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PubMed2025

Predicting breast cancer risk and its association to biopsychosocial factors among Taiwanese women with a family history of breast cancer: an investigation based on the Gail model.

BACKGROUND: First-degree relatives with breast cancer have a two-fold higher risk than women without a family history. The Gail model approach has been employed in numerous studies to investigate the risk of breast cancer among women in a variety of countries. Nevertheless, the studies investigating the correlation between the level of breast cancer risk and biopsychosocial factors among Taiwanese women with a family history of breast cancer (FHBC) are limited. By using the Gail model, we explored the breast cancer risk score and its relationship to biopsychosocial factors among Taiwanese women with FHBC. METHODS: The present study was a cross-sectional study from secondary data of the Taiwan Biobank from 2008 to 2018. Self-reports were conducted to determine biopsychosocial factors. A total of 3,060 women aged 35-70 years with and without FHBC were considered eligible for enrollment. The Gail model, which utilizes six questions, was used to estimate individual five-year absolute breast cancer risk. Women with scores at least 1.66% and above were categorized as high risk. In addition, we performed bivariate and multivariate logistic regression analysis using SPSS version 27 to predict the associations between biopsychosocial factors and the risk of breast cancer based on the Gail model. All analyses were stratified by age. RESULTS: Among the 3,060 Taiwanese women, there was a statistically significant difference in breast cancer risk score between the groups with and without FHBC (p = < 0.001), stratified by age, of which 574 in FHBC group (34.2%) were identified as having a high breast cancer risk based on the Gail model. Furthermore, six out of 15 biopsychosocial factors were significantly associated with breast cancer risk in women under 50 years of age, while seven factors showed significant associations in women aged 50 years and older. Logistic regression analysis identified five biopsychosocial factors as consistent and significant predictors of breast cancer risk in women aged 50 years and older, highlighting this group as particularly vulnerable. CONCLUSIONS: This study concludes that the Gail model identifies Taiwanese women who have a higher estimated risk of breast cancer based on cross-sectional data. Various biopsychosocial factors are associated with higher risk estimates in this population particularly in older women. Professionals can assist women in recognizing risk factors beyond the inevitable risk by encouraging regular screenings, positive behavior, and health promotion.

Humans↗

PubMed2004

Proline homozygosity in codon 72 of p53 is a factor of susceptibility for thyroid cancer.

A common germline polymorphism of p53 gene produces an Arginine to Proline change at aminoacid position 72. The resulting codon 72 variants have been reported associated with tumor susceptibility since they reduce p53 ability to activate apoptosis. Codon 72 polymorphism may play a role in subside vulnerability to different carcinogens and might account for ethnic variations in cancer frequency. Using an allele-specific polymerase chain reaction (PCR), we tested peripheral blood samples from 98 patients with thyroid cancer, including 21 follicular (FC) and 77 papillary carcinomas (PC), 44 patients with benign nodules, including 14 follicular adenomas and 30 goiters and 153 healthy individuals from the same geographical region. Data on lifetime occupational history, smoking history, general health conditions, previous diseases and other anamnestic data were obtained through interviews. Patients with FC (Pro/Pro = 19.0%, Arg/Arg = 42.9%, Arg/Pro = 38%) and with PC (Pro/Pro = 10.3%, Arg/Arg = 36.36%, Arg/Pro = 53.24%) showed a significant overrepresentation of codon 72 variants compared to the control population (Pro/Pro = 1.9%, Arg/Arg = 33.3%, Arg/Pro = 64.7%) (P = 0.0015). The Pro/Pro genotype, after adjusting for gender, age, tobacco and drugs, was associated with a markedly higher risk of FC (OR=9.714; CI: 2.334-40.436) and of PC (OR=5.299; CI: 2.334-40.436). These results provide evidence that p53 polymorphism is implicated in thyroid carcinogenesis and that individuals harboring the Pro/Pro genotype have an increased risk of developing thyroid cancer.

Adenocarcinoma, Follicular↗

PubMed2003

Intervention to reduce intentions to use tobacco among pediatric cancer survivors.

PURPOSE: In this randomized controlled trial, we sought to determine whether a risk counseling intervention would increase knowledge and perceived vulnerability to tobacco-related health risks and decrease future intentions to use tobacco among preadolescents and adolescents previously treated for cancer. PATIENT AND METHODS: Participants included 103 cancer survivors between the ages of 10 and 18 years who were randomly assigned to either a standard care control (SCC) group or a tobacco intervention (TI) group. Patients in the SCC group received standard advice about the risks of tobacco use. Patients in the TI group received more intensive late effects risk counseling in addition to an educational video, goal setting, written physician feedback, smoking literature, and follow-up telephone counseling. The effect of our intervention was assessed by self-reported knowledge, perceived vulnerability, and intentions at baseline, 6, and 12 months. RESULTS: Compared with the SCC group, patients who received our intervention had significantly higher knowledge scores, higher perceived vulnerability scores, and lower intention scores at 12 months. No significant differences between the SCC and TI groups at 6 months, across all measures, were found. CONCLUSION: Pediatric survivors' knowledge, perceived vulnerability to health risks, and intentions to use tobacco can be modified by a risk counseling intervention. The delayed effect of our intervention indicates that these changes may evolve over time. Implications for health care providers who engage in tobacco counseling with young cancer survivors are discussed. Additional longitudinal studies are needed to determine definitive long-term intervention effects on actual tobacco use in this high-risk population.

Adolescent↗

PubMed2003

Intrinsic oxidative stress in cancer cells: a biochemical basis for therapeutic selectivity.

PURPOSE: Therapeutic selectivity is one of the most important considerations in cancer chemotherapy. The design of therapeutic strategies to preferentially kill malignant cells while minimizing harmful effects to normal cells depends on our understanding of the biological differences between cancer and normal cells. We have previously demonstrated that certain agents generating reactive oxygen species (ROS) such as 2-methoxyestradiol (2-ME) preferentially kill human leukemia cells without exhibiting significant cytotoxicity in normal lymphocytes. The purpose of the current study was to investigate the biochemical basis for such selective anticancer activity. METHODS: Flow cytometric analyses were utilized to measure intracellular O(2)(-) levels and apoptosis. MTT assays were used as indicators of cellular viability. Western blot analysis was used to measure the expression of antioxidant enzymes in cancer and normal cells. RESULTS: Malignant cells in general are more active than normal cells in the production of O(2)(-), are under intrinsic oxidative stress, and thus are more vulnerable to damage by ROS-generating agents. The intrinsic oxidative stress in cancer cells was associated with the upregulation of SOD and catalase protein expression, likely as a mechanism to tolerate increased ROS stress. The increase in SOD and catalase expression was observed both in primary human leukemia cells and in primary ovarian cancer cells. Both malignant cell types were more sensitive to 2-ME than their normal counterparts, as demonstrated by the significant accumulation of O(2)(-) and subsequent apoptosis. The administration of ROS scavengers in combination with 2-ME prevented the accumulation of O(2)(-) and abrogated apoptosis induction. CONCLUSIONS: O(2)(-) is an important mediator of 2-ME-induced apoptosis. The increased oxidative stress in cancer cells forces these cells to rely more on antioxidant enzymes such as SOD for O(2)(-) elimination, thus making the malignant cells more vulnerable to SOD inhibition than normal cells.

2-Methoxyestradiol↗

PubMed2006

Stem cell aging and cancer.

Stem cells are capable of self-renewal, differentiation into various lineages, and proliferation; thus, they play critical roles in the functioning and maintenance of many biological systems. However, these unique qualities of stem cells also make them more vulnerable to mutations as the organism ages. The biggest risk factor in cancer development is age, and most scientists believe that cancers partly result from a buildup of mutations in different cell types over time. This accumulation of mutations takes place over the course of a person's lifetime, during which repeated rounds of cell division result in editing errors in the DNA. Genetic alterations can cause changes in the signaling pathways controlling proliferation, differentiation, and apoptosis. In the case of stem cells, such mutations would be passed on to all of the stem cell's progeny, ultimately resulting in a pool of stem cells that feeds neoplastic formation. Studies aiming to identify and characterize these putative cancer stem cells and to understand how they arise will shed light on the process of stem cell aging and its role in cancer.

Cell Transformation, Neoplastic↗

PubMed2002

A colony color method identifies the vulnerability of mitochondria to oxidative damage.

Mitochondrial dysfunction is a profound feature of cancer cells and is also known to cause several mitochondrial diseases. Mutations in mitochondrial DNA (mtDNA) have been reported frequently in these diseases. Although many environmental agents are known to cause damage to mitochondria, rapid methods need to be developed for testing agents that cause mitochondrial dysfunction and are involved in the development of mitochondrial and other diseases. Using Saccharomyces cerevisiae, we describe the development of a colorimetric method that identifies both physical and chemical agents that cause mitochondrial dysfunction and mutation of the mitochondrial genome. This method utilizes the previously reported ade2 mutant of S.cerevisiae that produces red colonies. However, when they lose mitochondrial function the colonies turn white. This colorimetric method has helped quantify the vulnerability of mtDNA to oxidative agents. Our study reveals that the oxidative agent adriamycin causes both mutation and extensive damage to mtDNA, which leads to loss of mtDNA. Our study also reveals that the lost mtDNA fragments migrate to the nucleus and integrate into the nuclear genome. Furthermore, our analysis reveals that loss of mtDNA leads to resistance to oxidative agents. The method described in this paper should aid in the rapid identification of environmental and other agents that cause mitochondrial dysfunction and mutagenesis, agents that may be involved in the development of mitochondrial and other diseases.

Adenine↗

PubMed2006

Effects of breast cancer risk counseling for sexual minority women.

Sexual minority women (lesbian and bisexual) represent a vulnerable group regarding their breast health. The participants in this study were 150 women aged 18-74 recruited via public announcements in mainstream and sexual minority communities in the greater Seattle metropolitan area. Potential participants were recruited to participate in a randomized trial of a breast cancer risk counseling intervention for sexual minority women. The counseling intervention produced significant reductions in perceived risk of breast cancer, anxieties and fears about breast cancer at 6 and 24 months, and increases in breast screening rates at 24 months in the intervention arm, compared with the control arm participants. These data add to the growing body of knowledge on sexual minority women's health and point to areas of community action and future research.

Adult↗

PubMed2000

K-ras point mutation in the nerve plexuses around the superior mesenteric artery in resectable adenocarcinoma of the pancreatic head: distribution pattern and related factors.

BACKGROUND: Adenocarcinoma of the pancreas is likely to spread into the nerve plexuses around the superior mesenteric artery (SMA) at a microscopic level. Since there has been no detailed report on how minute cancer invasion is distributed among the peri-SMA plexuses or which cases are more vulnerable to such an event, it has long been controversial how to treat this area when resecting the pancreatic head cancer. HYPOTHESIS: The K-ras mutation assay is more sensitive than the conventional histologic diagnosis in detecting minute cancer invasion around the SMA. DESIGN: Prospective consecutive series. SETTING: Cancer center hospital. PATIENTS AND METHODS: The entire circle of the peri-SMA tissues was obtained from 24 patients who had received an extended pancreatectomy for adenocarcinoma of the pancreatic head. They were divided into right and left hemicircular samples (48 samples), and each sample was used for both histologic and genetic diagnoses. Since all patients' primary tumors were positive for point mutation at codon 12 of the K-ras gene, the presence or absence of the mutation was determined for the peri-SMA plexuses using the mutant allele specific amplification method. RESULTS: Compared with results of the histologic examination, the K-ras mutation assay was more sensitive in detecting positive findings in the peri-SMA plexuses (12 samples from 9 patients). According to the distribution of the K-ras mutation into the right- and left-half samples, 24 patients were classified into the following 4 patterns (right/left): negative/negative in 15 patients; positive/negative in 6 patients; positive/positive in 3 patients; and negative/positive in 0 patients. In 3 patients who showed a positive/positive pattern in the genetic diagnosis, their right-half samples included more cancer cells that were detectable by routine microscopy. There was no relation between K-ras mutation and lymphatic invasion, while K-ras mutation was particularly related with the invasion of portal vein (P =.04) and posterior peripancreatic tissues (P =.002). All 3 patients with K-ras mutation in bilateral plexuses were classified by the TNM staging system as T4 using Union Internationale Contre le Cancer classification. CONCLUSIONS: The K-ras mutation (at codon 12) assay indicated a simple and regular pattern of cancer extension into the nerve plexuses around the SMA from adenocarcinoma of the pancreatic head: (1) The left half of the plexus was unlikely to be involved by cancer in cases in which the right half was intact. (2) Cancer extension into the peri-SMA plexuses occurred after the posterior confine of the pancreas had been involved by direct invasion from the primary pancreatic tumor. (3) The left half was not involved in cancerous tumors classified as T1 to T3 but was occasionally involved in those classified as T4 tumors. These data seem to provide a useful indicator of some additional treatments (resection, irradiation, etc) for the peri-SMA region when a locally advanced pancreatic head cancer is treated with a curative intent.

Adenocarcinoma↗

PubMed2005

Never too old? Age should not be a barrier to enrollment in cancer clinical trials.

Throughout Europe and the U.S., over 60% of the total incidence of cancer occurs in the elderly (> or =65 years) population, a patient group that requires particular consideration when making treatment decisions due to a number of factors. Despite this, elderly patients are generally under-represented in clinical trials such that study data should be interpreted with caution because results in younger cancer patients may not always extrapolate to the typical elderly cancer patient. Reports suggest that elderly cancer patients represent around 22% of patients enrolled in phase II clinical studies. Barriers to the accrual of elderly patients to clinical trials include lack of appropriate trials, high burden of comorbidity, study-imposed restrictions, and attitudes of physicians. There is a belief that elderly patients may be unable to tolerate various cancer therapies, which may result in this patient population being excluded from prospective trials. However, clinical data demonstrate that age alone is not a sufficient reason to withhold treatment. Lack of clinical trial data and the associated lack of evidence-based guidelines for elderly patients mean physicians have little to guide them, with the result that patients may not receive the optimal therapy. As clinical trials are the primary method of evaluating the efficacy and safety of adjuvant and palliative cancer therapies, trials that specifically target the elderly cancer patient are required to adequately assess the risks and benefits of treatment in this vulnerable population. This review aims to assess the clinical reality and clinical trial age mismatch to evaluate implications for elderly cancer patients and to identify how this situation may be addressed. Possible reasons for the disparity, and the resulting clinical consequences, are also considered.

Age Factors↗

PubMed2003

Screening behavior in brothers and sons of men with prostate cancer.

PURPOSE: We identified factors associated with screening behavior in the brothers and sons of men with prostate cancer. MATERIALS AND METHODS: We contacted 837 men with prostate cancer to invite their 40 to 70-year-old brothers or sons to participate in this study. We mailed the brothers and sons who contacted us a survey to explore sociodemographic and medical characteristics, prostate cancer family history, prostate cancer knowledge, self-efficacy, barriers to screening, perceived benefits, perceived vulnerability and medical support. RESULTS: Of the 138 candidates who participated in the study 86 (62%) had undergone prostate specific antigen and digital rectal examination within the last 2 years. Men older than 50 years, those who had discussed prostate cancer screening with their physician, those with good knowledge of recommended screening frequency and those with no co-morbidity had undergone screening more often than others. CONCLUSIONS: Physician support and prostate cancer screening knowledge were positively associated with previous screening. Effective interventions to increase screening in families at risk should target physicians.

Adult↗

PubMed2004

Adolescents' beliefs about the risks involved in smoking "light" cigarettes.

BACKGROUND: Light cigarettes have been marketed by the tobacco industry as being a healthier smoking choice, a safe alternative to cessation, and a first step toward quitting smoking altogether. Research, however, has failed to show a reduction in smoking-related health risks, an increase in rates of smoking cessation, a decrease in the amount of carbon monoxide or tar released, or a reduction in the rates of cardiovascular disease or lung cancer associated with light cigarette use, compared with regular cigarette use. Nevertheless, more than one-half of adolescent smokers in the United States smoke light cigarettes. This study is the first to investigate adolescents' perception of the risks associated with smoking light cigarettes, as well as adolescents' attitudes and knowledge about the delivery of tar and nicotine, health risks, social effects, addiction potential, and ease of cessation with light cigarettes, compared with regular cigarettes. DESIGN: Participants were 267 adolescents (mean age: 14.0 years) who completed a self-administered questionnaire during class time. After reading scenarios in which they imagined that they smoked regular or light cigarettes, participants estimated the chances that they would personally experience 7 smoking-related health risks and 3 addiction risks. Participants also responded to 14 items concerning their attitudes and knowledge about light cigarettes versus regular cigarettes. RESULTS: Participants thought that they would be significantly less likely to get lung cancer, have a heart attack, die from a smoking-related disease, get a bad cough, have trouble breathing, and get wrinkles when smoking light cigarettes, compared with regular cigarettes, for the rest of their lives. Furthermore, when participants were asked how long it would take to become addicted to the 2 cigarette types, they thought it would take significantly longer to become addicted to light versus regular cigarettes. Adolescents also thought that their chances of being able to quit smoking were higher with light versus regular cigarettes. Similarly, when participants were asked how easy it would be to quit smoking the 2 cigarette types, they thought it would be significantly easier for them to quit smoking light cigarettes than regular cigarettes. Adolescents agreed or strongly agreed that regular cigarettes deliver more tar than light cigarettes and that light cigarettes deliver less nicotine than regular cigarettes. CONCLUSIONS: Overall, the results of this study show that adolescents hold misperceptions in both their personal risk estimates and their general attitudes about the health risks, addictive properties, and ease of cessation associated with light cigarettes. With a variety of light and ultralight cigarettes on the market, adolescents are led to think that there is a progression of safety levels to choose from when deciding which cigarettes to smoke. This illusion of control over health outcomes contributes to an underestimation of risks associated with smoking light cigarettes and supports these misperceptions. These results are of concern, given evidence suggesting that, if adolescents think they are less vulnerable to smoking-related health risks (ie, lung cancer), then they are more likely to initiate smoking. Furthermore, there is evidence that adolescents are not fully aware of the addictive nature of cigarettes and therefore think that they can experiment with smoking during adolescence without becoming addicted or experiencing any health consequences. The data presented here support concerns regarding smoking addiction; adolescents might be even more inclined to smoke light cigarettes to delay addiction. Without correct information about light cigarettes, adolescents are unable to make informed decisions about their smoking behaviors. The findings presented here strongly suggest that health care practitioners need to talk to their adolescent clients not only about the overall risks of smoking but also about the specific risks associated with smoking light cigarettes and other tobacco varieties, including the potential for addiction and long-term health consequences. Information shared with adolescents about light cigarettes, both individually by health care practitioners and at the population level via counter-advertising campaigns, may be successful in changing current misperceptions, and ultimately light cigarette smoking patterns, among youth.

Adolescent↗

PubMed2006

Health-risk behaviors and health promotion in adolescent and young adult cancer survivors.

A diagnosis of cancer during adolescence, a period characterized by experimentation and risk-taking behaviors, has the potential to derail critical developmental tasks required for successful transition into adulthood. Health professionals caring for adolescents and young adults have an opportunity to influence behavioral practices by correcting knowledge deficits, addressing factors that enhance the survivor's sense of vulnerability to health problems, and providing personalized health counseling that encourages the practice of health promoting behaviors. The approach to health counseling in childhood cancer survivors should consider their unique educational needs related to their cancer experience. Previous investigations of adolescent and young adult survivor health behavior indicate that survivors perceive themselves as more vulnerable to health problems than their peers without cancer and recognize a need to protect their health. However, these perceptions of health vulnerability do not always correlate with health promoting behavioral practices, suggesting that factors other than health perceptions should be investigated to motivate behavioral change. Very few studies have been undertaken to prospectively evaluate the effectiveness of health promotion programs in adolescent and young adult survivors of cancer. The scarcity of knowledge in the issue of health promotion after childhood cancer underscores the need for more research to define 1) the optimal timing of health counseling; 2) the influence of developmental status and neurocognitive function; 3) the most effective methods and venues for health education; 4) the feasibility and cost-effectiveness of health promotion strategies; and 5) psychosocial and economic impediments to practice of healthy behaviors.

Adolescent↗

PubMed2006

Central nervous system toxicity from cancer therapies.

The central nervous system (CNS) is an organ with a unique profile of vulnerability to antineoplastic treatments. In many cases, CNS neurotoxicity is the dose-limiting side effect of treatment for systemic and CNS neoplasms. Novel methods of delivering radiation and chemotherapy agents have led to recognition of new forms of CNS neurotoxicity. In this article, the authors review the most important CNS toxicities of cancer treatment.

Antineoplastic Agents↗

PubMed2006

Trends in childhood cancer incidence in Wisconsin, 1980-1999.

OBJECTIVES: Characterizing the burden of childhood cancer in Wisconsin is the first step to assessing the impact of prevention efforts, identifying especially vulnerable subgroups, and directing etiologic research. To support these goals, population-level data were used to examine trends in childhood cancer incidence among children aged 0-14 years in Wisconsin from 1980 to 1999. METHODS: Data for Wisconsin was provided by the Wisconsin Cancer Reporting System and compared to national data. Annual age-adjusted childhood cancer incidence rates for the entire population and subgroups by age, sex, race, time period, diagnostic code, and geographic region were described. Correlational analysis was conducted to assess the relation between community socioeconomic status and childhood cancer incidence using census data. RESULTS: Overall, Wisconsin's annual incidence rate for childhood cancers was 14.4 cases per 100,000 children aged 0-14 years during 1980-1999. This rate increased 10.9% (95% confidence interval 1-22%) between 1980 and 1999. Children in the 0-4 age group (20.9 per 100,000 per year) had the highest incidence rates as compared to 5-9 year olds (10.4 per 100,000 per year) and 10-14 year olds (12.0 per 100,000 per year). In males, the age-adjusted incidence of childhood cancers between 1980 and 1999 was 15.5 cases per 100,000 per year, whereas females had an incidence rate of 13.1 per 100,000 per year. Rates for whites were similar to the rates for all other racial groups combined. Leukemia had the highest age-adjusted incidence rate among childhood cancer diagnostic subtypes (4.3 cases per 100,000 per year); leukemia incidence increased by 32% between 1980 and 1999. Among the 13 hospital referral regions in Wisconsin with reported cancer cases, the Dubuque region had the highest annual age-adjusted incidence rate of 24.6 cases per 100,000, followed by Madison with 15.6 per 100,000, and Milwaukee with 15.5 per 100,000. In general, higher socioeconomic status as reflected by census indicators was positively correlated with higher rates of childhood cancer. SUMMARY: Wisconsin experienced childhood cancer incidence rates and trends similar to those throughout the United States between 1980 and 1999. Analysis of Wisconsin data, which is subject to small numbers in absolute terms (3,138 cases during 1980-1999), suggests that not all children have similar risk--infants and younger children (<5 years of age) as well as children living in areas with higher socioeconomic status may be especially vulnerable.

Adolescent↗

PubMed2004

Age-related vulnerabilities of older adults with colon adenomas: evidence from Project Prevent.

BACKGROUND: This report addresses the interface between cancer and aging in the context of colorectal carcinoma (CRC), the second leading cause of cancer death in the U.S. overall and the first leading cause among individuals age > or = 75 years. Because polyp risk increases with age, interventions to prevent recurrent polyps among older adults likely would reduce CRC morbidity and mortality. METHODS: Data for this study derive from Project Prevent, a multisite, randomized controlled trial designed to reduce behavioral risk factors for CRC among 1247 adults who underwent the removal of > or = 1 adenomatous colon polyps. Middle-aged and older patients were compared on key cognitive-behavioral mechanisms associated with CRC risk and established age-related factors associated with adverse health outcomes. Relations between cognitive-behavioral mechanisms and age-related vulnerability factors identified subgroups of older polyp patients that may have an enhanced risk for CRC. RESULTS: Compared with middle-aged patients, older patients were less concerned about developing CRC, less motivated to reduce their risk, and less confident that their behavior change efforts would succeed. As expected, they also reported more age-related physical, social, and economic vulnerabilities, as expected. Evidence for enhanced CRC risk was found for older patients with multiple comorbid conditions, low social support for change, and perceptions of income inadequacy. CONCLUSIONS: The presence of age-related vulnerability factors may enhance the risk of CRC among older cancer patients by creating barriers to behavioral change. Efforts to reduce the cancer burden in older populations will require attention beyond early detection and surveillance to interventions that account for the unique physical and psychosocial characteristics of older adults.

Adenomatous Polyposis Coli↗

PubMed2002

Medication misadventure in cancer care.

OBJECTIVES: To describe the nature and scope of the problem of medication errors in health care, with specific implications for error reduction and prevention. DATA SOURCES: Articles and research studies. CONCLUSIONS: Because of the complexity of chemotherapeutic regimens, requirements for supportive care drugs, and the physiologic vulnerability of patients due to their malignancies and intensive therapies, patients with cancer should be the focus of interdisciplinary medication error prevention programs. IMPLICATIONS FOR NURSING PRACTICE: Nurses play a critical role in patient safety and the implementation of preventive and risk-reducing interventions to improve the drug delivery process.

Antineoplastic Agents↗

PubMed1997

Controversies surrounding diet and breast cancer.

What we know about prevention of breast cancer is related to lifetime oestrogen exposure and exposures to specific oestrogens at vulnerable periods of life. This can be influenced by diet. The strongest indicator of a diet-related effect to date is the fairly consistent increase in breast cancer among women who are tall or obese (Hunter & Willett, 1993). The other dietary factors summarized in Table 1 are less strongly associated with breast-cancer risk in epidemiological studies. The relationship between fat and breast-cancer risk has been extensively studied but remains somewhat uncertain. Fat, as a contributor to energy intakes and energy imbalance, is probably a factor in the higher breast-cancer rates in Western countries. Beyond its role as an energy source, the evidence for an independent effect of dietary fat on breast-cancer risk is weak. More focused analyses of the role of individual fatty acids, and on lipid-related pesticide exposures, may reveal strong effects which are currently masked by the use of inadequate exposure measures, as well as by measurement error. Currently, there is substantial evidence of a weak relationship with alcohol consumption, even at frequencies of drinking of less than once daily. The evidence of a protective role for antioxidants is weaker for breast cancer than for other cancers. This might by expected in a cancer which is not strongly associated with cigarette smoking. Specific foods are being studied for other potentially-active ingredients which may be involved in hormone metabolism, but conclusive results for soyabean or cruciferous vegetables are not yet available. Studying these relationships will continue to be a challenge for researchers because of the difficulties in measuring dietary exposures, which is complicated by the uncertainty of the relevant time frame for exposure assessment. While substantial attention has been focused on studying diet in relation to incidence, the potential for diet to reduce recurrence of breast cancer is thoroughly under-studied. There is little reason to believe that the factors which influence the incidence of breast cancer, perhaps during childhood and puberty, are the same as those which affect recurrence in adulthood. In this area, the very limited evidence available suggests that study of biologically-active fatty acids is promising.

Animals↗

PubMed1999

Lineage selection and the evolution of multistage carcinogenesis.

A wide array of proto-oncogenes and tumour suppressor genes are involved in the prevention of cancer. Each form of cancer requires mutations in a characteristic group of genes, but no single group controls all cancers. This lack of generality shows that the control of cancer is not an ancient, fixed property of cells. By contrast, it supports a dynamic evolutionary model, whereby genetic controls over unregulated cell growth are recruited independently through evolutionary time in different tissues within different taxa. The complexity of this genetic control can be predicted from a population genetic model of lineage selection driven by the detrimental fitness effects of cancer. Cancer occurs because the genetic control of cell growth is vulnerable to somatic mutations (or 'hits'), particularly in large, continuously dividing tissues. Thus, compared to small rodents, humans must have evolved more complex genetic controls over cell growth in at least some of their tissues because of their greater size and longevity; an expectation relevant to the application of mouse data to humans. Similarly, the 'two-hit' model so successfully applied to retinoblastoma, which originates in a small embryonic tissue, is unlikely to be generally applicable to other human cancers; instead, more complex scenarios are expected to dominate, with complexity depending upon a tissue's size and its pattern of proliferation.

Animals↗