Epidemiology of cervical cancer.
TL;DR: Variation in the incidence of cervical cancer is also present within countries, where rural and poor areas have the highest rates.
Abstract: In 1985, 7.6 million cases of cancer were diagnosed in 24 different regions all over the world (1). Globally, cervical cancer is the fifth most frequent malignancy and second among women, with an annual estimate of 471,000 new cases and 213,000 deaths. The age-adjusted incidence rates for developed countries are 7.6 to 11.8 per 105 and for developing countries, 17.6 to 46.8 per 105 (1,2). This variation in the incidence of cervical cancer is also present within countries, where rural and poor areas have the highest rates.
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TL;DR: Data demonstrate that p16INK4a is a specific biomarker to identify dysplastic cervical epithelia in sections of cervical biopsy samples or cervical smears and that Dysplastic cells could also be identified in cervicalsmears using a specific p16ink4a monoclonal antibody.
Abstract: Cytological screening for cervical cancer or its precursors using Papanicolaou's smear test (Pap test) has been highly efficient to reduce the morbidity and mortality of cervical cancer. However, evaluation of the Pap test relies on subjective diagnostic parameters and is affected by a high rate of false-positive and false-negative results. More objective diagnostic parameters to identify truly dysplastic or neoplastic cells in cervical smears as well as in cervical biopsy samples would therefore avoid insecurity for many patients and the high screening costs associated with repeated testing. Cervical dysplasia is induced by persistent infections through high-risk types of human papillomaviruses (HPVs). Outgrowth of dysplastic lesions is triggered by increasing expression of two viral oncogenes, E6 and E7, which both interact with various cell cycle-regulating proteins. Among these is the retinoblastoma gene product pRB, which is inactivated by E7. pRB inhibits transcription of the cyclin-dependent kinase inhibitor gene p16INK4a. Increasing expression of the viral oncogenes in dysplastic cervical cells might thus be reflected by increased expression of p16INK4a. In line with this hypothesis, we observed marked overexpression of p16INK4a in all cervical intraepithelial neoplasm (CIN) I lesions (n = 47) except those associated with low-risk HPV types (n = 7), all CIN II lesions (n = 32), all CIN III lesions (n = 60) and 58 of 60 invasive cervical cancers. In contrast, no detectable expression of p16INK4a was observed in normal cervical epithelium (n = 42), inflammatory lesions (n = 48) and low-grade cervical lesions (CIN I) associated with low-risk HPV types (n = 7). Dysplastic cells could also be identified in cervical smears using a specific p16INK4a monoclonal antibody. These data demonstrate that p16INK4a is a specific biomarker to identify dysplastic cervical epithelia in sections of cervical biopsy samples or cervical smears. © 2001 Wiley-Liss, Inc.
1,012 citations
Additional excerpts
...Normal 42 42 (100) HPV negative 31 31 (100) LR-HPV 1 1 (100) HR-HPV 10 10 (100) Inflammation 48 35 (73) 10 (21) 3 (6) HPV negative 30 23 (77) 6 (20) 1 (3) HR-HPV 18 12 (67) 4 (22) 2 (11) Reserve cell hyperplasia 21 12 (57) 6 (28) 2 (10) 1 (5) HPV negative 12 7 (58) 3 (14) 2 (9) LR-HPV 1 1 (100) HR-HPV 8 4 (50) 3 (38) 1 (12) CIN I 47 7 (14) 2 (4) 10 (21) 29 (61) HPV negative 17 2 (12) 15 (88) LR-HPV 15 7 (47) 2 (13) 6 (40) HR-HPV 15 2 (13) 13 (87) CIN II 32 32 (100) HPV negative 14 14 (100) HR-HPV 18 18 (100) CIN III 60 60 (100) HPV negative 9 9 (100) HR-HPV 51 51 (100) Invasive carcinoma 60 2 (3) 58 (97) HPV negative 5 5 (100) HR-HPV 55 2 (4) 53 (96) Squamous 53 1 (2) 52 (98) Adenomatous 7 1 (14) 6 (86)...
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862 citations
TL;DR: The model approximates the age-specific incidence of cervical cancer and provides a tool for evaluating the natural history of HPV infection and cervical cancer carcinogenesis as well as the effectiveness and cost-effectiveness of primary and secondary prevention strategies.
Abstract: The authors constructed a Markov model as part of a systematic review of cervical cytology conducted at the Duke University Evidence-based Practice Center (Durham, North Carolina) between October 1997 and September 1998. The model incorporated states for human papillomavirus infection (HPV), low- and high-grade squamous intraepithelial lesions, and cervical cancer stages I-IV to simulate the natural history of HPV infection in a cohort of women from ages 15 to 85 years. The age-specific incidence rate of HPV, and regression and progression rates of HPV and squamous intraepithelial lesions, were obtained from the literature. The effects of varying natural history parameters on cervical cancer incidence were evaluated by using sensitivity analysis. The base-case model resulted in a lifetime cervical cancer risk of 3.67% and a lifetime cervical cancer mortality risk of 1.26%, with a peak incidence of 81/100,000 at age 50 years. Age-specific distributions of precursors were similar to reported data. Lifetime risk of cancer was most sensitive to the incidence of HPV and the probability of rapid HPV progression to high-grade lesions (two- to threefold variations in risk). The model approximates the age-specific incidence of cervical cancer and provides a tool for evaluating the natural history of HPV infection and cervical cancer carcinogenesis as well as the effectiveness and cost-effectiveness of primary and secondary prevention strategies.
465 citations
TL;DR: Criteria for successful screening is described, recent evidence and policy changes that have implications for cancer screening are discussed, and guidelines reviews that are underway are described.
Abstract: Each year, the American Cancer Society (ACS) publishes a summary of its recommendations for early cancer detection, including guideline updates, emerging issues that are relevant to screening for cancer, and a summary of the most current data on cancer screening rates for US adults. In 2006, there were no updates to ACS guidelines for early cancer detection. In this issue of the journal, we describe criteria for successful screening, discuss recent evidence and policy changes that have implications for cancer screening, summarize the ACS guidelines and describe guidelines reviews that are underway, and provide an update of the most recent data pertaining to participation rates in cancer screening from the Centers for Disease Control and Prevention's (CDC's) Behavioral Risk Factor Surveillance System (BRFSS) and the National Health Interview Survey (NHIS).
395 citations
TL;DR: This review discusses the recent nanotechnological strategies for siRNA delivery by using different carriers such as liposomes, dendrimers and carbon nanotubes.
314 citations
References
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TL;DR: This timely monograph is a distillation of knowledge of hepatitis B, C and D, based on a review of 1000 studies by a small group of scientists, and it is concluded that hepatitis D virus cannot be classified as a human carcinogen.
Abstract: Viral hepatitis in all its forms is a major public health problem throughout the world, affecting several hundreds of millions of people. Viral hepatitis is a cause of considerable morbidity and mortality both from acute infection and chronic sequelae which include, in the case of hepatitis B, C and D, chronic active hepatitis and cirrhosis. Hepatocellular carcinoma, which is one of the 10 commonest cancers worldwide, is closely associated with hepatitis B and, at least in some regions of the world, with hepatitis C virus. This timely monograph is a distillation of knowledge of hepatitis B, C and D, based on a review of 1000 studies by a small group of scientists. (It is interesting to note in passing that some 5000 papers on viral hepatitis are published annually in the world literature.) The epidemiological, clinical and experimental data on the association between infection with hepatitis B virus and primary liver cancer in humans are reviewed in a readable and succinct format. The available information on hepatitis C and progression to chronic infection is also evaluated and it is concluded (perhaps a little prematurely) that hepatitis C virus is carcinogenic. However, it is concluded that hepatitis D virus, an unusual virus with a number of similarities to certain plant viral satellites and viroids, cannot be classified as a human carcinogen. There are some minor criticisms: there are few illustrations and some complex tabulations (for example, Table 6) and no subject index. A cumulative cross index to IARC Monographs is of little value and occupies nearly 30 pages. This small volume is a useful addition to the overwhelming literature on viral hepatitis, and the presentation is similar to the excellent World Health Organisation Technical Reports series on the subject published in the past. It is strongly recommended as a readable up-to-date summary of a complex subject; and at a cost of 65 Sw.fr (approximately £34) is excellent value. A J ZUCKERMAN
11,533 citations
TL;DR: The results confirm the role of genitalHPVs, which are transmitted sexually, as the central etiologic factor in cervical cancer worldwide and suggest that most genital HPVs are associated with cancer, at least occasionally.
Abstract: Background Epidemiologic studies have shown that the association of genital human papillomavirus (HPV) with cervical cancer is strong, independent of other risk factors, and consistent in several countries There are more than 20 different cancer-associated HPV types, but little is known about their geographic variation Purpose Our aim was to determine whether the association between HPV infection and cervical cancer is consistent worldwide and to investigate geographic variation in the distribution of HPV types Methods More than 1000 specimens from sequential patients with invasive cervical cancer were collected and stored frozen at 32 hospitals in 22 countries Slides from all patients were submitted for central histologic review to confirm the diagnosis and to assess histologic characteristics We used polymerase chain reaction-based assays capable of detecting more than 25 different HPV types A generalized linear Poisson model was fitted to the data on viral type and geographic region to assess geographic heterogeneity Results HPV DNA was detected in 93% of the tumors, with no significant variation in HPV positivity among countries HPV 16 was present in 50% of the specimens, HPV 18 in 14%, HPV 45 in 8%, and HPV 31 in 5% HPV 16 was the predominant type in all countries except Indonesia, where HPV 18 was more common There was significant geographic variation in the prevalence of some less common virus types A clustering of HPV 45 was apparent in western Africa, while HPV 39 and HPV 59 were almost entirely confined to Central and South America In squamous cell tumors, HPV 16 predominated (51% of such specimens), but HPV 18 predominated in adenocarcinomas (56% of such tumors) and adenosquamous tumors (39% of such tumors) Conclusions Our results confirm the role of genital HPVs, which are transmitted sexually, as the central etiologic factor in cervical cancer worldwide They also suggest that most genital HPVs are associated with cancer, at least occasionally Implication The demonstration that more than 20 different genital HPV types are associated with cervical cancer has important implications for cervical cancer-prevention strategies that include the development of vaccines targeted to genital HPVs
3,272 citations
TL;DR: This study shows that the E6 protein of HPV-16 is capable of binding to the cellular p53 protein, providing further evidence that the human papillomaviruses, the adenovirus type 5, and SV40 may effect similar cellular pathways in transformation.
Abstract: Human papillomavirus type 16 (HPV-16) is a DNA tumor virus that is associated with human anogenital cancers and encodes two transforming proteins, E6 and E7. The E7 protein has been shown to bind to the retinoblastoma tumor suppressor gene product, pRB. This study shows that the E6 protein of HPV-16 is capable of binding to the cellular p53 protein. The ability of the E6 proteins from different human papillomaviruses to form complexes with p53 was assayed and found to correlate with the in vivo clinical behavior and the in vitro transforming activity of these different papillomaviruses. The wild-type p53 protein has tumor suppressor properties and has also been found in association with large T antigen and the E1B 55-kilodalton protein in cells transformed by SV40 and by adenovirus type 5, respectively, providing further evidence that the human papillomaviruses, the adenoviruses, and SV40 may effect similar cellular pathways in transformation.
2,520 citations
TL;DR: The annual incidence rates and numbers of new cases of 18 different cancers have been estimated for the year 1985 in 24 areas of the world and tobacco smoking and chewing are almost certainly the major prevent able causes of cancer today.
Abstract: The annual incidence rates (crude and age-standardized) and numbers of new cases of 18 different cancers have been estimated for the year 1985 in 24 areas of the world. The total number of new cancer cases (excluding non-melanoma skin cancer) was 7.6 million, 52% of which occur in developing countries. The most common cancer in the world today is lung cancer, accounting for 17.6% of cancers of men worldwide, and 22% of cancers in men in the developed countries. Stomach cancer is now second in frequency (it was slightly more common than lung cancer in 1980) and breast cancer—by far the most important cancer of women (19.1% of the total)—is third. There are very large differences in the relative importance of the different cancers by world area. The major cancers of developed countries (other than the 3 already named) are cancers of the colon-rectum and prostate, and, in developing countries, cancers of the cervix uteri, mouth and pharynx, liver and oesophagus. The implications of these patterns for cancer control, and specifically prevention, are discussed. Tobacco smoking and chewing are almost certainly the major prevent able causes of cancer today.
1,685 citations
TL;DR: The American Cancer Society's Department of Epidemiology and Statistics reports its 29th annual compilation of cancer incidence, survival and mortality data for the United States and around the world.
Abstract: The American Cancer Society's Department of Epidemiology and Statistics reports its 29th annual compilation of cancer incidence, survival and mortality data for the United States and around the world.
1,441 citations