The incidence and prevalence of cancer in the United Arab Emirates.
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Adult↗
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Results for “Cancer Prevalence”
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Estimated point prevalence of cancer in Japan.
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Adult↗
Prevalence of cancer in older persons living at home and in institutions.
Even though the elderly have the greatest risk of developing and dying of cancer, screening for cancer occurs less often in older persons. Cancer screening is appropriate for nursing home residents with the cognitive ability to understand the screening method and its implications, who do not have comorbid illnesses that would preclude treatment, and who have at least a five-year life expectancy. Screening recommendations are provided for cancers of the breast, cervix, prostate, colon, skin, and mouth.
Age Distribution↗
Frequency of gallbladder cancer in Chile, a high-risk area.
We report an autopsy study of gallbladder cancer prevalence in Chile, where the risk of this disease is among the highest reported world-wide. In 14,768 autopsy protocols obtained from 3 university hospitals, 45% of women and 20% of men older than 20 years had gallstone disease (the major known risk factor for gallbladder cancer). The prevalence of gallbladder cancer in Chileans was compared to that found in a Swedish-Czechoslovakian autopsy study previously published. These countries were chosen because of their high frequency of gallstone disease. The comparison was performed by using logistic regression models adjusting for possible differences in the age-sex structure or the true incidence of gallstones in both populations. We found that the most important single risk factor for gallbladder cancer in Chile was gallstone disease, with an estimated effect on the logistic scale meaning that the cancer risk for subjects with gallstones is seven times higher than for those without the disease. Second in importance was the risk for sex, women being 2.8 times higher than for men. The estimated difference in the sex composition and the incidence of gallstones resulted in 17.9% higher odds of cancer in Chile than in Sweden and Czechoslovakia. However, this difference was not significant. This study suggests that the major etiologic factors of gallbladder cancer in Chileans, Swedes and Czechoslovakians are primarily related to gallstone disease.
Adult↗
Decreased prevalence of gallstones in gastric cancer.
The prevalence of gallstones and the frequency of previously performed cholecystectomy were examined in 498 autopsy subjects who had gastric cancer and their age- and sex-matched control subjects. The frequency of gallstones not treated by operation and previous cholecystectomy was significantly (p less than 0.01) lower in those with gastric cancer than in the matched-control subjects. It is not possible to determine on the basis of this study what the possible factors that cause this phenomenon are.
Adult↗
Advances in diagnostic practices affect thyroid cancer incidence in France.
OBJECTIVE: To analyse trends in diagnostic practices of thyroid diseases and to relate them to the increase in thyroid cancer incidence in France over time. DESIGN: From 1980 to 2000, a French retrospective multicentric (three endocrinology and three nuclear medicine centres) study of thyroid diseases was conducted on 20 consecutive unselected patients' records, sampled every 5 years in each centre. METHODS: Characteristics of the population and diagnosis procedures (thyroid ultrasonography (US), radionuclide scan, cytology and hormonal measurements) were described over time. Changing trends in operated patients and in cancer prevalence were analysed as well as the impact of practices on cancer incidence. RESULTS: The study included 471 patients (82% female, mean age 46.7, range 9-84 years), referred for nodular thyroid diseases (66.7%) or thyroid dysfunctions (33.3%). A significant increase in US (3 to 84.8%) and cytological practices (4.5 to 23%), and a decrease (89.4 to 49.6%) in radionuclide scan procedures were observed over time. Although the proportion of patients undergoing surgery remained constant (24.8%), the prevalence of cancer increased among operated patients from 12.5 to 37% (P=0.006). In a Cox's proportional hazard model stratified on the clinical characteristics of patients, only the cytological practice, regardless of its results, was significantly associated with the occurrence of cancer: relative risk (RR)=4.4 (95% confidence interval (CI): 1.1-16; P=0.04). CONCLUSIONS: From 1980 to 2000, a major evolution in clinical practices has led to the increase in thyroid cancer reported in France. Such changes in medical, as well as in surgical and pathological, practices must be taken into account in incidence measurement.
Adolescent↗
[Prevalence of thyroid cancer in hot nodules].
The prevalence of thyroid cancer is not nodules is low, as it is estimated to be between 0 and 4% in adults. In order to more accurately estimate this prevalence and to recommend optimal treatment, 93 hot nodules operated between 1976 and 1995 were reviewed. 52 of these subjects (56%) were euthyroid, 11 (12%) suffered from clinical hyperthyroidism and 30 (32%) a presented subclinical hyperthyroidism. All patients were operated for a hot nodule, 1.5 to 6 cm in diameter. Two groups of patients were considered on the basis on the histological examination. Group I consisted of 47 patients (39 F, 8 M, mean age: 44 years +/- 15) with multinodular goitre; 16 (34%) of them underwent total thyroidectomy. Group II was composed of 46 patients (38 F, 8 M, mean age: 44 years +/- 15) with a solitary hot nodule; 39 (85%) patients underwent unilateral lobectomy. Microscopic carcinoma (diameter less tha 1 cm) ws discovered in 2(4%) patients of group 1 and 5 (11%) patients of group 11, corresponding to a total prevalence of 7/93 (7.5%). The microscopic carcinoma was located in the nodule or in the capsule in four cases, and away from the nodule but in the ipsilateral lobe in three cases. In every case, this was an incidental finding and no clinical features distinguished patients with or without microscopic carcinoma. This study suggests that the probability of discovering a microscopic carcinoma associated with a hot nodule is considerable. However, microscopic carcinoma is an incidental discovery in a number of subjects undergoing thyroidectomy and is present in 10 to 20% of autopsied thyroids. As surgical treatment is devoid of risks, it appears indicated, particularly when the nodule exceeds 3 cm in diameter.
Adolescent↗
Racial differences in a prostate cancer screening study.
PURPOSE: We attempted to determine whether black men have a higher prostate cancer prevalence and more advanced disease. MATERIALS AND METHODS: We screened 17,157 white and 804 black men 50 years old or older by serum prostate specific antigen measurement and digital rectal examination. We recommended biopsy when either test was suspicious. RESULTS: Black men had a higher prevalence of elevated prostate specific antigen (13.1 versus 8.9%) and cancer (5.1 versus 3.2%) than white men, and a higher prevalence of clinically but not pathologically advanced cancer. Fewer black men in lower income zip codes complied with recommendations for biopsy. CONCLUSIONS: In our screening study black men had a higher prevalence of detectable cancer. However, unlike in clinical studies there was no striking racial difference in advanced cancer stage at diagnosis.
Aged↗
Human prostate cancer: a direct role for oestrogens.
We have studied the response to oestrogen and expression of oestrogen receptors in responsive LNCaP and androgen non-responsive PC3 human prostate cancer cell lines. Growth of LNCaP cells is significantly stimulated by physiological concentrations of oestradiol; this growth increase appears to be comparable to that induced by either testosterone or dihydrotestosterone. In contrast, oestradiol significantly inhibits the proliferation of PC3 cells. We also present novel evidence for functional oestrogen binding in LNCaP cells. This evidence was first obtained by means of radioligand binding assays and was further corroborated using: (a) immunocytochemical analysis of oestrogen and progesterone receptors; (b) reverse transcriptase polymerase chain reaction of oestrogen receptor mRNAs; and (c) immunofluorescence of the 27 kDa heat shock protein (Hsp27), which has been reported to be a marker of functional oestrogen receptors. There appeared to be significantly and consistently lower levels of oestrogen receptor expressed in PC3 cells than in LNCaP cells. The observation that oestradiol-induced growth of LNCaP cells is completely reversed by the pure anti-oestrogen ICI 182,780 clearly implies that the biological response of these cells to oestradiol is mediated mainly via its own receptor. On the other hand, use of a neutralizing antibody against transforming growth factor (TGF)-beta 1 results in a remarkable increase in the growth of PC3 cells; this effect is almost completely abolished after the addition of oestradiol. This suggests that the oestradiol-induced growth inhibition may be mediated by TGF-beta 1. These results suggest that the current model for hormone-dependence of human prostatic carcinoma should be revised. This is of special concern, because recent data indicate that prostate cancer has become the most prevalent cancer and the second principal cause of cancer death in western countries.
Cell Division↗
Growth inhibition, cell-cycle dysregulation, and induction of apoptosis by green tea constituent (-)-epigallocatechin-3-gallate in androgen-sensitive and androgen-insensitive human prostate carcinoma cells.
Prostate cancer (PCA) is the most prevalent cancer diagnosed and the second leading cause of cancer-related deaths among men in the United States. Descriptive epidemiological data suggest that androgens and environmental exposures play a key role in prostatic carcinogenesis. Since androgen action is intimately associated with proliferation and differentiation, at the time of clinical diagnosis in humans most PCA represent themselves as a mixture of androgen-sensitive and androgen-insensitive cells. Androgen-sensitive cells undergo rapid apoptosis upon androgen withdrawal. On the other hand, the androgen-insensitive cells do not undergo apoptosis upon androgen blocking, but maintain the molecular machinery of apoptosis. Thus, agents capable of inhibiting growth and/or inducing apoptosis in both androgen-sensitive and androgen-insensitive cells will be useful for the management of PCA. In the present study, we show that (-)-epigallocatechin-3-gallate (EGCG), the major polyphenolic constituent present in green tea, imparts antiproliferative effects against both androgen-sensitive and androgen-insensitive human PCA cells, and this effect is mediated by deregulation in cell cycle and induction of apoptosis. EGCG treatment was found to result in a dose-dependent inhibition of cell growth in both androgen-insensitive DU145 and androgen-sensitive LNCaP cells. In both the cell types, EGCG treatment also resulted in a dose-dependent G(0)/G(1)-phase arrest of the cell cycle as observed by DNA cell-cycle analysis. As evident by DNA ladder assay, confocal microscopy, and flow cytometry, the treatment of both DU145 and LNCaP cells with EGCG resulted in a dose-dependent apoptosis. Western blot analysis revealed that EGCG treatment resulted in (i) a dose-dependent increase of p53 in LNCaP cells (carrying wild-type p53), but not in DU145 cells (carrying mutant p53), and (ii) induction of cyclin kinase inhibitor WAF1/p21 in both cell types. These results suggest that EGCG negatively modulates PCA cell growth, by affecting mitogenesis as well as inducing apoptosis, in cell-type-specific manner which may be mediated by WAF1/p21-caused G(0)/G(1)-phase cell-cycle arrest, irrespective of the androgen association or p53 status of the cells.
Androgens↗
New chemotherapeutic strategies in colorectal cancer.
Since colorectal cancer is the second most prevalent cancer worldwide, its treatment remains a major challenge for researchers, gastroenterologists and oncologists. Despite curative resections, half of all patients diagnosed with colorectal cancer die because of their underlying disease. Integral chemotherapeutic components of standard regimens are 5-fluorouracil (5-FU), its modulation by folinic acid and irinotecan or oxaliplatin. All these drugs sequentially given have results in terms of median overall survival of more than 20 months in the palliative treatment of advanced colorectal cancer. Oral fluoropyrimidines, currently under clinical investigation, are likely to substitute continuous 5-FU. Inhibitors of growth factor receptors or their signaling may further prolong disease-free and overall survival rates. Preliminary evidence exists that improved adjuvant and neoadjuvant chemotherapy strategies may further improve the prognosis, mainly because more patients are able to go for primary or secondary surgery with curative intent.
Administration, Oral↗
Anticancer effects of ethanolic neem leaf extract on prostate cancer cell line (PC-3).
Prostate cancer (PC) is the most prevalent cancer and the leading cause of male cancer death. Azadirachta indica (neem tree) has been used successfully centuries to reduce tumors by herbalists throughout Southeast Asia. Here the present study indicated that an ethanolic extract of neem has been shown to cause cell death of prostate cancer cells (PC-3) by inducing apoptosis as evidenced by a dose-dependent increase in DNA fragmentation and a decrease in cell viability. Western blot studies indicated that treatment with neem extract showed decreased level of Bcl-2, which is anti-apoptotic protein and increased the level of Bax protein. So the neem extract could be potentially effective against prostate cancer treatment.
Antineoplastic Agents, Phytogenic↗
Multiple human papillomavirus genes affect the adeno-associated virus life cycle.
The risk of cervical cancer, one of the most prevalent cancers in the world, is determined by two viruses. Human papillomavirus (HPV) is the main risk factor for developing cervical cancer. However, although little known, it is well substantiated that the human Parvovirus adeno-associated virus type 2 (AAV), and its encoded Rep78 protein, interacts with HPV and lowers the risk of cervical cancer. HPV also contributes to AAV inhibition by serving as a helper virus for AAV and stimulating higher AAV replication levels. Here we surveyed four HPV-16 early genes, E1, E2, E6 and E7, for their ability to increase/decrease the basal level of AAV replication in stratifying squamous epithelium (the epithelial raft culture system). It was found that the HPV-16 E1, E2 and E6 genes were able to help/enhance AAV-2 replication in epithelial raft cultures. Under these conditions, with all the HPV genes being expressed from the AAV p5 promoter, E1 appeared to have the strongest enhancing effect on AAV DNA replication (Southern blot), RNA expression (RT-PCR), protein expression (Western blot) and AAV virion production (2 plate-Southern blot). Further study of E1 mutants showed that the carboxy-half of E1, the putative helicase/ATPase domain, was the main contributor of helper activity. These data are important for understanding the HPV-AAV interaction and its effect on modifying cervical cancer risk. These data also suggest the possibility that the identified HPV helper genes may be useful in the generation of recombinant (r)AAV virions for gene therapy, as rAAV is increasing in popularity for such purposes.
Capsid Proteins↗
Androgen receptor signaling in androgen-refractory prostate cancer.
Prostate cancer is the second most prevalent cancer in males in the United States. Standard therapy relies on removing, or blocking the actions of, androgens. In most cases, this therapy results in a regression of the cancer because the prostate and most primary prostate tumors depend on androgens for growth and the avoidance of apoptosis. However, a portion of the cancers eventually relapse, at which point they are termed "androgen refractory" and can no longer be cured by conventional therapy of any type. The precise molecular events that lead from androgen-sensitive prostate cancer to androgen-refractory prostate cancer are, therefore, of great interest. This review seeks to identify specific molecular events that may be linked directly to the progression to androgen-refractory cancer. Some of the mechanisms appear to involve the androgen receptor (AR) directly and include mutations in, or amplification of, the AR gene in a manner that allows the AR to respond to low doses of androgens, other steroids, or antiandrogens. In a less direct manner, coactivators may increase the sensitivity of the AR to androgens and even other nonandrogenic substances through a number of mechanisms. Additional indirect mechanisms that do not result from mutation of the AR may involve activation of the AR by peptide growth factors or cytokines or may involve bypassing the AR entirely via other cellular pathways. Identification of the role of these mechanisms in the progression to androgen-refractory prostate cancer is critical for developing therapies capable of curing this disease.
Androgens↗
Role of oxidative stress and the antioxidant network in cutaneous carcinogenesis.
Melanoma and nonmelanoma skin cancers are among the most prevalent cancers in the human population. Solar ultraviolet radiation is considered a major etiological factor but the relationship between dose, timing, and nature of exposure to tumor development is still unclear. Free radicals are generated by normal physiologic processes, including aerobic metabolism and inflammatory response, but may inflict cellular damage when generation is increased and antioxidant defense mechanisms are overwhelmed. Important findings supporting the free radical hypothesis in skin carcinogenesis are: (1) Reactive oxygen species (ROS) are generated in UVA- and UVB-irradiated skin in excessive doses, (2) the natural cutaneous antioxidant defense is impaired upon UV-exposure, (3) free radicals are involved in all steps of carcinogenesis, (4) supplementation with antioxidants can inhibit skin carcinogenesis, and (5) conditions that increase ROS generation enhance photocarcinogenesis. These findings provide a promising rationale for the development of powerful new antioxidant strategies in the prevention and therapy of skin cancer.
Antioxidants↗
Telomerase. A target for anticancer therapy.
Telomerase is absent in most normal tissues, but is abnormally reactivated in all major cancer types. Telomerase enables tumor cells to maintain telomere length, allowing indefinite replicative capacity. Albeit not sufficient in itself to induce neoplasia, telomerase is believed to be necessary for cancer cells to grow without limit. The presence of telomerase has been detected in virtually all cancer types including the most prevalent cancers of the prostate, breast, lung, colon, bladder, uterus, ovary, and pancreas as well as in lymphomas, leukemias, and melanomas. In addition, data from cancer patients indicate that telomerase levels correlate with clinical outcome in neuroblastomas, leukemias, and prostate, gastric, and breast cancers. Studies using an antisense to the human telomerase RNA component demonstrate that telomerase in human tumor lines can be blocked ex vivo. In these experiments, telomerase inhibition led to telomere shortening and cancer cell death, validating telomerase as a target for anticancer therapy. Telomerase is a uniquely appealing target for drug discovery because its dichotomic expression in normal versus cancer cells suggests that no serious side effects would result from a treatment abrogating telomerase activity. A variety of approaches to telomerase inhibition are being investigated and are discussed.
Enzyme Inhibitors↗
First- and second-line therapy of metastatic colorectal cancer.
In the USA, colorectal cancer is the fourth most prevalent cancer and is the second leading cause of cancer death after lung cancer. In 2006, 148,610 colorectal cancer cases are expected in the USA, with 55,170 deaths expected from this disease. After years of stagnation, the treatment of metastatic colorectal cancer has recently made dramatic advances. The previous standard of care, 5-fluorouracil, is the now the backbone of combination regimens with oxaliplatin or irinotecan. The addition of biological agents, such as the vascular endothelial growth factor inhibitor, bevacizumab, and the epidermal growth factor receptor inhibitors, cetuximab and panitumumab, have further enhanced the activity of conventional chemotherapy. These advances have increased the overall survival of advanced colorectal cancer patients, which was once 6 months with best supportive care, to over 2 years if all active agents are used in the course of the disease.
Antibodies, Monoclonal↗
Screening, prevention and socioeconomic costs associated with the treatment of colorectal cancer.
Colorectal cancer (CRC), the third most prevalent cancer worldwide, imposes a significant economic and humanistic burden on patients and society. One study conservatively estimated the annual expenditures for colorectal cancer to be approximately dollars US 5.3 billion in 2000, including both direct and indirect costs. However, other investigators estimated inpatient costs alone incurred in the US in 1994 to be around dollars US 5.14 billion. Therefore, the economic burden of colorectal cancer in the US could be projected to be somewhere in the range of dollars US 5.5-6.5 billion by considering that inpatient costs approximate 80% of total direct costs. No worldwide data have been published, but assuming that the US represents 25-40% of total expenditures in oncology, as seen for breast and lung cancers, a rough estimate for colorectal cancer would be in the range of dollars US 14-22 billion. Screening helps increase patient survival by diagnosing colorectal cancer early. The ideal method among the four tests most used (faecal occult blood test, flexible sigmoidoscopy, colonoscopy and double contrast barium enema) has not been identified. Economic studies of colorectal cancer screening are complex because of the many variables involved, as well as the fact that the outcomes must be followed for many years, and the lack of consensus on screening guidelines. Intuitively, modelling colorectal cancer is one way to overcome these hurdles; published modelling studies predict colorectal cancer screening programs to be within the threshold of dollars US 40000 per life-year saved. The faecal occult blood test appears to be the only clearly effective test, both from a clinical and an economic viewpoint. Important limitations are the invasiveness and inconvenience of the screening procedures, except faecal occult blood test. Patients' comfort and satisfaction are essential in improving compliance with screening recommendations, which appears to be low even in the US (35% of the general population aged over 40 years and 60% of the high-risk population), the country with the highest awareness and compliance in the world. Since colorectal cancer is generally a disease of the elderly, its economic burden is expected to grow in the near future, mainly due to population aging. Potential avenues to pursue in order to contain or reduce the economic burden of colorectal cancer would be the design and implementation of efficient screening programmes, the improvement of patient awareness and compliance with screening guidelines, the development of appropriate prevention programs (i.e. primary and secondary), and earlier diagnosis.
Antineoplastic Agents↗