Drug 'nukes' ovarian cancer.

Drug "nukes' ovarian cancer 

Ovarian cancer strikes some 19,000 U.S. women eacy year,ultimately killing almost three out of five of them--or about twice as many of its victims, proportionately, as breast cancer. Now researchers at the University of Chicago and Argonne (Ill.) National Laboratory have teamed up to tackle ovarian cancer with a new radioactive drug. Though tests are very preliminary, the drug appears to hold great promise of fighting this and estrogen-dependent cancers.

Cancers of the ovaries, breast, cervix and uterus frequentlyinvolve cells that have many hundreds or thousands of estrogen-receptor sites. Because most of these cancers also require estrogen for growth, postsurgical treatment to seek out and destroy metastatic disease (minute secondary tumors spawned by the original cancer) usually involves endorcrine therapy--starving these cancers of estrogen or providing a drug that counteracts the effects of estrogen.

Ovarian cancers, notes Eugene DeSombre of the Universityof Chicago, are the exception. Though roughtly half carry estrogen receptors that in fact bind with estrogen, these cancers apparently do not need or use the estrogen and therefore "have not responded at all well to any endocrine therapy.' But a new estrogen treatment he is investigating shows promise of hunting down and killing metastasized ovarian cancers despite this limitation, he says.

The treatment employs an estrogen or estrogen-like drug towhich a form of radioactive bromine (Br-80m) has been attached. Since estrogen receptors are "very tightly associated with DNA,' DeSombre explains, when the drug binds to a cell it locks in the bromine very close to its genetic material. As the bromine decays, its locally deposited Auger-electron radiation (SN: 2/22/86, p.124) destroys the cell's DNA.

Micrographs picturing the drug's damage to cells grown inculture show "very dramatic' results, DeSombre says: "The cells look like they've had a miniature atom blast in the middle of them.' Moreover, he told SCIENCE NEWS, because each cell suffers so many DNA breaks, "we're confident that they would not be able to recover.'

Though the drug might also harm normal ovarian tissue, inmost cases surgery for the primary tumor would have removed the ovaries prior to treatment, he says. And because most other tissues reached by the drug would have far fewer estrogen receptors per cell than the cancers, DeSombre says, they should be much less vulnerable to the drug.

The drug, shown to work in cultured cells, is expected toundergo animal testing soon. If all goes well, human trials could get under way in as little as three years.