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PubMedDate not supplied

Cancer Prevention Study II. The American Cancer Society Prospective Study.

Over the past 40 years, the American Cancer Society has led in large-scale, prospective studies of behavioral and environmental risk factors in association with cancer development. Through results of its 1952 study, cigarette smokers were found to have a 10-fold higher risk of lung cancer than nonsmokers. Cancer Prevention Study I (1959-1972) extended these results and also showed the relationship between age smoking began, depth of inhalation, smoking cessation, air pollution, body weight, etc., on all causes of death as well as specific cancer sites. Cancer Prevention Study II began in 1982 and after six years of follow-up has confirmed many earlier findings, and additionally has found: aspirin may be protective against colon cancer; persons reporting themselves to be heavy exercisers had higher standardized mortality ratios (SMR) for lung, colorectal, and pancreas cancer than moderate exercisers; more women who were long-term users of artificial sweeteners reported gaining weight during the past year than nonusers; diesel fume exposure elevated the risk of lung cancer among men ages 40-79; pesticide exposure was associated with an increased risk of multiple myeloma; and based on CPS II mortality rates, an estimated 250 million of the 1.25 billion persons living in developed countries will die because they smoke.

Age Factors↗
PubMed2004

Is gastric cancer preventable?

Gastric cancer is a major health burden worldwide and prevention is the most promising strategy to control the disease. The available scientific evidence indicates that curing Helicobacter pylori infection results in a modest retardation of the precancerous process but does not prevent all cancers. Individuals at the highest risk should be cured of their infection and monitored endoscopically to detect dysplasia and "early" cancer, amenable to successful treatment.

Helicobacter Infections↗
PubMed2000

Life expectancy gains from cancer prevention strategies for women with breast cancer and BRCA1 or BRCA2 mutations.

CONTEXT: Women with BRCA1- or BRCA2-associated breast cancer are at increased risk for contralateral breast cancer and ovarian cancer and therefore may consider secondary cancer prevention strategies, such as prophylactic surgery and tamoxifen therapy. It is not proven to what extent these strategies reduce risk of second cancers in such patients. OBJECTIVE: To examine the effect of tamoxifen therapy, bilateral prophylactic oophorectomy (PO), prophylactic contralateral mastectomy (PCM), and combinations of these strategies on life expectancy for women with unilateral breast cancer and a BRCA1 or BRCA2 gene mutation. DESIGN AND SETTING: Decision analysis using a Markov model. Probabilities for developing contralateral breast cancer and ovarian cancer, dying from these cancers, dying from primary breast cancer, and the reduction in cancer incidence and mortality due to prophylactic surgeries and/or tamoxifen were estimated from published studies. PARTICIPANTS: Hypothetical breast cancer patients with BRCA1 or BRCA2 mutations facing decisions about secondary cancer prevention strategies. INTERVENTIONS: Seven strategies, including 5 years of tamoxifen use, PO, PCM, and combinations of these strategies, compared with careful surveillance. MAIN OUTCOME MEASURES: Total and incremental life expectancy (LE) with each intervention strategy. RESULTS: Depending on the assumed penetrance of the BRCA mutation, compared with surveillance alone, 30-year-old early-stage breast cancer patients with BRCA mutations gain in LE 0.4 to 1.3 years from tamoxifen therapy, 0.2 to 1.8 years from PO, and 0.6 to 2.1 years from PCM. The magnitude of these gains is least for women with low-penetrance mutations (assumed contralateral breast cancer risk of 24% and ovarian cancer risk of 6%) and greatest for those with high-penetrance mutations (assumed contralateral breast cancer risk of 65% and ovarian cancer risk of 40%.) Older age and poorer prognosis from primary breast cancer further attenuate these gains. CONCLUSIONS: Interventions to prevent second cancers, particularly PCM, may offer substantial LE gain for young women with BRCA-associated early-stage breast cancer. Estimates of LE gain may help women and their physicians consider the uncertainties, risks, and advantages of these interventions and lead to more informed choices about cancer prevention strategies.

Adult↗
PubMed2006

Inhibition of p38 by vitamin D reduces interleukin-6 production in normal prostate cells via mitogen-activated protein kinase phosphatase 5: implications for prostate cancer prevention by vitamin D.

Although numerous studies have implicated vitamin D in preventing prostate cancer, the underlying mechanism(s) remains unclear. Using normal human prostatic epithelial cells, we examined the role of mitogen-activated protein kinase phosphatase 5 (MKP5) in mediating cancer preventive activities of vitamin D. Up-regulation of MKP5 mRNA by 1,25-dihydroxyvitamin-D3 (1,25D) was dependent on the vitamin D receptor. We also identified a putative positive vitamin D response element within the MKP5 promoter that associated with the vitamin D receptor following 1,25D treatment. MKP5 dephosphorylates/inactivates the stress-activated protein kinase p38. Treatment of prostate cells with 1,25D inhibited p38 phosphorylation, and MKP5 small interfering RNA blocked this effect. Activation of p38 and downstream production of interleukin 6 (IL-6) are proinflammatory. Inflammation and IL-6 overexpression have been implicated in the initiation and progression of prostate cancer. 1,25D pretreatment inhibited both UV- and tumor necrosis factor alpha-stimulated IL-6 production in normal cells via p38 inhibition. Consistent with inhibition of p38, 1,25D decreased UV-stimulated IL-6 mRNA stabilization. The ability of 1,25D to up-regulate MKP5 was maintained in primary prostatic adenocarcinoma cells but was absent in metastases-derived prostate cancer cell lines. The inability of 1,25D to regulate MKP5 in the metastasis-derived cancer cells suggests there may be selective pressure to eliminate key tumor suppressor functions of vitamin D during cancer progression. These studies reveal MKP5 as a mediator of p38 inactivation and decreased IL-6 expression by 1,25D in primary prostatic cultures of normal and adenocarcinoma cells, implicating decreased prostatic inflammation as a potential mechanism for prostate cancer prevention by 1,25D.

Calcitriol↗
PubMed2002

New approaches to lung cancer prevention.

Lung cancer is the most common cause of cancer death worldwide. The overall 5-year survival rate remains disappointing at 14% or less. Several clinician- and community-based interventions show promise for reducing lung cancer incidence through prevention and smoking cessation. However, long-term heavy smokers retain a significant lung cancer risk despite smoking cessation. Half of newly diagnosed lung cancers are now found in former smokers. An additional strategy of lung cancer control through chemoprevention needs to be developed. Advances in optical imaging technologies and genome science will continue to improve our ability to identify individuals with the highest risk of lung cancer for chemoprevention. More accurate surrogate endpoint biomarkers are becoming available for phase II trials of new agents. A number of promising agents are currently being tested in phase II and III trials for prevention of lung cancer.

Animals↗
PubMed1999

Synergistic effects of (--)-epigallocatechin gallate with (--)-epicatechin, sulindac, or tamoxifen on cancer-preventive activity in the human lung cancer cell line PC-9.

The study on incorporation of [3H](-)-epigallocatechin gallate (EGCG) into human lung cancer cell line PC-9 indicated that the [3H]EGCG incorporation was significantly enhanced by (-)-epicatechin, an inert tea polyphenol without a galloyl moiety. (-)-Epicatechin enhanced apoptosis, growth inhibition of PC-9 cells, and inhibition of tumor necrosis factor-alpha release from BALB/c-3T3 cells by EGCG and other tea polyphenols with a galloyl moiety in a dose-dependent manner. Moreover, the effects of EGCG on induction of apoptosis were also synergistically enhanced by other cancer-preventive agents, such as sulindac and tamoxifen. This paper reports significant evidence that whole green tea is a more reasonable mixture of tea polyphenols for cancer prevention in humans than EGCG alone and that it is even more effective when it is used in combination with other cancer preventives.

3T3 Cells↗
PubMed2004

Should tamoxifen be used in breast cancer prevention?

Breast cancer is the most commonly diagnosed cancer in women. The risk of developing breast cancer can be lowered by maintaining a healthy bodyweight and avoiding long-term use of combined estrogen and progestogen replacement after menopause. However, many women are at an increased risk of developing breast cancer secondary to age, early menarche, a family history of breast cancer or a personal history of benign breast disease. These women may now be offered tamoxifen as a chemoprevention therapy. Five years of tamoxifen treatment results in a reduction in the relative risk of developing estrogen receptor-positive breast cancer of 48%. This benefit outweighs the risk of tamoxifen-related adverse events for many healthy women. However, the benefit-risk ratio of tamoxifen chemoprevention varies for individual women. The randomized clinical trials evaluating standard-dose tamoxifen versus placebo as chemoprevention therapy are reviewed and analyzed to determine which particular women are most likely to benefit and least likely to experience a tamoxifen-related adverse event. Tamoxifen decreases the risk of breast cancer associated with aging, having a first-degree relative with disease, and a personal diagnosis of atypical ductal hyperplasia or lobular carcinoma in situ. Women who have had a hysterectomy and are at low risk of a thromboembolic event have a decreased risk of adverse effects associated with tamoxifen therapy. The strengths and weaknesses of the Gail model (frequently used to assess an individual's risk of developing invasive breast cancer over the next 5 years) are highlighted. A method for assessing the benefit-risk ratio for an individual woman is presented. Alternative breast cancer chemoprevention strategies are considered, including the use of aromatase inhibitors. This article discusses the pros and cons of these various preventive therapies and concludes that at this time, tamoxifen remains the gold standard for breast cancer prevention.

Adult↗
PubMedDate not supplied

Evaluation of N-4-(hydroxycarbophenyl) retinamide as a cancer prevention agent and as a cancer chemotherapeutic agent.

In this review, a retinoid analogue (N-4-hydroxycarbophenyl) retinamide (R11) has been evaluated for its pharmacological and clinical properties. R11 has been studied both as a cancer prevention agent, as well as, a cancer chemotherapeutic agent. R11 alone and in combination with other agents can be used for the treatment of cervical dysplasia or leukemia. This review will examine novel strategies and mechanisms of action for retinoids in the treatment and prevention of cancer.

Animals↗
PubMed1994

Toward a physiological approach to breast cancer prevention.

Breast cancer is one of the most frequent malignancies in women, and its incidence is increasing. No reduction in the mortality rate has resulted from advances in early diagnosis and new therapeutic modalities; therefore, new approaches to the understanding of this disease are required. The observation that, in an experimental animal model, full-term pregnancy prior to exposure to a carcinogenic agent protects the mammary gland from malignant transformation led us to study the mechanisms underlying this phenomenon. The protective effect observed after pregnancy did not depend upon gestational or lactational hyperplasia of the mammary gland, but upon structural changes induced in the mammary parenchyma by those processes. Those changes are permanent, since the protective effect is maintained after pregnancy and consists in the complete differentiation of terminal end buds to lobules. The protective effect exerted by pregnancy can be mimicked by treating young virgin rats with a single placental hormone, chorionic gonadotropin. Since the possibility of preventing breast cancer by treating young nulliparous females with hormones that mimic a fullterm pregnancy that results in complete differentiation of the gland is of practical interest to the human female population, we undertook the study of the human breast. The breast of postpubertal nulliparous women is composed of lobular structures reflecting different stages of development. Lobules type 1 (lob 1) are the most undifferentiated ones. Lobules type 2 evolve from the previous ones and have a more complex morphology, being composed of a higher number of ductular structures per lobule. They progress to lobules type 3 and 4, which are present in the pregnant and lactational periods of the mammary gland. In nulliparous women the structure most frequently found at all ages is the lob 1, whereas in parous women, lob 3 is the most frequent one. Lob 1 are considered to be the site of origin of ductal carcinoma in situ, which progresses to invasive carcinoma. Lob 2 originate lobular carcinoma and lob 3 originate adenomas, fibroadenomas, sclerosing adenosis, and apocrine cysts. These observations led us to test if the degree of lobular development influences the transformation of human breast epithelial cells exposed in vitro to chemical carcinogens. We found that primary cultures derived from breast tissues composed of lobules type 1 and 2 express phenotypes of cell transformation which were not observed in cells derived from lobules type 3.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed2004

Green tea and tea polyphenols in cancer prevention.

The cancer-preventive effects of green tea and its main constituent (-)-epigallocatechin gallate [(-)-EGCG] are widely supported by results from epidemiological, cell culture, animal and clinical studies in the recent decade. In vitro cell culture studies show that tea polyphenols potently induce apoptotic cell death and cell cycle arrest in tumor cells but not in their normal cell counterparts. Green tea polyphenols affect several signal transduction pathways, including growth factor-mediated, the mitogen-activated protein kinase (MAPK)-dependent, and ubiquitin/proteasome degradation pathways. Epidemiological studies have suggested that the consumption of green tea lowers the risk of cancer. Various animal studies have revealed that treatment by green tea inhibits tumor incidence and multiplicity in different organ sites such as skin, lung, liver, stomach, mammary gland and colon. Phase I and II clinical trials were carried out recently to explore the anticancer effects of green tea in patients with cancer. At this time, more mechanistic research, animal studies, and clinical trials are necessary to further evaluate the role of green tea in cancer prevention.

Anticarcinogenic Agents↗
PubMed1981

[Examination for the prevention of gynecologic cancer in young women: when should cancer prevention begin?].

Since the Swiss Gynecological Society suggests that cervical smears be taken only from patients age 25 years or over, we have investigated the validity of an age limitation. Analyzing the patients at our dysplasia clinic, the following statistics emerged: of the 4255 patients in the period 1970-1980, 897 or 21.08% were under 25 years of age; 190 or 4.46% were under 20. Of these women, 153 had or developed (cytologically at least) serious dysplasia or carcinoma in situ. On the basis of the data presented and the literature we are obliged to concluded that an age limit is not medically meaningful and that every sexually active woman, regardless of age, should be accepted into the preventive examination program.

Adult↗