromosomes & Cancer (MLL chimeric protein activation renders cells vulnerable to chromosomal damage: An explanation for the very short latency of infant leukemia. Genes Chromosomes Cancer, 2006;45(8):754-760).
For additional information, contact M. Greaves, Institute of Cancer Research, Chester Beatty Laboratories, Hematology Oncology Sect, 237 Fulham Rd., London SW3 6JB, England.
Publisher contact information for the journal Genes Chromosomes & Cancer is: Wiley-Liss, Division John Wiley & Sons Inc., 111 River St., Hoboken, NJ 07030, USA.
Keywords: London, England, Acute Myeloid Leukemia, Apoptosis, Chemotherapy, Chimeric Protein, DNA Damage, DNA Research, Deoxyribonucleic Acid, Etoposide, Hormones, Oncology, Progenitor Cell, Proteomics, Stem Cell Research, Cancer Therapy, Infant, In Utero.
This article was prepared by Hematology Week editors from staff and other reports. Copyright 2006, Hematology Week via NewsRx.com. |