A new research shows how the absence of an important tumor-suppressing protein gives rise to acute myeloid leukemia (AML).
CSHL Professor Scott W. Lowe. Ph.D., an Investigator of the Howard Hughes Medical Institute and colleagues found that disabling protein P53 combined with a genetic mutation caused cell proliferation.
P53 has the ability to induce a cell to commit suicide (apoptosis) or to enter a quiescent state in which it can no longer multiply (senescence). So its absence causes a cell's "braking" system to be disabled.
"We showed that it has the ability to reinforce cell-fate and differentiation programs. In AML, p53 loss leads to cancer by disabling this reinforcement. The question we are now eager to answer is whether p53 has similar functions in other types of cancer," said Johannes Zuber, M.D.
The results are published in the July 1 issue of Genes and Development.