A new study, "p21 delays tumor onset by preservation of chromosomal stability," is now available

04-17-2007

According to a study from the United States, "The p53 protein suppresses tumorigenesis by initiating cellular functions such as cell cycle arrest and apoptosis in response to DNA damage. A p53 mutant, p53R172P, which is deficient for apoptosis but retains a partial cell cycle arrest function, delays tumor onset in mice."

"Remarkably, lymphomas arising in Trp53(515C/515C) mice (encoding p53R172P) retain stable genomes. Given the dominant role of p21 in p53 cell cycle control, we crossed Trp53(515C/515C) mice onto a p21-null background to determine whether p21 was required for maintaining chromosomal stability and delaying tumor onset. Loss of p21 completely abolished the cell cycle arrest function of p53R172P and accelerated tumor onset in Trp53(515C/515C) mice. Cytogenetic examination of Trp53(515C/515C) p21(-/-) sarcomas and lymphomas revealed aneuploidy and chromosomal aberrations that were absent in Trp53(515C/515C) malignancies," wrote J.A. Barboza and colleagues, University of Texas, M. D. Anderson Cancer Center.

The researchers concluded: "Thus, p21 coupled p53-dependent checkpoint control and preservation of chromosomal stability, and cooperated with apoptosis in suppressing tumor onset in mice."

Barboza and colleagues published the results of their research in Proceedings of the National Academy of Sciences of the United States of America (p21 delays tumor onset by preservation of chromosomal stability. Proceedings of the National Academy of Sciences of the United States of America, 2006;103(52):19842-7).

For additional information, contact J.A. Barboza, University of Texas M D Anderson Cancer Center, Dept. of Cancer Genetics and Pathology, 1515 Holcombe Boulevard, Houston, TX 77030 U.S.

This article was prepared by Hematology Week editors from staff and other reports. Copyright 2007, Hematology Week via NewsRx.com.