March 4 (HealthDay News) -- A protein called Lefty that regulates development of human embryonic stem cells can inhibit the growth and spread of deadly melanomas and aggressive breast cancers, says a study by researchers at Northwestern University in Chicago.

The findings, published in this week's online issue of the Proceedings of the National Academy of Sciences, add to the team's previous efforts to identify the genes and cellular pathways involved in cancer metastasis, and may help lead to new kinds of cancer treatments.

Lefty is secreted only in human embryonic stem cells (hESCs) and not in any other types of stem cells, including those isolated from amniotic fluid, umbilical cord blood or adult bone marrow, the researchers said.

In an earlier study, the Northwestern team found that aggressive melanoma and breast cancer produce a protein called Nodal, which may serve as a marker of aggressive behavior in human cancers.

In this new study, the researchers exposed metastatic melanoma and breast cancer cells to hESCs containing Lefty and noted a dramatic reduction in Nodal production in the cancer cells, along with decreased growth and an increase in programmed cell death (apoptosis).

"The remarkable similarity of the responses of the two tumor types is likely attributable to the commonality of plasticity (for example, the aberrant and unregulated expression of Nodal) that indiscriminately unifies highly aggressive cancer cells, regardless of their tissue of origin," team leader Dr. Mary J. C. Hendrix, scientific director of the Children's Memorial Research Center and professor in The Robert H. Lurie Comprehensive Cancer Center of Northwestern University and the Feinberg School of Medicine, said in a prepared statement.

"Further, the tumor suppressive effects of the hESC microenvironment, by neutralizing the expression of Nodal in aggressive tumor cells, provide previously unexplored novel therapeutic modalities for cancer treatment," Hendrix said.

SOURCE: Northwestern University, news release, March 3, 2008