220 research outputs found
Chapter 3: Cofactors in Human Papillomavirus Carcinogenesis--Role of Parity, Oral Contraceptives, and Tobacco Smoking
No full textPIN90 Towards Best Practices for Handling Uncertainties in Health Technology Assessments for HPV Vaccination to Better Inform Decision Making
No full textHead and neck cancers in Australia
No full textThis report on head and neck cancers in Australia presents the latest available information on incidence, mortality, survival and hospitalisations.
Overview
Head and neck cancer is a term used to describe a range of cancers that occur in the throat (pharynx and larynx), nose, sinuses and mouth.
This report presents the most recent data available on head and neck cancer incidence, mortality, survival and hospitalisations and also describes risk factors that can contribute to a person developing head and neck cancer.
The report also includes a \u27spotlight\u27 section which discusses the human papillomavirus (HPV) and how it contributes to head and neck cancers.
Incidence
The number of head and neck cancers diagnosed in Australia is increasing. From 1982 to 2009, the number of head and neck cancers diagnosed rose from 2,475 to 3,896.
While the number of cases diagnosed is rising, the age-standardised incidence rate for head and neck cancers fell from 19.3 per 100,000 persons in 1982 to 16.8 per 100,000 in 2009. Increases in the overall number of cases diagnosed are occurring, despite decreases in age-standardised incidence rates, because of Australia\u27s increasing and ageing population.
The number of cases diagnosed in 2009 was higher for males than females. Males accounted for 73.8% (2,875) of head and neck cancers compared to 26.2% (1,021) for females.
Mortality
Similar to the number of cases diagnosed, the number of deaths from head and neck cancers rose from 752 in 1982 to 944 in 2011.
The age-standardised mortality rate fell from 6.1 per 100,000 persons in 1982 to 3.8 per 100,000 in 2011. Increases in the overall number of deaths due to head and neck cancers are occurring, despite a drop in the age-standardised mortality rates, because of the growth and ageing of Australia\u27s population.
Males accounted for a higher number of deaths in 2011 than females, with 73.2% (691) of deaths from head and neck cancers among males compared to 26.8% (253) for females.
Survival
Overall survival from head and neck cancers is improving. There was a rise in 5-year relative survival from 61.8% in 1982-1987 to 68.2% in 2006-2010. One-year relative survival for males and females in 2006-2010 were broadly comparable. However, 5-year relative survival for females was higher at 70.4% compared to males at 67.4%.
Hospitalisations
Hositalisations for head and neck cancers are also rising. In 2011-12, there were 8,478 hospitalisations where head and neck cancer was the principal diagnosis. This was an increase of 13.8% from 2002-03 when there were 7,448 hospitalisations.
The number of hospitalisations for surgery where head and neck cancer was the principal diagnosis also increased over time, from 3,305 in 2002-03 to 3,725 in 2011-12. This was an overall increase of 12.7%
Human papillomavirus genotype distribution and cervical squamous intraepithelial lesions among high-risk women with and without HIV-1 infection in Burkina Faso.
No full textHuman papillomavirus (HPV) infection and cervical squamous intraepithelial lesions (SILs) were studied in 379 high-risk women. Human papillomavirus DNA was detected in 238 of 360 (66.1%) of the beta-globin-positive cervical samples, and 467 HPV isolates belonging to 35 types were identified. Multiple (2-7 types) HPV infections were observed in 52.9% of HPV-infected women. The most prevalent HPV types were HPV-52 (14.7%), HPV-35 (9.4%), HPV-58 (9.4%), HPV-51 (8.6%), HPV-16 (7.8%), HPV-31 (7.5%), HPV-53 (6.7%), and HPV-18 (6.4%). Human immunodeficiency virus type 1 (HIV-1) seroprevalence was 36.0%. Human papillomavirus prevalence was significantly higher in HIV-1-infected women (87 vs 54%, prevalence ratio (PR) = 1.61, 95% confidence interval (CI): 1.4-1.8). High-risk HPV types (71 vs 40%, PR = 1.79, 95% CI: 1.5-2.2), in particular HPV-16+18 (22 vs 9%, PR = 2.35, 95% CI: 1.4-4.0), and multiple HPV infections (56 vs 23%, PR = 2.45, 95% CI: 1.8-3.3) were more prevalent in HIV-1-infected women. High-grade SIL (HSIL) was identified in 3.8% of the women. Human immunodeficiency virus type 1 infection was strongly associated with presence of HSIL (adjusted odds ratio = 17.0; 95% CI 2.2-134.1, P = 0.007) after controlling for high-risk HPV infection and other risk factors for HSIL. Nine of 14 (63%) HSIL cases were associated with HPV-16 or HPV-18 infection, and might have been prevented by an effective HPV-16/18 vaccine
N-2-Ethyldeoxyguanosine as a Potential Biomarker for Assessing Effects of Alcohol Consumption on DNA
No full textHead and neck cancers are causally related to alcohol consumption, but the underlying mechanisms are unclear. Ethanol is metabolized to acetaldehyde, an experimental carcinogen. Quantitation of the major DNA adduct of acetaldehyde, N-2-ethylidenedeoxyguanosine, in human tissues could help to elucidate the mechanism of alcohol carcinogenicity. We applied a quantitative method for the analysis of this adduct, measured as the NaBH3CN reduction product N-2-ethyldeoxyguanosine (N-2-ethyl-dGuo) by liquid chromatography-electrospray ionization-tandem mass spectrometry-selected reaction monitoring, on DNA (0.04 +/- 0.03 mg) isolated from blood collected from control subjects recruited from two studies conducted in different areas of Europe between 1999 and 2005. The group selected from the first study (n = 127) included alcohol drinkers and abstainers while the group from the second study (n = 50) included only heavy drinkers. N-2-ethyl-dGuo was detected in all DNA samples. After adjusting for potential confounders, in the first study, drinkers showed a higher level of N-2-ethyl-dGuo (5,270 +/- 8,770 fmol/mu mol dGuo) compared with nondrinkers (2,690 +/- 3040 fmol/mu mol dGuo; P = 0.04). A significant trend according to dose was observed in both studies (P = 0.02 and 0.04, respectively). Taking into account the amount of alcohol consumption, adduct levels were higher in younger compared with older subjects (P = 0.01), whereas no differences were observed comparing men with women. These results show the feasibility of quantifying N-2-ethyl-dGuo in small-volume blood samples and are consistent with the hypothesis that ethanol contributes to carcinogenesis through DNA adducts formation. (Cancer Epidemiol Biomarkers Prev 2008;17(11):3026-32
Alcohol-related cancers and genetic susceptibility in Europe: the ARCAGE project: study samples and data collection
No full textCancers of the upper aerodigestive tract (UADT) include those of the oral cavity, pharynx (other than nasopharynx), larynx, and esophagus. Tobacco smoking and consumption of alcoholic beverages are established causes of UADT cancers, whereas reduced intake of vegetables and fruits are likely causes. The role of genetic predisposition and possible interactions of genetic with exogenous factors, however, have not been adequately studied. Moreover, the role of pattern of smoking and drinking, as well as the exact nature of the implicated dietary variables, has not been clarified. To address these issues, the International Agency for Research on Cancer initiated in 2002 the alcohol-related cancers and genetic susceptibility (ARCAGE) in Europe project, with the participation of 15 centers in 11 European countries. Information and biological data from a total of 2304 cases and 2227 controls have been collected and will be used in a series of analyses. A total of 166 single nucleotide polymorphisms of 76 genes are being studied for genetic associations with UADT cancers. We report here the methodology of the ARCAGE project, main demographic and lifestyle characteristics of the cases and controls, as well as the distribution of cases by histology and subsite. About 80% of cases were males and fewer than 20% of all cases occurred before the age of 50 years. Overall, the most common subsite was larynx, followed by oral cavity, oropharynx, esophagus and hypopharynx. Close to 90% of UADT cancers were squamous cell carcinomas. A clear preponderance of smokers and alcohol drinkers among UADT cases compared with controls was observed. European Journal of Cancer Prevention 18:76-84 © 2009 Wolters Kluwer Health
Is Hospital in the Home as safe and effective as inpatient care?
No full textWhen Activity-Based Funding (ABF) for public hospitals begins on 1 July this year, it should make it easier for hospitals to establish Hospital in the Home (HITH) services. The pricing framework underpinning the ABF system stipulates that public hospital services should be priced in a way that facilitates the timely roll-out of evidence-based innovations in the most appropriate care setting.
HITH services have been operating in some Australian hospitals for nearly 20 years. However before starting up a service of their own, many hospital managers will want to know if HITH is safe, and for which patients. This paper briefly outlines the evidence on the safety, quality and costs of HITH services. A list of resources is provided for those who want to know more.
What does the evidence say?
Many health services provide care in patients’ homes. To qualify as a HITH service it must provide active treatment by health care professionals in patients’ homes for conditions that otherwise would require hospital in-patient care. Examples of acute treatments delivered in the home include blood transfusions, intravenous antibiotic treatments for infections, and anticoagulation for patients with deep venous thrombosis and pulmonary emboli.
Some HITH services (early - discharge HITH) also provide subacute treatment such as rehabilitation at home after orthopaedic injuries and procedures. The range of conditions that are treatable at home continues to expand as technology and confidence in HITH improves.
Cochrane Reviews are generally regarded as an authoritative source of research evidence. A systematic review of the evidence on HITH was conducted by the Cochrane Collaboration in 2008 (it was updated in 2011 and no changes were made to the conclusions).
After searching the main medical databases, the Cochrane reviewers found 10 randomised controlled trials (RCTs) that compared HITH with inpatient care; RCTs are generally thought to produce high quality evidence. Data from five of the RCTs on admission - substitution HITH services were broadly comparable, so they were pooled and used to conduct a more high-powered statistical analysis, a meta-analysis
A genome-wide association study of upper aerodigestive tract cancers conducted within the INHANCE consortium
No full textGenome-wide association studies (GWAS) have been successful in identifying common genetic variation involved in susceptibility to etiologically complex disease. We conducted a GWAS to identify common genetic variation involved in susceptibility to upper aero-digestive tract (UADT) cancers. Genome-wide genotyping was carried out using the Illumina HumanHap300 beadchips in 2,091 UADT cancer cases and 3,513 controls from two large European multi-centre UADT cancer studies, as well as 4,821 generic controls. The 19 top-ranked variants were investigated further in an additional 6,514 UADT cancer cases and 7,892 controls of European descent from an additional 13 UADT cancer studies participating in the INHANCE consortium. Five common variants presented evidence for significant association in the combined analysis (p≤5×10−7). Two novel variants were identified, a 4q21 variant (rs1494961, p = 1×10−8) located near DNA repair related genes HEL308 and FAM175A (or Abraxas) and a 12q24 variant (rs4767364, p = 2×10−8) located in an extended linkage disequilibrium region that contains multiple genes including the aldehyde dehydrogenase 2 (ALDH2) gene. Three remaining variants are located in the ADH gene cluster and were identified previously in a candidate gene study involving some of these samples. The association between these three variants and UADT cancers was independently replicated in 5,092 UADT cancer cases and 6,794 controls non-overlapping samples presented here (rs1573496-ADH7, p = 5×10−8; rs1229984-ADH1B, p = 7×10−9; and rs698-ADH1C, p = 0.02). These results implicate two variants at 4q21 and 12q24 and further highlight three ADH variants in UADT cancer susceptibility
Socioeconomic factors associated with risk of upper aerodigestive tract cancer in Europe
No full textIntroduction<p></p>
In the European Union, there are 180,000 new cases of upper aerodigestive tract (UADT) cancer cases per year – more than half of whom will die of the disease. Socioeconomic inequalities in UADT cancer incidence are recognised across Europe. We aimed to assess the components of socioeconomic risk both independently and through their influence on the known behavioural risk factors of smoking, alcohol consumption and diet.<p></p>
Patients and methods<p></p>
A multicentre case–control study with 2198 cases of UADT cancer and 2141 controls from hospital and population sources was undertaken involving 14 centres from 10 countries. Personal interviews collected information on demographics, lifetime occupation history, smoking, alcohol consumption and diet. Socioeconomic status was measured by education, occupational social class and unemployment. Odds ratios (ORs) and 95% confidence intervals (CIs) were computed using unconditional logistic regression.<p></p>
Results<p></p>
When controlling for age, sex and centre significantly increased risks for UADT cancer were observed for those with low versus high educational attainment OR = 1.98 (95% CI 1.67, 2.36). Similarly, for occupational socioeconomic indicators – comparing the lowest versus highest International Socio-Economic Index (ISEI) quartile for the longest occupation gave OR = 1.60 (1.28, 2.00); and for unemployment OR = 1.64 (1.24, 2.17). Statistical significance remained for low education when adjusting for smoking, alcohol and diet behaviours OR = 1.29 (1.06, 1.57) in the multivariate analysis. Inequalities were observed only among men but not among women and were greater among those in the British Isles and Eastern European countries than in Southern and Central/Northern European countries. Associations were broadly consistent for subsite and source of controls (hospital and community).<p></p>
Conclusion<p></p>
Socioeconomic inequalities for UADT cancers are only observed among men and are not totally explained by smoking, alcohol drinking and diet.<p></p>
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