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DISEASE RESEARCH SUPPORT In response to a perceived need for increased clinical research funding, the Doris Duke Charitable Foundation recently established the Doris Duke Distinguished Clinical Scientist Award Program. The Foundation will give $600,000 a year for five years to four research teams studying either cancer, AIDS, heart disease, or sickle cell anemia and related blood disorders. According to Alan Altschuler, the Foundation's acting program director for medical research, the clinical awards program is geared toward "bench to bedside" research involving scientists who are "seeking to convert scientific findings into real treatments for people." The grants are not meant to support specific research proposals, but rather to supplement the salaries and laboratory expenses of clinical researchers who are already receiving National Institutes of Health funding. They will only be offered to senior medical scientists at the 25 medical schools that receive the greatest amount of support from the NIH for research focusing on each of the four designated diseases. Altschuler notes that these grants, and the $4.2 million in grants established by the foundation last July, are partly in response to the conclusion of a recent NIH Director's Panel on Clinical Research that available funds for physician clinical investigators were inadequate. The program, says Altschuler, will try to assist university researchers who, in an era of managed care, are often forced to see more and more patients to the exclusion of doing research. The first grants will be given out in the first quarter of 1999; the program will later be reviewed and possibly renewed. Craig B. Thompson SEEKING IMMUNITY The first scientific director of the Leonard and Madlyn Abramson Family Cancer Research Institute at the University of Pennsylvania Cancer Center, Craig B. Thompson, hopes to harness the body's immune system--with the help of the $100 million pledge that formed the center in 1997--to fight cancer. "Your immune system is supposed to recognize something that's foreign," Thompson said in a 1998 news conference announcing his 1999 appointment to the post. The body's immune system largely ignores cancers when they develop. Making the body recognize cancer as foreign could lead to methods to selectively kill cancer cells, he adds. Thompson also hopes to focus on interdisciplinary and translational research at the cancer center by attracting researchers from a variety of backgrounds. (See page 6 for a related story about the possible role of the immune system and cancer.) HEALTHY HOPS? A study by Okayama researchers suggests that beers, especially stouts, may stave off the mal-effects of some carcinogens. GOT BEER? Might a pint a day keep the doctor away? Researchers at Okayama University near Hiroshima report in an American Chemical Society journal (S. Arimoto-Kobayashi et al., "Inhibitory Effects of Beer and Other Alcoholic Beverages," Journal of Agricultural and Food Chemistry, 47 :221-30, Jan. 18, 1999) that most types of beer, when given to mice and bacteria, actually inhibited the mutagenicity of heterocyclic amines (HAs), a group of carcinogens produced during the cooking of food. According to the paper, which reports the effects of 24 beers--17 lagers, four stouts, two ales, and one nonalcoholic--from England, France, Germany, Ireland, Italy, Japan, The Netherlands, Russia, Scotland, South Africa, and the United States, stouts are the best HA fighters. The nonalcoholic beer and one of the lagers had no effect. The Okayama team did the study in the wake of several recent conflicting reports on the correlation between beer or alcohol consumption and cancer risk. They chose to investigate beer primarily because compounds related to some beer ingredients had been shown, in their lab and others, to inhibit the mutagenic activities of meat-derived carcinogens in bacterial systems. Beer's high percentage of dissolved solids--100 ml of evaporated beer yields 4 g of residual solids--also made it a good candidate for study. According to lead author and Okayama pharmaceutical sciences researcher Sakae Arimoto-Kobayashi, who corresponded via E-mail, one of the possible mechanisms for the inhibition of mutagens is the enhanced degradation of the active metabolites of carcinogens. "More studies are needed to elucidate the mechanism," she suggests. First on the agenda, however, is an attempt to isolate the specific substance responsible; Okayama researchers suspect that the plant components derived from the hops are somehow involved. MARKS TO STEP DOWN After nearly two decades at the helm, Paul A. Marks, the president and chief executive officer of Memorial Sloan-Kettering Cancer Center in New York, announced publicly on Dec. 30 and via an interoffice memo on Dec. 1, that he intends to step down as president some time during 1999 pending the appointment of a successor. He will participate in the appointment process. According to Richard Rifkind, the chairman of Sloan-Kettering, Marks, who was previously a provost at Columbia University, met the challenge handed to him when he became the president in 1980: to create a biological research environment attached to an effective clinical arena at a freestanding institution. Rifkind suggests that Marks, who plans to keep an active role in the laboratory after stepping down, also improved the recruitment of biological scientists and clinical scientists based on his own experience as both a developmental biologist and a clinician. "The success of the institution ... lulled most of us into believing that he was going to be with us forever, because his energy never seemed to slack and it hasn't yet," notes Rifkind. "And what he's doing, which has impressed all of us, ... is turning over the reins ... at a time of enormous institutional success." Rifkind notes that the next president, who he says will need demonstrated ability to manage and balance the biological and the clinical aspects of Sloan-Kettering, will be assigned the difficult task of trying to continue that success. (See also Commentary, page 12) Pamela Bechtel DOWNSTREAM MARKER In every type of breast cancer tumor Pamela Bechtel examined, one commonality emerged--a form of proliferating cell nuclear antigen (PCNA) different from that of healthy cells. Bechtel thinks the protein may be a sound diagnostic marker for breast cancer, because it doesn't appear as a result of any one gene mutation or problem in transcription. The University of Maryland Medical School postdoc suspects the difference emerges farther downstream; therefore, the protein may mark cancers arising from various causes, unlike mutation tests for single breast cancer oncogenes such as BRCA1 or BRCA2. The alteration's presence in several varieties of breast cancers also suggests that several different biochemical pathways may lead to the same conclusion. But Bechtel and colleagues still don't understand what causes that disparity between healthy and abnormal breast cells: "We're trying to pin down what exactly causes the difference," she comments. Understanding when and why the altered form of PCNA emerges could help Bechtel and colleagues develop an antibody, which could then serve as a universal breast cancer diagnostic test. Several basic questions about the protein's role in cancer also remain unanswered, Bechtel concludes: "How does this affect DNA replication? How does this affect DNA repair?"

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