NEW YORK, September 9, 2004 - Many cancers, including colon, prostate, and leukemia, continue to grow unchecked because they do not respond to a signal to die and stop proliferating from Transforming Growth Factor-beta (TGF-b). The cause of this signaling disruption of the normal cell cycle has not been fully understood. For the first time, scientists at Memorial Sloan-Kettering Cancer Center have discovered the biologic function of the cytoplasmic form of the Promyelocytic Leukemia protein (PML), and identified it as an essential factor in maintaining TGF-b signaling. Their findings, published in the September 9 issue of the journal Nature, explain the link between these two proteins in the development of cancer and suggest that restoring their activity may provide a possible cancer treatment.
"Through our discovery of the biologic function of PML and its essential role in maintaining TGF-b signaling, we can better understand the progression of many human cancers," said Pier Paolo Pandolfi, M.D., Ph.D., Head of the Molecular and Developmental Biology Laboratory at Memorial Sloan-Kettering and the study's senior author. "Restoring PML function may correct this signaling defect therefore providing a novel therapeutic target for cancer drugs."
TGF-b is a protein that can suppress tumor development by signaling a cell to stop growing. The unresponsiveness to TGF-b signaling has been associated with a variety of human cancers. In addition to this loss of TGF-b, loss of PML is associated with tumor progression in many human cancers, including prostate, breast, colon, and lung, as shown by Dr. Pandolfi and colleagues in a recently published study in the Journal of the National Cancer Institute. In a later work published in Nature Cell Biology, they also demonstrated an unexpected role for PML in affecting the nucleolar network for tumor suppression and in regulating the function of a gene crucial to the suppression of the genesis of cancer.
Page: 1 2 Related biology news :1
Contact: Joanne Nicholas
Memorial Sloan-Kettering Cancer Center
. New molecular link key to cellular proteins involved in cancer progression, other diseases2
. Researchers identify protein promoting vascular tumor growth3
. UCI scientists successfully target key HIV protein; breakthrough may lead to new drug therapies4
. Experimental drug shown to block mutant protein causing blood disease5
. Loss of the neuronal adhesion protein d-catenin leads to severe cognitive dysfunction6
. Images of tail of protein needed for cell multiplication suggest anticancer drug targets7
. New dye directly reveals activated proteins in living cells8
. Disruption of protein-folding causes neurodegeneration, mental retardation9
. Optimizing proteins death domain halts leukemia in laboratory study10
. Stuck on you: Scientists lay bare secrets of bacterial attachment proteins11
. Scientists discover proteins involved in spread of HIV-1 infection