PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cancer prevention”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1993

Multistage carcinogenesis--genetic and epigenetic mechanisms in relation to cancer prevention.

The prevention of cancer is, at our present state of knowledge, the most effective and inexpensive mode of controlling this disease. Passive cancer prevention is practiced voluntarily or, in part, through governmental regulation in many parts of the world. However, active cancer prevention by the administration of vaccines, dietary factors, antihormones, or other agents is likely to be the most effective mechanism of cancer prevention in humans. Carcinogenesis develops in three defined stages--initiation, promotion, and progression--the first and third resulting from irreversible genetic changes in the cell, whereas the intermediate stage of promotion involves an epigenetic alteration of the expression of the genome and cell division. Thus, the stage of promotion is the most effective site to target for both active and passive cancer prevention. A review of the modalities presently used in cancer prevention, both active and passive, demonstrates that all such methods involve an inhibition and/or reversal of this intermediate stage, thus preventing the development of the malignant process. Future advances in cancer prevention will depend on better knowledge of the mechanisms of the stages of carcinogenesis in order that rational preventive agents and formats may be used in altering or modifying the appropriate stage(s) of neoplastic development.

Humans↗
PubMed1991

What healthy women think, feel and do about cancer, prevention and breast cancer screening in Italy.

In preparation for a major campaign to encourage participation in a breast screening programme for all women between 50-70 years old in Florence, Italy, an in-depth study of 200 women's attitudes and practices regarding cancer and its prevention was undertaken. 72% participated in semistructured interviews, and inclination to participate was analysed in terms of Yes (39%), Uncertain (36%), and No (20%) (5% were unspecified). Age (P = 0.03), area of birth (P = 0.01), education level of husband (P = 0.04) and prior Pap smear (P = 0.00) or mammography (P = 0.00) were among the variables statistically associated with inclination to participate. While the women shared more or less common images of cancer, concern for health, and belief in the importance of God and destiny, those less inclined to participate felt less personally vulnerable, had less faith in medicine's ability to cure or prevent cancer, were more distant from the medical system and culture in general and regarded information about health or illness more as unnecessary or dangerous than beneficial. Understanding and consideration of both "popular" and "medical" cultures need to be encouraged.

Aged↗
PubMed1994

The alpha-tocopherol, beta-carotene lung cancer prevention study: design, methods, participant characteristics, and compliance. The ATBC Cancer Prevention Study Group.

The Alpha-Tocopherol, Beta-Carotene (ATBC) Lung Cancer Prevention Study was a randomized, double-blind, placebo-controlled, 2 x 2 factorial design, primary prevention trial testing the hypothesis that alpha-tocopherol (50 mg/day) and beta-carotene (20 mg/day) supplements reduce the incidence of lung cancer and possibly other cancers. Total and disease-specific mortality and incidence of various diseases and symptoms were monitored for safety. Between 1985 and 1993, 29,133 eligible male smokers aged 50 to 69 years at entry were randomized to receive daily active supplements or placebo capsules for 5 to 8 years (median 6.1 years), accumulating 169,751 follow-up years. This report describes the study design, methods, and protocol as well as the baseline characteristics and capsule compliance of the participants. The ATBC Study is the largest lung cancer chemoprevention trial conducted to date.

Adjuvants, Immunologic↗
PubMed2002

Cancer prevention clinical trials.

Prevention of cancer through interventions based on sound scientific research remains an important strategy of oncology research at the National Cancer Institute (NCI). Reducing the burden of cancer in the United States is focused on clinical investigations in medical settings and public health intervention research on cancer risk factors regarding lifestyle and diet. Chemoprevention research at the NCI has progressed systematically to identify potential agents that reduce cancer risk and to develop public health strategies that take advantage of basic research results. In addition, advances in our understanding of molecular targets and pathways and our use of new and emerging technologies have become important tools for oncology research. Priority areas for chemoprevention research, identified from experimental and clinical research, are investigated in clinical trials to determine their ability to reduce cancer risk in selected populations or in the general population. Priority areas discussed in this review are the relationship of the arachidonic acid pathway to carcinogenesis, lung cancer prevention in former smokers, breast cancer prevention, and prostate cancer prevention. In addition, two lifestyle factors that have potential to influence cancer risk-obesity and functionally enhanced foods-are discussed in the context of their link between clinical and public health-related research.

Anticarcinogenic Agents↗
PubMed2003

Cyclooxygenase inhibitors: drugs for cancer prevention.

Evidence that chronic intake of non-steroidal anti-inflammatory drugs, especially aspirin, prevents cancer development continues to accumulate. The data are particularly convincing for colorectal cancer; however, because of well-known side effects, they cannot routinely be recommended for this purpose. An appreciation of the mechanisms that underlie their anti-cancer effects might permit the development of safer agents. Intensive investigation has led to the characterization of several potential chemopreventive mechanisms of action of these drugs. Antineoplastic actions could result from effects on overlapping processes in the different cell-types that comprise tumors, such as epithelial and stromal cells.

Angiogenesis Inhibitors↗
PubMed1995

The evidence for soybean products as cancer preventive agents.

There is much evidence suggesting that compounds present in soybeans can prevent cancer in many different organ systems. The evidence for specific soybean-derived compounds having a suppressive effect on carcinogenesis in animal model systems is limited, however. There is evidence that the following isolated soybean derived products suppress carcinogenesis in vivo: a protease inhibitor, the Bowman-Birk inhibitor, inositol hexaphosphate (phytic acid) and the sterol beta-sitosterol. Other compounds that may be able to suppress carcinogenesis in animals are the soybean isoflavones. Soybean compounds reported to have other types of anticarcinogenic activity include soybean trypsin inhibitor, saponins and genistein. There is much evidence to suggest that diets containing large amounts of soybean products are associated with overall low cancer mortality rates, particularly for cancers of the colon, breast and prostate. It is believed that supplementation of human diets with certain soybean products shown to suppress carcinogenesis in animals could markedly reduce human cancer mortality rates.

Animals↗
PubMed1999

Dietary compounds that induce cancer preventive phase 2 enzymes activate apoptosis at comparable doses in HT29 colon carcinoma cells.

Dietary agents that induce glutathione S-transferases and related detoxification systems (Phase 2 enzyme inducers) are thought to prevent cancer by enhancing elimination of chemical carcinogens. The present study shows that compounds of this group (benzyl isothiocyanate, allyl sulfide, dimethyl fumarate, butylated hydroxyanisole) activated apoptosis in human colon carcinoma (HT29) cells in culture over the same concentration ranges that elicited increases in enzyme activity (5-25, 25-100, 10-100, 15-60 micromol/L, respectively). Pretreatment of cells with sodium butyrate, an agent that induces HT29 cell differentiation, resulted in parallel increases in Phase 2 enzyme activities and induction of apoptosis in response to the inducers. Cell death characteristics included apoptotic morphological changes, appearance of cells at sub-G1 phase on flow cytometry, caspase activation, DNA fragmentation and TUNEL-positive staining. The results suggest that dietary Phase 2 inducers may protect against cancer by a mechanism distinct from and in addition to that associated with enhanced elimination of carcinogens. If this occurs in vivo, diets high in such compounds could eliminate precancerous cells by apoptosis at time points well after initial exposure to chemical mutagens and carcinogens.

Apoptosis↗
PubMed1997

Inhibition of cyclooxygenase: a novel approach to cancer prevention.

An expanding body of evidence indicates that downregulation of the cyclooxygenases (Cox-1 and Cox-2) will be an important strategy for preventing cancer because cyclooxygenases catalyze the formation of prostaglandins (PGs), and PGs have multiple effects that favor tumorigenesis. PGs also are more abundant in cancers than in the normal tissues from which cancers arise. Overexpression of Cox-2 in epithelial cells inhibits apoptosis and increases the invasiveness of tumor cells; inhibitors of Cox (e.g., NSAIDS) are chemopreventive; and tumorigenesis is inhibited in Cox-2 knockout mice. We focus in this review on strategies to selectively inhibit and downregulate the Cox-2 isoform. This is important because simultaneous inhibition of Cox-1 (constitutively expressed) and Cox-2 (inducible isoform), which is achieved with classical NSAIDs, interferes with the housekeeping functions of Cox-1 and thereby causes serious side effects, such as peptic ulcer disease. Simultaneous inhibition of Cox-1 and Cox-2 hence is not a realistic approach for chemoprevention in individuals at low to moderate risk for cancer. On the other hand, it appears possible to avoid many NSAID-dependent side effects by selective inhibition of Cox-2, which is also the isoform that is upregulated in benign and malignant tumors. Through understanding the biochemistry of these enzymes and the regulation of Cox-1 and Cox-2 gene expression, we review how Cox-2 can be regulated selectively as a target for chemopreventive therapy. We also discuss the potential importance and advantages of a multifaceted approach to diminishing the function of Cox-2 (i.e., combining inhibitors of enzyme function with inhibitors of gene expression).

Animals↗
PubMed1995

Potential impact of genetic testing on cancer prevention trials, using breast cancer as an example.

Using breast cancer as an example, we explored the potential impact that a highly predictive genetic test could have on the design and analysis of cancer prevention trials. We discuss three situations in this article: 1) trials that are in progress when the genetic test first becomes available as a research tool but is not available for general use, 2) trials in progress when the genetic test becomes generally available to the public, and 3) trials that begin after the test becomes generally available. We have concluded that the availability of a highly predictive genetic test will provide impediments to prevention trials in the form of increased noncompliance and also will provide opportunities in the form of new trials that include only persons at very high risk of developing cancer. Such trial designs could, under favorable circumstances, substantially reduce the size, duration, and cost of cancer prevention trials. The availability of a highly predictive genetic test will make the discovery of effective interventions even more urgent, and the randomized trial will still provide the most reliable method of evaluating prevention strategies.

Adult↗
PubMed2002

[Cancer prevention in familial cancer].

We established a protocol for and will conduct an interventional randomized controlled trial for the prevention of colorectal cancer. The subjects will be 100 patients with hereditary non-polyposis colorectal cancer. Two regimens were formulated for the prevention of colorectal cancer. Regimen A is dietary guidance and ingestion of aged garlic extract (AGE) capsules, and regimen B is dietary guidance and non-function capsules. The main end point of the trial is number and size of colorectal adenomas after 2 years. Subject recruiting was started in March, 2002. The trial will be completed in September, 2005.

Colorectal Neoplasms, Hereditary Nonpolyposis↗
PubMed2006

A methodologic analysis of chemoprevention and cancer prevention strategies for gastrointestinal cancer.

Gastroenterology lags behind other specialties such as cardiology in the quality of its evidence base for clinical practice. One area where this is particularly evident is in cancer prevention, despite developments in chemoprevention strategies for high-risk patients. For chemoprevention strategies to be successful, we need appropriate clinical networks and translational science infrastructures, model chemoprevention agents and multiple, large, flexible and randomized clinical trials. Translational science must also be embedded into large-scale, long-term, randomized clinical trials that have hard endpoints, so that irrefutable evidence of the longevity of treatment efficacy can be gathered. We also need to be able to identify an individual's cancer risk using valid global patient populations, so that medical benefits can be applied to all, regardless of ethnicity, sex, economic status, age and comorbidities. The future success of gastrointestinal chemoprevention relies on fostering a closer link between basic pharmaceutical research and clinical applications, in a 'bench to bedside and back' manner. In this review we systematically assess the evidence for various cancer prevention strategies, especially chemoprevention, and highlight the obstacles to further exploitation of this knowledge base.

Chemoprevention↗
PubMed2001

COX-2 inhibition in clinical cancer prevention.

Colorectal cancer is an excellent model for studying cancer prevention by means of secondary (e.g., polypectomy to remove a precursor adenoma) and primary (chemoprevention) strategies. Evidence has shown that regular users of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) have a reduction in risk of colorectal cancer. A possible mechanism of this benefit is decreased prostaglandin production, which is achieved through inhibition of cyclooxygenase (COX) activity, and possibly other pathways. Two isoforms of COX--COX-1 and COX-2--have been identified. COX-2 is expressed in colorectal adenomas and carcinomas, both in humans and rodents. Inhibition of COX-2 has been shown to decrease the incidence of carcinogen-induced neoplasia in rats and to lower the incidence of adenomas in murine models. Several COX-2 inhibitors, with the potential for less toxicity than that associated with traditional NSAIDs, are under development. This paper reviews potential chemoprevention of colorectal cancer using COX-2 inhibitors in patients at increased risk, e.g., patients with familial adenomatous polyposis, hereditary nonpolyposis colorectal cancer, and sporadic adenomas. Included are the rationale for use of such agents, results of a study showing a significant reduction in adenoma burden in familial adenomatous polyposis patients who received the selective COX-2 inhibitor celecoxib (Celebrex), and the design of other ongoing or planned clinical trials.

Adenocarcinoma↗
PubMed1995

Hormonally induced differentiation: a novel approach to breast cancer prevention.

Breast cancer, one of the most common neoplasms in women, develops more frequently in those who are nulliparous or late parous, who experience early menarche and late menopause and have a family history of breast cancer. Early parity, late menarche, early menopause, and hormone deprivation exert a protective effect. The mechanisms modulating these variations in malignancy susceptibility are not known. Epidemiologic and experimental studies indicate that malignancies develop in the mammary gland as a result of exposure to carcinogenic stimuli (i.e., chemical carcinogens, radiation). Neoplastic transformation requires that the gland be under specific developmental and age-related conditions at the time of exposure to such agents. In the rat, maximal susceptibility to neoplastic transformation is exhibited by the highly proliferating and undifferentiated gland of the young, virgin, intact females, whereas the fully differentiated gland of parous rats and virgin rats treated with the placental hormone human chorionic gonadotropin is protected from tumor development. Hormonally induced differentiation of the mammary gland is a novel approach to breast cancer prevention and therapy. The development of clinical protocols capitalizing on the protective effect of hormonal treatments mimicking pregnancy in humans is required to validate observations in experimental animal models, and to determine how they relate to epidemiologic and clinical findings. The feasibility of this approach is supported by the observed parallelism between humans and experimental models in both the site of cancer origin and the changes in breast development occurring with parity. Breast cancer initiates in terminal ductal lobular units or lobules type 1, the most undifferentiated structures frequently found in the breast of young nulliparous women.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

The molecular pathogenesis of prostate cancer: Implications for prostate cancer prevention.

Prostate cancer has become 1 of the most commonly diagnosed cancers in the United States and 1 of the leading causes of cancer death in North America and Western Europe. Survey studies of prostate tissues obtained at autopsy indicate that the development of life-threatening prostate cancer in the US likely occurs over decades. Insights from epidemiologic studies implicate environmental factors, principally dietary components, as major risk factors for prostate cancer development. An accumulating body of basic research data suggests that normal and neoplastic prostate cells may be subjected to a relentless barrage of genome-damaging stresses, and that dietary components and male sex steroids might modulate the level of genome threatening insults. Finally, over the past 5 years, analyses of somatic genome alterations in prostatic carcinoma cells have revealed that somatic inactivation of GSTP1, encoding the carcinogen-detoxification enzyme glutathione S-transferase pi, may serve as an initiating genome lesion for prostatic carcinogenesis. These diverse observations can be integrated into a transcendent mechanistic hypothesis for the pathogenesis of prostate cancer: normal prostate cells acquiring somatic GSTP1 defects may suffer chronic genome damage, influenced by dietary practices, that promote neoplastic transformation, while prostatic carcinoma cells, which characteristically contain defective GSTP1 alleles, remain susceptible to further genome-damaging stresses that promote malignant cancer progression. This hypothesized critical role for GSTP1 inactivation in the earliest steps of prostatic carcinogenesis provides several attractive opportunities for prostate cancer prevention strategies, including (1) restoration of GSTP1 function, (2) compensation for inadequate GSTP1 activity (via use of therapeutic inducers of other glutathione S-transferases (GST), and (3) abrogation or attenuation of genome-damaging stresses.

Atrophy↗
PubMed2005

Non-steroidal anti-inflammatory drugs and colorectal cancer prevention.

Colorectal cancer is the second leading cause of cancer deaths in the United States. Currently, the most effective strategy available for colon cancer prevention is endoscopic screening, with polypectomy or surgical resection for advanced lesions. This intervention carries with it many concerns regarding cost, patient acceptance, and the growing burden of surveillance colonoscopies for patients with polyps. Further improvements in the understanding of the multistep model of colorectal carcinogenesis will probably lead to the development of other primary and secondary prevention strategies. Data obtained from animal and epidemiological studies and most recently from randomised, placebo controlled trials, suggest that non-steroidal anti-inflammatory drugs may prove effective chemopreventive agents in different groups of people, from patients with familial adenomatous polyposis to those with sporadic adenomas.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

Hormonal approach to breast cancer prevention.

Breast cancer is more frequent in nulliparous women, while its incidence is significantly reduced by full-term pregnancy. The fact that the protection conferred by pregnancy is observed in women from different countries and ethnic groups, regardless of the endogenous incidence of this malignancy, indicates that this protection does not result from extrinsic factors specific to a particular environmental, genetic, or socioeconomic setting, but rather from an intrinsic effect of parity on the biology of the breast. Using an experimental system we have shown that treatment of young virgin rats with human chorionic gonadotropin (hCG), like full-term pregnancy, efficiently inhibits the initiation and progression of chemically induced mammary carcinomas. Treatment of young virgin rats with hCG induced a profuse lobular development of the mammary gland, reduced the proliferative activity of the mammary epithelium, and induced the synthesis of inhibin, a secreted protein with tumor-suppressor activity. HCG treatment also increased the expression of the programmed cell death (PCD) genes testosterone repressed prostate message 2 (TRPM2), interleukin 1-beta-converting enzyme (ICE), p53, c-myc, and bcl-XS, induced apoptosis, and downregulated cyclins. PCD genes were activated through a p53-dependent process, modulated by c-myc, and with partial dependence on the bcl-2 family-related genes. The possibility that this hormonal treatment activates known or new genes was tested by differential display technique. We have identified a series of new genes, hormone-induced-1 (HI-1) among them. The characterization of their functional role will contribute to clarify the mechanisms through which hCG inhibits the initiation and progression of mammary cancer. Of great significance was the observation that PCD genes remained activated even after lobular formations had regressed due to the cessation of hormone administration. We postulate that this mechanism plays a major role in the long-lasting protection exerted by hCG from chemically induced carcinogenesis, and might be also involved in the lifetime reduction in breast cancer risk induced in women by full-term pregnancy. The implications of these observations are two-fold: on one hand, they indicate that hCG, as pregnancy, may induce early genomic changes that control the progression of the differentiation pathway, and on the other, that these changes are permanently imprinted in the genome, regulating the long-lasting refractoriness to carcinogenesis. The permanence of these changes, in turn, makes them ideal surrogate markers of hCG effect in the evaluation of this hormone as a breast cancer preventive agent.

Animals↗
PubMed1986

Clinical trials in cancer prevention.

Research in cancer prevention can be divided into laboratory research, epidemiologic research, and clinical trials. When results from laboratory and/or epidemiologic research support the possibility of clinical cancer prevention, these leads should be subjected to study in clinical trials. If clinical trials produce positive results, wide application of these results to the relevant segments of the general population should then be emphasized. Why are clinical trials needed in cancer prevention? There are several considerations: epidemiologic studies may lack specificity, that is, the ability to reach conclusions that apply to only one specific factor; the predictive value of animal models based on laboratory studies is not entirely known; clinical trials quantitate the level of participant acceptance of the intervention; and clinical trials address the issues of risk/benefit ratios. Over the last 3 years, the National Cancer Institute has supported the development of a program of clinical trials in cancer prevention. The aim of these studies includes the reversal of precursor lesions, prevention of progression from a precursor state to overt malignancy, reduction in the incidence of malignancy, reduction in cancer mortality, and reduction in overall mortality. Interventions under study include a diet with less than 20% of calories from fat, and the administration of single agents or combinations of agents, including beta carotene, vitamin A, 13-cis-retinoic acid, vitamins C, E, and B12, and folacin.

Clinical Trials as Topic↗