Next Friday, the journal Cell will publish a paper titled: "hEST2, the putative human telomerase catalytic subunit gene, is up-regulated in tumor cells and during immortalization."

The article's senior author is molecular biologist Robert Weinberger, a founding member of the Whitehead Institute for Biomedical Research, at the Massachusetts Institute of Technology.

Weinberger told BioWorld Today that hEST2 stands for "human ever-shortening-telomeres 2." He said that the difference between his forthcoming paper in the Aug. 22, 1997, Cell, and that by Thomas Cech in today's Science (see cover story) is that "The Cech paper is really focusing on the enzyme, and we're focusing on the cancer connection in our paper, which I believe is not addressed in the Cech paper."

Specifically, Weinberg explained, "We were interested in the mystery of how telomerase suddenly becomes activated in cancer cells. How do they resurrect the expression of the enzyme, which has been so tightly repressed in the antecedent cells?

"What we now find in our paper," he continued, "which is to my mind its most interesting aspect, is that the RNA for the catalytic subunit is not expressed in normal cells, but in cancer cells it is expressed in a readily assayable fashion. Therefore, we may have stumbled across the mechanism by which telomerase becomes activated when normal cells evolve into cancer cells." —David N. Leff