Editor's note: Science Scan is a quick round-up of recently publishedbiotechnology related research

Chronic myeloid leukemia (CML) comes in like a lamb, and goes outlike a lion.

After it's diagnosed, the malignant blood dyscrasia holds a steadycourse for several years, typically three. During this chronic phase,periodic chemotherapy with cytotoxic drugs steers a patient throughalternating ups and downs of relapse and remission.

Eventually, this regimen fails, and the disease suddenly puts onspeed, shifting from chronic to acute. At that point, the outcome israpidly fatal.

Interferon-alpha has for some years been touted and tried asmaintenance therapy for CML, but only now does a 7.5-year, large-scale (597-patient), randomized clinical trial confirm its quasi-anecdotal benefits.

This week's Lancet, dated June 3, reports the U.K. ResearchCouncil's experience, comparing 293 patients who receivedWellferon (human lymphoblastoid interferon-a, provided by theWellcome Research Laboratories, of Beckenhamn, Kent),supplementing conventional therapy, with 294 who got everythingbut interferon.

Results: Median survival was 61 months for the INF-a cohort (52percent); 41 months (34 percent) for no-interferon. Deaths numbered128 in the INF-a arm; 158 in the no-INF group.

To follow up, contact N. C. Allen, Western General Hospital,Edinburgh, U.K.

Mutant Colorectal Gene Blazes Tumor Trail

Despite its name, transforming growth-factor-b (TGF-b) is in fact agrowth-curbing factor. It potently inhibits epithelial cells. Hence, amutated TGF-b receptor gene found in human colon cancer cell linesis being blamed for allowing colorectal tumors to proliferate. Themutation, which defeats DNA mismatch repair, runs in the families ofpatients with hereditary nonpolyposis colorectal cancer.

Sanford Markowitz of Case Western University in Cleveland is leadauthor of a report in the current issue of Science, dated June 2, titled:"Inactivation of the Type II TGF-b receptor in colon cancer cellswith microsatellite instability."

The mutation occurs, according to the paper, "by inducing the escapeof cells from TGF-b-mediated growth control, links DNA repairdefects with a specific pathway of tumor progression."

In an editorial commenting on the research, Science writer Jean Marxobserves that "Screening for the mutant TGF-b receptor gene may aidin diagnosing colon cancer, and two other cancers common in [thesame] families, ovarian and endometrial." Ultimately," she adds, "itmay even be possible to treat [such] cancers by using gene therapy totransplant functional copies of the gene into patients' cells."

To follow up, contact Sanford Markowitz at (216) 844-8236.

For Parasite, No Is A No-No

When nitrogen and oxygen, the atmosphere's two main gases,combine chemically into nitric oxide (NO), they spell bad news andgood news for the human body.

On the minus side, the cytotoxic compound turns out to be the guiltyparty in pertussis _ whooping cough. (See BioWorld Today, Jan. 5,1994, p. 1.) In the plus column, NO is a key transmitter of nerveimpulses and regulator of blood-vessel tone.

An enzyme called nitric oxide synthase (NOS) keeps the bodysupplied with NO by cleaving it from the amino acid, L-arginine.NOS does its job when induced by cytokines, which the immunesystem releases on demand.

To get a better handle on NO's biological functions, immunologistsat the University of Glasgow, Scotland, constructed transgenic micelacking the gene for inducible NOS.

Their paper in Nature, dated June 1, reports "Altered immuneresponses in mice lacking inducible nitric oxide synthase." Theyfound these NO-minus mice to be "viable, fertile and without evidenthistopathological abnormalities."

But the mutant rodents did display one significant handicap: Unliketheir wild-type brethren, which stoutly resist infection by theprotozoal parasite Leishmania major, the lab-created mice proveduniformly susceptible to L. major infection.

Chalk up another plus for NO.

To follow up, contact Foo Y. Liew, Department of Immunology,University of Glasgow, (011) 44 141 337 3122.

_ Compiled By Science Editor David N. Leff

(c) 1997 American Health Consultants. All rights reserved.