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PubMed2006

The cost of prostate cancer chemoprevention: a decision analysis model.

BACKGROUND: The Prostate Cancer Prevention Trial found reduced prostate cancer prevalence for men treated with finasteride. The public health cost of wide-scale chemoprevention is unclear. We developed a model to help clarify the cost effectiveness of public use of prostate cancer-preventive agents. METHODS: A Markov decision analysis model was designed to determine the lifetime prostate health-related costs, beginning at the age of 50 years, for men treated with finasteride compared with placebo. Model assumptions were based on data from the Prostate Cancer Prevention Trial, a literature review of survival and progression rates for patients treated with radical prostatectomy, and costs associated with prostate cancer disease states. RESULTS: Chemoprevention with finasteride resulted in a gain of 8.7 [corrected] life years per 1,000 men at a cost of $1.107 million [corrected] per life year saved (LYS). However, if finasteride is assumed to not increase the incidence of high-grade tumors, it renders a gain of 16.9 [corrected] life years per 1,000 men at a cost of $578,400 [corrected] per LYS; finasteride must cost $160 per year [corrected] to reach $100,000 [corrected] per LYS. When applied to a population at higher risk (lifetime prevalence >or=40%) [corrected]for developing prostate cancer, the cost of finasteride must be reduced from its current cost ($62/month) to <$15/month [corrected]for the cost effectiveness to fall below $50,000 [corrected] per LYS. CONCLUSIONS: Given the natural history of treated prostate cancer, implementation of chemoprevention would require an inexpensive medication with substantial cancer risk reduction to be cost effective. Targeting populations at higher risk for developing prostate cancer, however, allows for considerable flexibility in the medication cost to make prostate cancer chemoprevention a more attainable goal.

Aged↗

PubMed2004

Cancer in the Commonwealth of the Northern Marianas Islands (CNMI).

The purpose of this study, funded by the National Cancer Institute, was to document the state of cancer awareness and services in the Commonwealth of the Northern Mariana Islands (CNMI) and to begin to identify cancer-care needs. Findings suggest that cancer is the second-leading cause of death in the CNMI, and that the most prevalent cancers are those that can be prevented and/or cured with early detection and treatment. Key informants identified a number of cancer-related service needs, and an action plan was developed based on three priority areas: 1) developing a cancer registry; 2) increasing resources dedicated to cancer prevention and control programs, and 3) increasing capacity of health professionals and support staff.

Awareness↗

PubMed1990

The epidemiology of cancer among Hispanic women. The experience in Florida.

To explore cancer incidence among Hispanic women living in Dade County, Florida, data were analyzed from the statewide cancer registry. For all but three sites, Hispanics had lower rates of the 15 most prevalent cancers than non-Hispanics. However, higher rates of cancer among Hispanics were noted for cancers of the gallbladder, liver, and heart and soft tissue. Subgroups of women had significantly higher rates of cervical cancer and thyroid cancer. Lower rates among Hispanics were observed for cancers of the esophagus, vagina, breast, colon, buccal cavity and pharynx, and malignant melanoma. These data suggest that most cancer sites traditionally higher among US Latino women were not higher among Dade Hispanics, and that sites more common among non-Hispanics have not yet shown an increased incidence among Hispanic women in Dade County.

Aged↗

PubMedDate not supplied

Risk of cancer among women with AIDS in New York City.

To evaluate the risk of cancer among women with AIDS in New York City (NYC), we compared the cancer experience of AIDS-infected women in NYC with that of the general population of women in NYC by matching the population-based New York State Cancer Registry with the New York City AIDS Registry. A probabilistic algorithm was used to match names, birth dates, and, where available, Social Security numbers between 15,146 women with AIDS and 232,902 women with cancer. Standardized incidence ratios (SIR) were calculated as the ratio of observed to expected cancer cases in the population of NYC women matched for age, race, and calendar period of cancer diagnosis. Period-specific relative risks (RR) of cancer prevalence prior to AIDS, and incidence at or after AIDS were calculated to determine which cancers increased in proximity to an AIDS diagnosis, a surrogate marker of increasing immunodeficiency. Analysis was limited to women between the ages of 15 to 69 who were diagnosed with AIDS between 1981 and 1994. Among 15,146 women diagnosed with AIDS, we found 1,194 matches with the Cancer Registry. For cancers included in the 1993 AIDS case definition, the SIR was 178.49 for Kaposi's sarcoma, 48.97 for non-Hodgkin's lymphoma, and 9.20 for invasive cervical cancer. The overall SIR for all non-AIDS-defining cancers was 2.20. Among non-AIDS-defining cancers, elevated SIRs were found for cancers of the lung (7.95), esophagus (7.69), multiple myeloma (7.37), oral cavity and pharynx (6.55), Hodgkin's disease (5.65), leukemias (4.52), and rectal/anal cancers (3.23). Statistically significant increases in period-specific risks were found for all non-AIDS-defining cancers combined, but not for individual cancers. Dual screening by two registries and unknown behavioral factors complicate the ascertainment of cancer risk. Our results show significantly elevated risks for several non-AIDS-defining cancers; these results are consistent with other studies of cancers among persons with AIDS. Extension of the time period of analysis is required to test for the effects of new anti-viral treatments and their association with cancer development among HIV-infected women.

Acquired Immunodeficiency Syndrome↗

PubMed1997

[Campaign for cervical cancer screening with vaginal smears in women aged 50-69 years in Isère (France). Results of the first round (January 1991-June 1993)].

The department of Isère, which is involved since 1990 in a breast cancer screening campaign concerning women aged 50 to 69, has managed to associate a cervical and colorectal cancers screening program. The target sample size is 98,000 individuals. Women are asked to refer their general practitioner or gynaecologist for cervicovaginal smears. Each woman is invited at a screening interval of 30 months. The results of the first invitation (November 1990-December 1992) are reported. Thus 29,570 women did referred, so that the screening uptake is 30% and 20,083 women (68%) had Pap smears inside the screening program. 1.1% of the smears were unsatisfactory and 1.2% of the tests showed abnormalities. Ninety-six percent of the women who had been referred for further examinations have been followed up. Thirty-eight women (representing 17% of smears with abnormalities) had surgery (conisation, hysterectomy, Wertheim). Among them, 5 cases of invasive cervical carcinoma and 25 in situ carcinoma were detected. The detected cancer prevalence per 1,000 women screened is 1.5/1000. An organised screening program for cervical cancer in association with breast cancer screening, seems to be an effective way of increasing smears realisation in women aged 50 to 69, and of involving general practitioners in cervical cancer screening.

Aged↗

PubMed1991

Comutagenesis of sodium arsenite with ultraviolet radiation in Chinese hamster V79 cells.

Solar ultraviolet radiation has been associated with the induction of skin cancer. Recent studies have indicated that near-ultraviolet, especially UVB, is mutagenic. Exposure to trivalent inorganic arsenic compounds has also been associated with increased skin cancer prevalence. Trivalent arsenic compounds are not mutagenic per se, but are comutagenic with a number of cancer agents. Here, we test the hypothesis that arsenite enhances skin cancer via its comutagenic action with solar ultraviolet radiation. Irradiation of Chinese hamster V79 cells with UVA (360 nm), UVB (310 nm) and UVC (254 nm) caused a fluence-dependent increase in mutations at the hprt locus. On an energy basis, UVC was the most mutagenic and UVA the least. However, when expressed as a function of toxicity, UVB was more mutagenic than UVC. Nontoxic concentrations of arsenite increased the toxicity of UVA, UVB and UVC. Arsenite acted as a comutagen at the three wavelengths; however, higher concentrations of arsenite were required to produce a significant (P less than 0.05) comutagenic response with UVB. The increased mutagenicity of UVB and UVA by arsenite may play a role in arsenite-related skin cancers.

Animals↗

PubMed1992

[The significance of the family anamnesis in women with breast carcinoma].

A cancer-related family history was ascertained in 600 women with breast cancer. Prevalence data in the families were compared to the data of the population-based Basel cancer registry. Breast cancer occurrence was increased in first degree female relatives (relative risk: 1.7; 95% confidence interval: 1.4-1.9; p less than 0.0001). Breast cancer risk in relatives decreased with increasing age of the probands. Women at elevated breast cancer risk can be identified by obtaining a family history of breast cancer patients.

Adult↗

PubMed1991

Pollution, carcinogenesis and cancer prevention.

Epidemiological and other data indicate that most cancer is due to environmental factors in the broader sense of the term and, therefore, presumably preventable to a great extent. Consequently, the identification of carcinogens in the environment is of fundamental importance in cancer prevention. Oncogene research has given new insight into the cellular signal pathways, as well as genetic alterations leading to neoplastic growth. This information provides a foundation for improvement of the current testing strategy for carcinogenic chemicals released into the environment. The testing protocols must take into consideration the carcinogenic agents that act through both genotoxic and non-genotoxic mechanisms. Also, it should be pointed out that human exposure often involves complex mixtures of chemicals, and the possibility of interactions between initiating and promoting carcinogens. Current test procedures rarely deal with such chemical interactions. Analyses of environmental factors responsible for the induction of cancer in humans indicate that naturally-occurring, rather than man-made, chemicals constitute a prevalent cancer risk. It must, however, be stressed that this conclusion applies to Western industrialized countries. In eastern European and developing countries, environmental pollutants, synthetic pesticides and other man-made chemicals very likely pose a larger cancer risk for the general population.

Animals↗

PubMed1998

[Prevalence of thyroid cancer in Réunion from scintigraphic data].

This work is a retrospective two years study of thyroid cancer, diagnosed in Reunion Island, using scintigraphic cold regions. Between April 1993 and April 1995, 1,364 thyroid scintigraphic studies were performed in the CHD F. Guyon at Saint Denis, Réunion). These studies resulted from all types of indication and of them 691 had cold regions, with 22 thyroid cancers among them, (i.e. a prevalence of 3.20% of cold areas). Analysis of these cancers allowed recognition of various characteristics. A large majority (82%) were in females, whose median age at the time of diagnosis was 49 years (as opposed to 48 years for the male patients). The associated cold zones were usually isolated cold nodules. Anatomical pathology investigation indicated six were papillary, five mixed, three vesicular nodule, four microcarcinoma, one each of anaplastic, one follicullar thyroid carcinoma, and two were metastases. Their geographical distribution was superposed on their medical demography. Treatment was surgical, but a variety of procedures was used. Generally the diagnostical, therapeutical and follow up procedures were not standardised. Needle cell biopsy was virtually excluded from the decision-making trees and a variety of protocols was used. In addition there are no local epidemiological data available concerning thyroid cancers. An improved method for dealing with these cancers appears to be essential for Reunion. It must be associated with a greater awareness from medical practitioners, agreement on procedures for diagnosis, treatment and follow up and the setting up of a register for thyroid cancer in the "Department". Some thought before detailed involvement should be given to the setting up of a team, trained in needle cell biopsy, and an associated metabolic radiotherapy facility, so allowing appropriate procedures and follow up for thyroid cancers in this "Department".

Adenocarcinoma, Follicular↗

PubMed2005

Cancer-related anemia: pathogenesis, prevalence and treatment.

Cancer-related anemia is a cytokine-mediated disorder resulting from complex interactions between tumor cells and the immune system. Overexpression of certain inflammatory cytokines results in shortened survival of red blood cells, suppression of erythroid progenitor cells, impaired iron utilization, and inadequate erythropoietin production. Numerous other factors may also contribute to the development of anemia in cancer patients. The European Cancer Anaemia Survey (ECAS) has provided the most current, comprehensive, prospectively collected data on the incidence and prevalence of anemia among cancer patients, as well as important perspectives on anemia treatment and relationship of hemoglobin and performance status. ECAS enrolled over 15,000 treated and untreated patients with various malignancies from cancer centers in 24 European countries and followed them for up to 6 months. The initial analysis of the ECAS data revealed that 39% of the total cancer patient population was anemic (hemoglobin <12.0 g/dl) at enrollment, although the rate varied according to tumor type, disease status, and cancer treatment status. Of the patients who were not anemic at enrollment and started cancer treatment during the survey, those undergoing chemotherapy--either alone or in combination with radiotherapy--had the highest incidence of anemia (63 and 42%, respectively). Low hemoglobin levels correlated with poor performance status and only 40% of patients who were anemic at some time during the survey received treatment for their anemia. These findings are noteworthy, since a growing body of clinical evidence indicates that the treatment of anemia can significantly improve patients' quality of life and may also improve the clinical outcome.

Anemia, Hypochromic↗

PubMed2026

Systemic treatment of advanced pancreatic cancer: A Comprehensive Review.

IMPORTANCE: Pancreatic adenocarcinoma (PDAC) is an uncommon but potentially catastrophic diagnosis with historically poor prognosis. It is the tenth most prevalent cancer in the US & UK. Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies worldwide, with a five-year survival rate of approximately 10%. Despite increasing understanding of its molecular biology, systemic treatment options for advanced disease remain limited, and survival outcomes have improved only modestly over the past decade. OBSERVATIONS: This narrative review traces the evolution of systemic therapy for advanced PDAC from gemcitabine monotherapy through the landmark FOLFIRINOX (PRODIGE trial) and gemcitabine/nab-paclitaxel (MPACT trial) combination regimens, which remain the standard of care. Second-line options including liposomal irinotecan plus 5-FU/LV (NAPOLI-1) and maintenance olaparib for germline BRCA1/2-mutated disease (POLO) are also reviewed. Emerging data on sequential treatment strategies (SEQUENCE trial), biomarker-driven treatment selection (PRIMUS-001, PASS-01), and precision medicine approaches targeting actionable molecular subgroups, including dMMR/MSI-H, NTRK fusions, and homologous recombination deficiency are discussed. Real-world evidence comparing FOLFIRINOX and gemcitabine/nab-paclitaxel is critically appraised, including the challenges of patient selection, tolerance, and applicability outside clinical trial settings. CONCLUSION AND RELEVANCE: Despite incremental progress, the treatment landscape of advanced PDAC remains challenging. Molecular stratification and biomarker-driven precision oncology represent the most promising path forward. This review serves as a clinical reference for physicians managing advanced pancreatic cancer, highlighting current evidence, evidence limitations, and future research priorities including prospective biomarker-driven trials and improved access to genomic testing.

Biomarkers↗

PubMed1988

The elderly population. Opportunities for cancer prevention and detection.

Interest in the elderly population, persons 65 years of age or older, as a target group for cancer control has not been great. Age recommendations rarely are made for prevention and early detection of cancer for elderly persons. However, cancer incidence and mortality rates are known to rise rapidly with increasing age. This paper takes a long-term public-health perspective to look toward the year 2030 to discuss the challenges of organizing and implementing prevention and early detection incentives for our nation's current and future elderly population. Cancer prevalence estimates in the context of the geriatric imperative of the 21st century are provided for three cancers--breast, prostate, and lung and bronchus. The sheer magnitude of numbers created by the aged population expansion can greatly increase the number of cancer survivors and newly diagnosed cases. Current efforts in cancer prevention and early detection should anticipate the health-care demands of the elderly in the first three decades of the next century.

Adult↗

PubMed2005

Gastrointestinal stem cells and cancer: bridging the molecular gap.

Cancer is believed to be a disease involving stem cells. The digestive tract has a very high cancer prevalence partly owing to rapid epithelial cell turnover and exposure to dietary toxins. Work on the hereditary cancer syndromes including familial adenomatous polyposis (FAP) has led to significant advances, including the adenoma-carcinoma sequence. The initial mutation involved in this stepwise progression is in the "gatekeeper" tumor suppressor gene adenomatous polyposis coli (APC). In FAP somatic, second hits in this gene are nonrandom events, selected for by the position of the germ-line mutation. Extensive work in both the mouse and human has shown that crypts are clonal units and mutated stem cells may develop a selective advantage, eventually forming a clonal crypt population by a process called "niche succession." Aberrant crypt foci are then formed by the longitudinal division of crypts into two daughter units--crypt fission. The early growth of adenomas is contentious with two main theories, the "top-down" and "bottom-up" hypotheses, attempting to explain the spread of dysplastic tissue in the bowel. Initial X chromosome inactivation studies suggested that colorectal tumors were monoclonal; however, work on a rare XO/XY human patient with FAP and chimeric Min mice showed that 76% of adenomas were polyclonal. A reduction in tumor multiplicity in the chimeric mouse model has been achieved by the introduction of a homozygous tumor resistance allele. This model has been used to suggest that short-range interaction between adjacent initiated crypts, not random polyp collision, is responsible for tumor polyclonality.

Adenomatous Polyposis Coli↗

PubMed1990

[Are industrial toxic substances a risk factor in gallbladder cancer?].

Increased prevalence of gallbladder cancer has been related to specific occupations and suggests a possible professional exposure to carcinogens. The authors report the case of a 64-year-old woman who had a squamous cell carcinoma of the gallbladder with hepatic metastases, and professional exposure to trichloroethylene in a degreasing metal laboratory. Although trichlorothylene could not be assumed to be a true carcinogen for gallbladder cancer, this case underscores that epidemiologic studies taking into account professional exposure, in addition to the usual risk factors of gallbladder cancer, are requested, in order to detect a new patient group at risk for gallbladder cancer.

Carcinoma, Squamous Cell↗

PubMed1998

Alcohol-related cancers and aldehyde dehydrogenase-2 in Japanese alcoholics.

Aldehyde dehydrogenase-2 (ALDH2) eliminates most of the acetaldehyde produced during alcohol metabolism. In some drinkers, a mutant ALDH2 allele contributes to diminished activity of the enzyme, dramatically increasing the risk for esophageal cancer. This study was designed to evaluate the ALDH2 gene polymorphism as a predictor of the development of cancers prevalent in Japanese alcoholics. We performed ALDH2 genotyping on lymphocyte DNA samples from Japanese alcoholic men (487 cancer-free; 237 with cancer, including 34 oropharyngolaryngeal, 87 esophageal, 58 stomach, 46 colon, 18 liver, 7 lung, 9 other sites, and 19 multiple primary cancers in two or three organs). The frequencies of the mutant ALDH2*2 allele were significantly higher in alcoholics with oropharyngolaryngeal (52.9%), esophageal (52.9%), stomach (22.4%), colon (21.7%) and esophageal cancer concomitant with oropharyngolaryngeal and/or stomach cancer (78.6%), than in cancer-free alcoholics (9.0%). After adjustment for age, daily alcohol consumption and amount of cigarette smoking, significantly increased risks (odds ratios) in the presence of the ALDH2 *2 allele were found for oropharyngolaryngeal (11.14), esophageal (12.50), stomach (3.49), colon (3.35), lung (8.20) and esophageal cancer concomitant with oropharyngolaryngeal and/or stomach cancer (54.20) but not for liver or other cancers. These results suggest a general role of acetaldehyde, a recognized animal carcinogen, in the development of human cancers.

Adult↗

PubMed2003

Role of DNA mismatch repair defects in the pathogenesis of human cancer.

The DNA mismatch repair (MMR) system is necessary for the maintenance of genomic stability. In a broad sense, all main functions of the MMR system, including the correction of biosynthetic errors, DNA damage surveillance, and prevention of recombination between nonidentical sequences serve this important purpose. Failure to accomplish these functions may lead to cancer. It is therefore not surprising that inherited defects in the MMR system underlie one of the most prevalent cancer syndromes in humans, hereditary nonpolyposis colon cancer (HNPCC). In addition, acquired defects of the same system may account for 15% to 25%, or even a higher percentage, of sporadic cancers of different organs of the "HNPCC spectrum," including the colon and rectum, uterine endometrium, stomach, and ovaries. Recent studies indicate that the MMR genes may be involved in the pathogenesis of even a broader spectrum of tumors in one way or another. An updated review of the different features of the human MMR system will be provided, with the emphasis on their implications in cancer development.

Colorectal Neoplasms, Hereditary Nonpolyposis↗

PubMed1994

Cancer mortality in Maryland: when being a leader is not best.

Maryland has the second highest statewide cancer mortality rate in the nation. This ranking is primarily due to high death rates for the most prevalent cancers: lung, breast, colon, and prostate. Based on the recent literature and the October 1991 preventive medicine grand rounds at the Johns Hopkins University School of Hygiene and Public Health, this paper summarizes several current viewpoints on cancer mortality in Maryland and the progress that has been made by recently instituted state and community initiatives.

Female↗

PubMed2003

Association of a polymorphism of the phospholipase D2 gene with the prevalence of colorectal cancer.

Phospholipase D plays an important role in transmembrane signaling in a variety of cell types and its activity is increased in certain cancers, suggesting that it also contributes to tumorigenesis. A C-->T transition at nucleotide 1814 of the human phospholipase D(2) gene, which results in a Thr-->Ile substitution at amino acid 577, was noted in the GenBank database. The relationship of this polymorphism to the prevalence of cancer of the esophagus, stomach, colon-rectum, lung, and breast in Japanese was investigated in a case-control study. The genotype of the phospholipase D(2) gene was determined by the polymerase chain reaction with confronting two-pair primers. Multivariate logistic regression analysis with adjustment for age, gender, and smoking status revealed that the frequency of the T allele of the 1814C-->T polymorphism was significantly higher in individuals with colorectal cancer than in controls. A significant association of the polymorphism with the prevalence of colorectal cancer was found in analyses assuming either dominant (TT+CT vs. CC) or additive (CT vs. CC) effects of the T allele, but the T allele was not associated with the prevalence of esophageal, gastric, lung, or breast cancer. The activities of phospholipase D in cell lysates or membrane fractions did not differ between cells transfected with cDNAs encoding the Thr-577 or Ile-577 variants of phospholipase D(2). These results suggest that the phospholipase D(2) gene is a susceptibility locus for colorectal cancer in Japanese individuals, although a functional effect of the 1814C-->T (Thr577Ile) polymorphism was not detected.

Colorectal Neoplasms↗