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Biomedical subjects

P Greenwald

Publications and source records attributed to P Greenwald.

At least 73 records · Page 4Linked to original sources
PubMed1992

Role of biology and prevention in aerodigestive tract cancers.

Primary prevention aimed at smoking control and chemoprevention for high-risk persons or patients at risk for a second cancer provide strong potential for cancer prevention and control of aerodigestive cancers. The National Cancer Institute (NCI) has a major effort to build this area of research. The Third Upper Aerodigestive Tract Cancer Task Force Workshop, held in 1989 under the auspices of the National Cancer Institute's Organ System Program, reviewed the opportunities for chemoprevention research on aerodigestive epithelial cancers such as the regulation of growth and differentiation in normal and malignant cells. The chemoprevention program's drug development effort is evaluating several promising candidate agents for future clinical testing and the NCI clinical intervention program is supporting several trials of selected chemoprevention agents with demonstrated potential for inhibiting cancers of the lung, bronchus, oral cavity, and esophagus. Of special interest to this program is the assessment of beta-carotene, retinol and related synthetic retinoids, and several vitamin and mineral combinations under study in high-risk international populations. Chemoprevention in the medical setting is a major focus of NCI's Community Oncology Program (CCOP), a network designed not only to increase accrual of patients to trials but also to speed adoption of state-of-the-art therapies. Public health strategies are directed toward control of exposure to tobacco. The focal point for these activities is NCI's Smoking, Tobacco, and Cancer Program (STCP). STCP smoking cessation efforts are targeted at specific populations that are at greater risk for developing cancer including youth, minority and ethnic groups, women, smokeless tobacco users, and heavy smokers. Two of the world's largest controlled intervention trials conducted by the STCP are underway: the Community Intervention Trial for Smoking Cessation (COMMITT), which focuses on 6.5 million heavy smokers in 11 pairs of matched communities in North America, and the American Stop Smoking Intervention Study (ASSIST), a coalition model designed to reach millions of Americans through existing health promoting systems.

Adolescent↗
PubMed1992

Keynote address: cancer prevention.

Life-style factors that have a major impact on cancer risk are smoking, alcohol consumption, and diet. Current evidence suggests that dietary fat is an etiologic factor for colorectal and postmenopausal breast cancer and that foods high in dietary fiber may be beneficial against colorectal cancer. Clinical prevention trials, augmented by molecular and biological marker studies, will provide new knowledge for diet modification and chemoprevention. These studies are likely to influence the scope of oncology and public health practices of the future.

Breast Neoplasms↗
PubMed1991

Socioeconomic factors and cancer incidence among blacks and whites.

Findings from previous studies suggest that differences in socioeconomic status may be responsible for some, if not all, of the elevated incidence of cancer among blacks as compared with whites. Using incidence data from the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program, we tested this hypothesis by correlating black and white cancer incidence rates in three US metropolitan areas between 1978 and 1982 with data from the 1980 census on socioeconomic status within individual census tracts. The study analyzed data on the incidence of cancer at all sites combined (greater than 100 cancer sites) and at seven major sites separately. As in other studies, income and educational levels served as surrogates for socioeconomic status. The present study also used census-tract data on population density as a surrogate factor. Each of these measures of socioeconomic status was analyzed independently. Before correlation with census-tract data, age-adjusted data on cancer incidence showed statistically significant elevated risks among blacks for cancer at all sites combined and at four of the seven separate sites; whites showed an elevated risk for cancer at two sites. Cancer at only one site, the colon, showed no significant association with race. When age-adjusted incidence data were correlated with socioeconomic status, the comparative black-white risks changed: Whites showed an elevated risk of cancer at all sites combined and at three of the seven separate sites; blacks maintained their elevated risk at three sites. These findings suggest that the disproportionate distribution of blacks at lower socioeconomic levels accounts for much of the excess cancer burden among blacks. They also suggest that for both blacks and whites unidentified racial factors, which may be either cultural or genetic and which are not closely linked to socioeconomic status, may play a role in the incidence of some cancers.

Black or African American↗
PubMed1991

Issues in the early termination of the aspirin component of the Physicians' Health Study. Data Monitoring Board of the Physicians' Health Study.

The Physicians' Health Study is a randomized, double-blind, placebo-controlled prevention trial of 22,071 US physicians, using a factorial design to evaluate the role of aspirin in the prevention of cardiovascular mortality and beta carotene in the reduction of cancer incidence. After approximately 5 years of follow-up, the aspirin component was terminated, 3 years ahead of schedule. Several factors were considered in the decision to terminate, including a cardiovascular mortality rate markedly lower than expected in both aspirin and placebo subjects, precluding the evaluation of the primary aspirin hypothesis, and a highly significant (P < .00001) and impressive (44%) reduction in the risk of first myocardial infarction in the aspirin group. Issues in the decision to terminate are described in this report.

Adult↗
PubMed1990

Lung cancer and exposure to tobacco smoke in the household.

BACKGROUND: The relation between passive smoking and lung cancer is of great public health importance. Some previous studies have suggested that exposure to environmental tobacco smoke in the household can cause lung cancer, but others have found no effect. Smoking by the spouse has been the most commonly used measure of this exposure. METHODS: In order to determine whether lung cancer is associated with exposure to tobacco smoke within the household, we conducted a population-based case--control study of 191 patients with histologically confirmed primary lung cancer who had never smoked and an equal number of persons without lung cancer who had never smoked. Lifetime residential histories including information on exposure to environmental tobacco smoke were compiled and analyzed. Exposure was measured in terms of "smoker-years," determined by multiplying the number of years in each residence by the number of smokers in the household. RESULTS: Household exposure to 25 or more smoker-years during childhood and adolescence doubled the risk of lung cancer (odds ratio, 2.07; 95 percent confidence interval, 1.16 to 3.68). Approximately 15 percent of the control subjects who had never smoked reported this level of exposure. Household exposure of less than 25 smoker-years during childhood and adolescence did not increase the risk of lung cancer. Exposure to a spouse's smoking, which constituted less than one third of total household exposure on average, was not associated with an increase in risk. CONCLUSIONS: The possibility of recall bias and other methodologic problems may influence the results of case-control studies of environmental tobacco smoke. Nonetheless, our findings regarding exposure during early life suggest that approximately 17 percent of lung cancers among nonsmokers can be attributed to high levels of exposure to cigarette smoke during childhood and adolescence.

Adolescent↗
PubMed1990

Dietary fiber, vegetables, and colon cancer: critical review and meta-analyses of the epidemiologic evidence.

Whether colon cancer risk can be modified by a diet rich in vegetables, grains, and fruit, and, if so, whether the protective factor is dietary fiber or other biologically active components correlated with a high-fiber diet are questions of active research interest. Because studies on diet are susceptible to bias from a number of sources, in this review we evaluated the adequacy of study methodology as well as study results to clarify how much protection, if any, is conferred by a high-fiber diet. The review consisted of an aggregate assessment of the strength of evidence from 37 observational epidemiologic studies as well as meta-analyses of data from 16 of the 23 case-control studies. Both types of analyses revealed that the majority of studies gave support for a protective effect associated with fiber-rich diets; an estimated combined odds ratio (OR) of 0.57 (95% confidence interval = 0.50, 0.64) was obtained when the highest and lowest quantiles of intake were compared. Risk estimates based on vegetable consumption (OR = 0.48) were only slightly more convincing than those based on an estimate of fiber intake (OR = 0.58), but the data do not permit discrimination between effects due to fiber and nonfiber effects due to vegetables.

Case-Control Studies↗
PubMed1990

Concepts in cancer chemoprevention research.

Cancer prevention through the use of chemical intervention regimens (chemoprevention) is an emerging field with broad potential for impacting on cancer incidence rates in defined high-risk groups and the general population. Information from cancer epidemiologic studies coupled with that from basic research on cancer biology have combined to reveal several categories of agents with potential for clinical application, including natural and synthetic tumor suppressive retinoids and antioxidants. Chemopreventive agents may inhibit the development of cancer by limiting exposure to initiators or promoters through stimulation of inactivation or excretion mechanisms. Biological consequences of exposure to carcinogens may also be interfered with, e.g., by inhibiting the activation of proto-oncogenes or by antagonizing the effects of oncogene expression. Hundreds of compounds with chemopreventive efficacy in vitro have been isolated from foods and plant products. The testing and development of candidate chemopreventives proceeds through a series of preclinical efficacy screens, followed by controlled clinical trials.

Animals↗
PubMed1990

Strategies for cancer prevention through diet modification.

Diet and cancer research at the National Cancer Institute has grown from a budget of $2.5 million in 1974 to $55 million in 1988. The emphasis is partially on demonstrations of prevention strategies and chemoprevention trials. Studies to disseminate dietary goals in practical ways are undertaken with the aid of the food industry.

Diet↗
PubMed1989

The dietary fat--breast cancer hypothesis is alive.

Data from animal experiments and human correlation studies strongly support the dietary fat-breast cancer hypothesis. Moreover, a causal relation between dietary fat and breast malignancy is biologically plausible. Negative findings from recent analytic epidemiologic studies of dietary fat and breast cancer, however, have fueled the notion that the hypothesis is no longer viable. We argue that only limited conclusions should be drawn from epidemiologic studies to date because of the narrow range of dietary fat intake among subjects and the substantial measurement error in dietary assessment. Although many doubts remain about the dietary fat--breast cancer hypothesis, the question is of such importance that intensive efforts at designing better studies of the hypothesis are urgently needed. Such studies might include (1) laboratory investigations in humans that examine possible mechanisms for the effects of fat, (2) large, prospective epidemiologic studies, and (3) randomized, controlled diet trials.

Animals↗
PubMed1989

Advanced-stage endometrial cancer: contributions of estrogen use, smoking, and other risk factors.

The contributions of estrogen replacement therapy, smoking, and other risk factors to the development of advanced-stage (2-4) endometrial cancer were evaluated in a case-control study of women 40-69 years old from upstate New York. Eighty-four cases and 168 matched community controls were interviewed in person about estrogen exposure and other risk factors. Despite a statistically significant increase in risk with longer use of estrogen pills (P less than 0.05), estrogen exposure actually contributed little to the overall risk of advanced-stage endometrial cancer. Other physical conditions (increased weight, lower parity, diabetes) and socioeconomic factors (education, access to medical services) largely accounted for advanced-stage disease. The evidence in this study does not support the hypothesis that women who smoke have a lower risk than nonsmokers of developing advanced-stage endometrial cancer.

Adult↗
PubMed1989

Strengths and limitations of methodologic approaches to the study of diet and cancer: summary and future perspectives with emphasis on dietary fat and breast cancer.

For many years, scientists have been studying the relationship between diet and certain cancers in animal and human population studies. With the exception of leukemia, nine of the leading cancers in humans may be associated positively or negatively with diet. Extensive literature reviewed by an expert group convened by the National Academy of Sciences concluded that the strongest evidence of an association between the incidence of certain cancers and dietary components is that for dietary fat, particularly for breast cancer (Committee on Diet, Nutrition and Cancer, National Research Council, National Academy of Sciences; Diet, Nutrition and Cancer; Washington, DC: National Academy Press, 1982). The conclusions reached by this group and the consensus of other advisory experts provided the rationale for the National Cancer Institute (NCI) to sponsor a multi-institutional breast cancer prevention trial. This trial was designed to test whether a diet containing 20% of calories from fat compared with the usual diet containing twice that amount would reduce breast cancer incidence in 45- to 69-year-old women. Ensuing controversies about the nature of the research evidence and methodologic issues related to the conduct of this trial led NCI, on advice of its counselors, to discontinue the full-scale implementation. It is clear from these debates that experts have looked at the same data and differed both in their interpretation and in their conception of what constitutes convincing evidence.

Breast Neoplasms↗
PubMed1989

Neurofibromatosis and other disorders among children with CNS tumors and their families.

We conducted a population-based case-control study with 338 patients, less than 15 years of age, diagnosed with a primary tumor of the central nervous system from January 1968 through December 1977 in 53 New York State counties. The study also included 676 controls selected from the birth certificate files of the New York State Department of Health. We collected information on neurofibromatosis and congenital anomalies in study subjects, their siblings and parents by telephone interview with the mother of each case and control. We obtained supplemental information on neurofibromatosis in the patients and their families from hospital medical records. This study confirmed the strong association of neurofibromatosis with risk of CNS tumors. Thirteen cases and no controls had neurofibromatosis. Two fathers and 3 mothers of cases had neurofibromatosis. Five cases had siblings with neurofibromatosis. None of the first-degree relatives of controls had neurofibromatosis. We observed a relative risk of 4.49 for history of seizures. Seizures are often among the presenting symptoms for CNS tumors. We observed no difference between cases and controls in the occurrence of congenital anomalies. There was a nonsignificant excess of congenital anomalies among siblings of cases compared with controls. This decreased to 1.13 when adjusted for number of siblings.

Brain Neoplasms↗