The most comprehensive analysis yet of the genome of childhood acute myeloid leukemia (AML) found only a few mistakes in the genetic blueprint, suggesting the cancer arises from just a handful of missteps, according to new findings from St. Jude Children's Research Hospital. The research appears in the July 27 online edition of the Proceedings of the National Academy of Sciences.

New research describes a molecular tool that shows great promise as a therapeutic for human acute myeloid leukemia (AML), a notoriously treatment-resistant blood cancer. The study, published by Cell Press in the July 2nd issue of the journal Cell Stem Cell, describes exciting preclinical studies in which a new therapeutic approach selectively attacks human cancer cells grown in the lab and in animal models of acute myeloid leukemia.

The Myelodysplastic Syndromes (MDS) Foundation announced today that data presented at this year's American Society of Hematology (ASH) Meeting in San Francisco demonstrate that patients with acute myeloid leukemia (AML) who were treated with VIDAZA (azacitidine) had significantly increased overall survival compared to those treated with conventional care regimens (CCR).

Oregon Health & Science University Cancer Institute researcher Jeff Tyner, Ph.D., has created a way to identify proteins that are candidates for targeted therapy in acute myeloid leukemia using an assay that yields results in just four days.

The genetic abnormalities that cause acute myeloid leukemia (AML) are many and varied. Although mice engineered to mimic a single genetic abnormality eventually develop leukemia, it is thought that a second genetic defect occurring as the mice age is required for this to happen. Support for this “2-hit” hypothesis has now been generated by Pier Giuseppe Pelicci and colleagues from the European Institute of Oncology, Italy.

In people with chronic myeloid leukemia (CML), the drug Imatinib has been shown to drive cancer into remission, but the disease often returns when treatment is stopped. New research by UC Irvine scientists indicates that Imatinib could cure CML under certain circumstances if it is taken over a long enough period of time.

Tumor suppressor proteins are so called because their functions oppose the development of cancer. Studies in mice indicate that the protein PU.1 is a tumor suppressor. Mice lacking a specific portion of the DNA (known as the upstream regulatory element; URE) that controls the level of expression of the PU.1 gene develop acute myeloid leukemia (AML).

A new study shows that the activity of a particular gene can identify people who have a more lethal form of acute myeloid leukemia, singling out those patients who should receive more intense therapy.