nts with ALL had
deletions or mutations in one of three so-called "master genes"
that control the normal differentiation of immature progenitor
cells into mature B lymphocytes. In ALL, the leukemic cells fail to
differentiate normally and remain blocked at an immature stage of
development. Locked in this state, the leukemic cells continue to
proliferate, and this continual growth of leukemic cells eventually
kills the child. The mutations identified in three genes, "PAX5,"
"EBF" and "Ikaros," are likely to directly contribute to this block
in normal lymphocyte differentiation.
"The more we learn about why progenitor cells get stuck in the
primitive, cancerous stage, the more likely we'll be able to design
new therapies that eliminate them. That could help us continue our
successful efforts to increase the survival rate of ALL," said
Ching-Hon Pui, M.D., chair of the Oncology department and American
Cancer Society Professor at St. Jude. Pui co-authored the
paper.
The other authors of this paper include William E. Evans, Mary
V. Relling, Charles G. Mullighan, Salil Goorha, Ina Radtke,
Christopher B. Miller, Elaine Coustan-Smith, James D. Dalton, Kevin
Girtman, Susan Mathew, Jing Ma, Stanley B. Pounds, Xiaoping Su and
Sheila A. Shurtleff.
This work was supported in part by the National Cancer
Institute, the National Institute of General Medical Sciences, the
National Health and Medical Research Council (Australia), the Royal
Australasian College of Physicians, the Haematology Society of
Australia and New Zealand, and ALSAC.
St. Jude Children's Research Hospital
St. Jude Children's Research Hospital is internationally
recognized for its pioneering work in finding cures and saving
children with cancer and other catastrophic diseases. Founded by
late entertainer Danny Thomas and based in Memphis, Tenn., St. Jude
freely shares its discoveries with scientific and medical
communities around the world. No family ever pays for treatments
not
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