Isolated Molecule Said To Trigger Breast Cancer
Researchers at the State University of New YorkStony Brook have isolated a molecule believed to trigger breast cancer, a scientist said Tuesday.
A research team led by Dr. Craig C. Malbon, vice dean of Stony Brook’s University Medical Center, found that levels of the molecule, mitogen-activated protein kinase - or MAP kinase are between five and 20 times higher in cancerous breast tissue cells than in normal breast tissue cells.
The discovery, reported in the April issue of The Journal of Clinical Investigation, could lead to new methods for early detection and treatment of breast cancer, Malbon said in a telephone interview with The Associated Press.
Malbon said the migration of MAP kinase into the nucleus of a cell signals the cell to begin replicating itself, causing cancer.
“The trip switch is this molecule and its migration into the nucleus,” he said.
Details of the discovery were to be announced at a news conference today in Manhattan.
Previous research has shown that MAP kinase signals cells to proliferate, Malbon said. The new research, he said, established a link between extremely high levels of the molecule and the growth and spread of breast cancer.
Malbon said elevated levels of MAP kinase also were found in the lymph nodes of breast cancer patients whose cancer spread to other parts of their body, making the molecule a marker for those so-called metastatic cancers.
The discovery could allow doctors to test for high levels of MAP kinase in breast cells, allowing detection of breast cancer even before noticeable tumors develop, Malbon said.
And it raises the possibility of breast cancer treatments based on “programmed cell death,” he said. In such treatments, doctors would introduce to cancerous cells special molecules designed to “turn off” the MAP kinase cell.
In cases of early-detection breast cancer, such targeted treatment can be preferable to the more scattershot approaches of radiation therapy or chemotherapy, Malbon said.
© Copyright 1997 Associated Press. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed.