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South Africa's HIV epidemic has evolved over time in terms of numbers of people living with HIV, access to antiretroviral treatment (ART) and age. These changes have profoundly influenced local cancer patterns. The Johannesburg Cancer Study has, over a period of 22 years (1995-2016), recruited over 20 000 incident black cancer patients who consented to provide answers to a questionnaire and blood samples (serum, DNA). This has presented a unique opportunity to examine the evolving association of HIV with cancer in Africa. We used logistic regression models to explore case-control associations between specific cancers and HIV, using participants with non-infection related cancers as controls. Using data of 20 835 cancer patients with confirmed HIV status, we found the following cancers to be associated with HIV: Kaposi's sarcoma (OR

Summary Background Prevention, control, and treatment of respiratory tract cancers are important steps towards achieving target 3.4 of the UN Sustainable Development Goals (SDGs)—a one-third reduction in premature mortality due to non-communicable diseases by 2030. We aimed to provide global, regional, and national estimates of the burden of tracheal, bronchus, and lung cancer and larynx cancer and their attributable risks from 1990 to 2019. Methods Based on the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 methodology, we evaluated the incidence, mortality, years lived with disability, years of life lost, and disability-adjusted life-years (DALYs) of respiratory tract cancers (ie, tracheal, bronchus, and lung cancer and larynx cancer). Deaths from tracheal, bronchus, and lung cancer and larynx cancer attributable to each risk factor were estimated on the basis of risk exposure, relative risks, and the theoretical minimum risk exposure level input from 204 countries and territories, stratified by sex and Socio-demographic Index (SDI). Trends were estimated from 1990 to 2019, with an emphasis on the 2010–19 period. Findings Globally, there were 2·26 million (95% uncertainty interval 2·07 to 2·45) new cases of tracheal, bronchus, and lung cancer, and 2·04 million (1·88 to 2·19) deaths and 45·9 million (42·3 to 49·3) DALYs due to tracheal, bronchus, and lung cancer in 2019. There were 209 000 (194 000 to 225 000) new cases of larynx cancer, and 123 000 (115 000 to 133 000) deaths and 3·26 million (3·03 to 3·51) DALYs due to larynx cancer globally in 2019. From 2010 to 2019, the number of new tracheal, bronchus, and lung cancer cases increased by 23·3% (12·9 to 33·6) globally and the number of larynx cancer cases increased by 24·7% (16·0 to 34·1) globally. Global age-standardised incidence rates of tracheal, bronchus, and lung cancer decreased by 7·4% (−16·8 to 1·6) and age-standardised incidence rates of larynx cancer decreased by 3·0% (−10·5 to 5·0) in males over the past decade; however, during the same period, age-standardised incidence rates in females increased by 0·9% (−8·2 to 10·2) for tracheal, bronchus, and lung cancer and decreased by 0·5% (−8·4 to 8·1) for larynx cancer. Furthermore, although age-standardised incidence and death rates declined in both sexes combined from 2010 to 2019 at the global level for tracheal, bronchus, lung and larynx cancers, some locations had rising rates, particularly those on the lower end of the SDI range. Smoking contributed to an estimated 64·2% (61·9–66·4) of all deaths from tracheal, bronchus, and lung cancer and 63·4% (56·3–69·3) of all deaths from larynx cancer in 2019. For males and for both sexes combined, smoking was the leading specific risk factor for age-standardised deaths from tracheal, bronchus, and lung cancer per 100 000 in all SDI quintiles and GBD regions in 2019. However, among females, household air pollution from solid fuels was the leading specific risk factor in the low SDI quintile and in three GBD regions (central, eastern, and western sub-Saharan Africa) in 2019. Interpretation The numbers of incident cases and deaths from tracheal, bronchus, and lung cancer and larynx cancer increased globally during the past decade. Even more concerning, age-standardised incidence and death rates due to tracheal, bronchus, lung cancer and larynx cancer increased in some populations—namely, in the lower SDI quintiles and among females. Preventive measures such as smoking control interventions, air quality management programmes focused on major air pollution sources, and widespread access to clean energy should be prioritised in these settings. Funding Bill & Melinda Gates Foundation.

We reviewed the literature on the importance of selected anti-high-risk human papillomavirus (HR-HPV) antibodies (namely, 16/18 and early oncoproteins E6 and E7) as potential serological markers for early detection of individuals at high risk of cervical cancer. We searched for studies in PubMed and Embase databases published from 2010 to 2020 on antibodies against HR-HPV E6 and E7 early proteins and cervical cancer. Pooled sensitivity and specificity for HPV16 and HPV18 antibodies were calculated using a bivariate hierarchical random-effects model. A total of 69 articles were identified; we included three studies with 1550 participants. For the three HPV16/18 E6 and E7 antibody tests, enzyme-linked immunosorbent assay-based assays had a sensitivity of 18% for detecting CIN2+ (95% confidence interval [CI]: 15-21) and a specificity of 96% (95% CI: 92-98), for slot-blot, sensitivity was 28.9% (95% CI: 23.3-35.1) and specificity was 72% (95% CI: 66.6-77.0) for detecting CIN2+, and for multiplex HPV serology assay based on a glutathione S-transferase, sensitivity was 16% (95% CI: 8.45-28.6) and specificity was 98% (95% CI: 97-99) for detecting invasive cervical cancer. HR-HPV16/18 E6 and E7 serological markers showed high specificity, but sensitivity was suboptimal for the detection of cervical cancer in either population screening settings or as point-of-care screening tests.

Background This population-based cross-stional and panel study investigated disparities in the management of coronary heart disease (CHD) by level of socioeconomic status. Methods CHD patients (aged ≥18 years), treated in 438 general practices in Australia, with ≥3 recent encounters with their general practitioners, with last encounter being during 2016–2018, were included. Secondary prevention prescriptions and number of treatment targets achieved were each modelled using a Poisson regression adjusting for demographics, socioeconomic indicators, remoteness of patient’s residence, comorbidities, lifetime follow-up, number of patient–general practitioner encounters and cluster effect within the general practices. The latter model was constructed using the Generalised Estimating Equations approach. Sensitivity analysis was run by comorbidity. Results Of 137,408 patients (47% women), approximately 48% were prescribed ≥3 secondary prevention medications. However, only 44% were screened for CHD-associated risk factors. Of the latter, 45% achieved ≥5 treatment targets. Compared with patients from the highest socioeconomic status fifth, those from the lowest socioeconomic status fifth were 8% more likely to be prescribed more medications for secondary prevention (incidence rate ratio (95% confidence interval): 1.08 (1.04–1.12)) but 4% less likely to achieve treatment targets (incidence rate ratio: 0.96 (0.95–0.98)). These disparities were also observed when stratified by comorbidities. Conclusion Despite being more likely to be prescribed medications for secondary prevention, those who are most socioeconomically disadvantaged are less likely to achieve treatment targets. It remains to be determined whether barriers such as low adherence to treatment, failure to fill prescriptions, low income, low level of education or other barriers may explain these findings.

Kaposi’s sarcoma (KS) has become a common AIDS-defining cancer in sub-Saharan Africa. Kaposi’s sarcoma-associated human herpesvirus strongly modulated by HIV-related immune suppression are the principal causes of this cancer. No other risk factors have been identified as playing a strong role. HIV prevention programs and good coverage of antiretroviral therapy (ART) in developed countries resulted in a remarkable decline in HIV-KS incidence and better KS prognosis. By contrast, in sub-Saharan Africa, population ART rollout has lagged, but clinical studies have shown positive results in reduction of KS incidence and better KS prognosis. However, the effect of ART rollout in relation to population KS incidence is unclear. We describe the incidence of KS in sub-Saharan Africa, in four time-periods, (1) before 1980 (before HIV/AIDS era); (2) 1981–2000 (early HIV/AIDS era, limited or no ART coverage); (3) 2001–2010 (early ART coverage period); and (4) 2011–2016 (fair to good ART coverage period). We used KS incidence data available from WHO-International Agency for Research on Cancer (IARC) publications and the Africa Cancer Registry Network. National HIV prevalence and ART coverage data were derived from UNAIDS/WHO. A rapid increase in KS incidence was observed throughout sub-Saharan Africa as the HIV epidemic progressed, reaching peak incidences in Period 2 (pre-ART rollout) of 50.8 in males and 20.3 per 100 000 in females (Zimbabwe, Harare). The overall unweighted average decline in KS incidence between 2000 and 2010 and 2011–2016 was 27%, but this decline was not statistically significant across the region. ART rollout coincides with a decline in KS incidence across several regions in sub-Saharan Africa. The importance of other risk factors such as reductions in HIV incidence could not be ascertained.

Background In populations with high rates of human immunodeficiency virus (HIV)-coinfection, the nature of the relationship between human papillomavirus (HPV)-16 and -18 (L1, E6 and E7) antibodies and cervical cancer is still uncertain. We measured the association between seropositivity to HPV (L1, E6 and E7) proteins and cervical cancer among black South African women with and without HIV co-infection. Methods We used questionnaire data and serum collected from consecutively recruited patients with a newly diagnosed cancer from the Johannesburg Cancer Study from 1346 cervical cancer cases and 2532 controls (diagnosed with other non-infection related cancers). Seropositivity to HPV proteins was measured using a multiplex serological assay based on recombinant glutathione S-transferase (GST) fusion proteins. We measured associations between their presence and cervical cancer using unconditional logistic regression models and evaluated the sensitivity and specificity of these HPV biomarkers. Results Among controls, HIV-negative women from rural areas compared to urban had significantly higher HPV seroprevalence, HPV16 E7 (8.6% vs 3.7%) and HPV18 E7 (7.9% vs 2.0%). HPV16 E6 and E7 antibodies were positively associated with cervical cancer in HIV-positive (Adjusted Odds Ratio (AOR) = 33; 95% CI 10–107) and HIV-negative women (AOR = 97; 95% CI 46–203). In HIV-positive women, HPV E6/E7 antibodies had low sensitivity (43.0%) and high specificity (90.6%) for cervical cancer detection. In HIV-negative women, HPV E6/E7 antibodies sensitivity was 70.6% and specificity was 89.7%. Conclusions Our data show that HPV (L1, especially E6 and E7) antibody positivity is associated with cervical cancer in both HIV-positive and HIV-negative women. Nonetheless, being HIV-positive plays an important role in the development of cervical cancer.

Background: Sun exposure causes cutaneous squamous (SCC) and basal cell (BCC) carcinomas. Human papillomavirus (HPV) infection might cause SCC. Methods: We examined associations of β and γ HPV infection in skin-swab DNA and serum antibodies with skin cancer risk, and modification of the carcinogenic effects of sun exposure by them, in case–control studies of 385 SCC cases, 832 BCC cases, and 1,100 controls nested in an Australian prospective cohort study (enrolled 2006–2009). Results: Presence of β-1 and β-3 HPV DNA appeared to increase risks for SCC and BCC by 30% to 40% (P adjusted Conclusions: Our substantive findings are at the level of genus β HPV. Like SCC, BCC risk may increase with increasing numbers of β HPV types on skin. Impact: The consistency in our findings that HPV infection may moderate the effects of sun exposure, the main environmental cause of SCC and BCC, merits further investigation.

The Johannesburg Cancer Study (JCS) aims were to examine whether cancer risk factors identified in Western countries applied to black patients in Johannesburg, South Africa and to understand the impact of HIV on cancer risk, with a view to identifying previously unrecognised HIV associated cancers. A total of 24 971 black patients with an incident histologically proven (>95%) cancer of any type were enrolled between 1995-2016. Response rates were >90%. Patients provided informed consent, lifestyle and demographic information using a structured questionnaire; 19 351 provided a serum sample and 18 972 a whole blood sample for genomic analyses. This is currently the largest cancer epidemiological biobank in Africa. JCS uses a cancer case-control method; controls being cancer types unrelated to exposures of interest. Published results show the importance of HIV in several cancers known to be infection associated e.g. Kaposi sarcoma (OR = 1683; CI = 595-5194) in those with high Kaposi-sarcoma-associated-herpesvirus titres; no effect of HIV on lung or liver cancer-in the latter showing a strong association with HBVDNA, sAg and c positivity (OR = 47; CI = 21-104). Comparable data to higher-income country studies include lung cancer ORs in relation to smoking (15+g tobacco/day) (ORMales = 37; CI = 21-67, ORFemales = 18.5; CI = 8-45) and associations between alcohol and oesophageal cancer in smokers (ORM&F = 4.4; CI = 3-6). Relationship between hormonal contraception declined to null 10 or more years after stopping for breast (OR = 1.1; CI = 0.9-1.4) and cervical cancer (OR = 1.0;CI = 0.8-1.2), and protective effects shown, five or more years after stopping for ovarian (OR = 0.6; CI = 0.4-1) and endometrial cancer (OR = 0.4; CI = 0.2-0.9). Preferential access is based on data requests promoting data pooling, equal collaborative opportunities and enhancement of research capacity in South Africa. The JCS is a practical and valid design in otherwise logistically difficult settings.

We describe our experience in several settings, following a suggestion in 1983 to add questions on the smoking status of the deceased on the UK death certificate as an effective way to monitor the evolution of the smoking epidemic. In South Africa in 1997 and in Tianjin Municipality, China, in 2010, questions about the smoking habits of the deceased were inserted on the official death certificates. In both places a system now exists to routinely collect information on smoking status in relation to causes of death. Results from two million South African and 300 000 Chinese deceased individuals have been reported, and the sample size in both places continues to grow. An unsuccessful attempt was made in 2008 to insert smoking questions on the Australian death notification forms but comments and concerns from the registrars of births, marriages and deaths have international applicability. In both China and South Africa, inserting questions on smoking on the death notification forms was not a trivial task-in each it required, as a minimum, significant commitment from several government agencies. Benefits, however, include a better local understanding of the smoking epidemic and allowing for planning and monitoring of tobacco control programmes. Documenting the varied experiences of collecting information on smoking on death notification forms is useful to those wishing to introduce such questions in their own settings. This is pertinent especially at a time when vital registration systems are being improved, with an aim to monitoring sustainable development goals.

Background Over two-thirds of the world’s cancer deaths occur in economically developing countries; however, the societal costs of cancer have rarely been assessed in these settings. Our aim was to estimate the value of productivity lost in 2012 due to cancer-related premature mortality in the major developing economies of Brazil, the Russian Federation, India, China and South Africa (BRICS). Methods We applied an incidence-based method using the human capital approach. We used annual adult cancer deaths from GLOBOCAN2012 to estimate the years of productive life lost between cancer death and pensionable age in each country, valued using national and international data for wages, and workforce statistics. Sensitivity analyses examined various methodological assumptions. Results The total cost of lost productivity due to premature cancer mortality in the BRICS countries in 2012 was $46·3 billion, representing 0·33% of their combined gross domestic product. The largest total productivity loss was in China ($28 billion), while South Africa had the highest cost per cancer death ($101,000). Total productivity losses were greatest for lung cancer in Brazil, the Russian Federation and South Africa; liver cancer in China; and lip and oral cavity cancers in India. Conclusion Locally-tailored strategies are required to reduce the economic burden of cancer in developing economies. Focussing on tobacco control, vaccination programs and cancer screening, combined with access to adequate treatment, could yield significant gains for both public health and economic performance of the BRICS countries.

Introduction Physical activity (PA) has been associated with lower risk of cardiovascular diseases, but the evidence linking PA with lower cancer risk is inconclusive. We examined the independent and interactive effects of PA and obesity using body mass index (BMI) as a proxy for obesity, on the risk of developing prostate (PC), postmenopausal breast (BC), colorectal (CRC), ovarian (OC) and uterine (UC) cancers. Methods We estimated odds ratios (OR) and 95% confidence intervals (CI), adjusting for cancer specific confounders, in 6831 self-reported cancer cases and 1992 self-reported cancer-free controls from the Cancer Lifestyle and Evaluation of Risk Study, using unconditional logistic regression. Results For women, BMI was positively associated with UC risk; specifically, obese women (BMI ≥30 kg/m2) had nearly twice the risk of developing UC compared to women with healthy-BMI-range (

Background: Human papillomavirus (HPV) infection is highly prevalent worldwide and may have a role, with sun exposure, in causing cutaneous squamous cell carcinoma. Little is known about the relationship of UV exposure and seroprevalence of cutaneous HPVs in the general population. Methods: Using multiplex serology, we estimated the seroprevalence of 23 beta and 7 gamma HPVs and 7 other antigens (mu HPV1, HPV63, nu HPV41, alpha HPV16; polyomaviruses HPyV7 and MCV; p53) in a population-based sample of 1,161 Australian 45 and Up Study participants with valid data from blood specimens collected from 2010 to 2012. We calculated prevalence ratios (PR) for the association of each antigen with residential ambient solar UV and other UV-related variables. Results: Seropositivity for at least one beta or gamma HPV was high at 88% (beta HPVs 74%, gamma HPVs 70%), and less in women than men [e.g., PR beta-2 HPV38 = 0.70; 95% confidence interval (CI), 0.56–0.87; any gamma = 0.90; 95% CI, 0.84–0.97]. A high ambient UV level in the 10 years before study enrollment was associated with elevated seroprevalence for genus beta (PRtertile3vs1 any beta = 1.17; 95% CI, 1.07–1.28), and beta-1 to beta-3 species, but not for gamma HPVs. Other UV-related measures had less or no evidence of an association. Conclusions: Seroprevalence of cutaneous beta HPVs is higher with higher ambient UV exposure in the past 10 years. Impact: The observed association between ambient UV in the past 10 years and cutaneous HPVs supports further study of the possible joint role of solar UV and HPV in causing skin cancer.

ObjectivesTo determine whether sex differences exist in the management of patients with a history of coronary heart disease (CHD) in primary care.MethodsGeneral practice records of patients aged ≥18 years with a history of CHD in a large general practice dataset in Australia, MedicineInsight, were analysed. Sex-specific, age-standardised proportions of patients prescribed with recommended medications; assessed for cardiovascular risk factors; and achieved treatment targets according to the General Practice Management Plan were reported.ResultsRecords of 130 926 patients (47% women) from 438 sites were available from 2014 to 2018. Women were less likely to be prescribed with recommended medications (prescribed ≥3 medications: women 44%, men 61%; pConclusionGaps in preventative management including prescription of indicated medications and risk factor monitoring have been reported from the late 1990s and this large-scale general practice data analysis indicate they still persist. Moreover, the gap is larger in women compared to men. We need new ways to address these gaps and the sex inequity.

Prostate cancer (PC) is the most common non-cutaneous cancer in men worldwide. The relationships between PC and possible risk factors for PC cases (n = 1,181) and male controls (n = 875) from the New South Wales (NSW) Cancer, Lifestyle and Evaluation of Risk Study (CLEAR) were examined in this study. The associations between PC risk and paternal history of PC, body mass index (BMI), medical conditions, sexual behaviour, balding pattern and puberty, after adjusting for age, income, region of birth, place of residence, and PSA testing, were examined. Adjusted risk of PC was higher for men with a paternal history of PC (OR = 2.31; 95%CI: 1.70–3.14), personal history of prostatitis (OR = 2.30; 95%CI: 1.44–3.70), benign prostatic hyperplasia (OR = 2.29; 95%CI: 1.79–2.93), being overweight (vs. normal; OR = 1.24; 95%CI: 0.99–1.55) or obese (vs. normal; OR = 1.44; 95%CI: 1.09–1.89), having reported more than seven sexual partners in a lifetime (vs.

Background Obesity and physical activity (PA) are predictors of colon (CC) and rectal (RC) cancers. Prolonged sitting is also emerging as a potential predictor for these cancers. Little knowledge exists about the interactive effects of obesity, PA and prolonged sitting on cancer risk. This analysis assessed independent and interactive effects of PA, body mass index (BMI) and sitting time on CC and RC risks. Methods This analysis used data from a prospective study of 226,584 participants aged 45 years and over in New South Wales (NSW), Australia, who joined the 45 and Up study between 2006 and 2009. Baseline data were linked with data relating to mortality, cancer registration, hospital admission and Department of Human Services to December 2010. Multivariable Cox regression was used to estimate adjusted hazard ratios (referred to as relative risks, RRs) and 95% confidence intervals (Cis). Statistical significance was defined as p

A small percentage of women with cervical HPV infection progress to cervical neoplasia, and the risk factors determining progression are incompletely understood. We sought to define the genetic loci involved in cervical neoplasia and to assess its heritability using unbiased unrelated case/control statistical approaches. We demonstrated strong association of cervical neoplasia with risk and protective HLA haplotypes that are determined by the amino-acids carried at positions 13 and 71 in pocket 4 of HLA-DRB1 and position 156 in HLA-B. Furthermore, 36% (standard error 2.4%) of liability of HPV-associated cervical pre-cancer and cancer is determined by common genetic variants. Women in the highest 10% of genetic risk scores have approximately >7.1% risk, and those in the highest 5% have approximately >21.6% risk, of developing cervical neoplasia. Future studies should examine genetic risk prediction in assessing the risk of cervical neoplasia further, in combination with other screening methods., Author summary Around 1% of women with cervical human papillomavirus (HPV) infection progress to cervical cancer. Previous studies had indicated that a person’s genetic makeup could predispose to HPV-associated cervical cancer, and that some of the genes likely to be involved include the immune-related human leukocyte antigen (HLA) genes among the major histocompatibility complex (MHC). However, it has been difficult to determine which alleles might be associated with cervical pre-cancer or cancer due to the complex and high level of co-inheritance of MHC alleles. Here, we performed a genome-wide association study that assessed the correlation of genetic variants among those with cervical cancer and healthy controls. We show that host genetics is a major determinant of HPV-associated cervical cancer, with 36% of liability due to common genetic variants in the population, and identify both risk and protective HLA alleles. Our study was also sufficiently powerful to identify particular residue variants on a number of the immune-related proteins that provide risk or protection, providing further insight into the biological basis for cervical cancer development. Our findings could lay the foundation for screening for people at increased risk of developing cancer following HPV infection, and aid in the treatment and prognosis of cervical cancer.

Epidemiological and mechanistic evidence on the causative role of human papillomaviruses (HPV) in esophageal squamous cell carcinoma (ESCC) is unclear. We retrieved alcohol- and formalin-fixed paraffin-embedded ESCC tissues from 133 patients seropositive for antibodies against HPV early proteins, from high-incidence ESCC regions: South Africa, China and Iran. With rigorous care to prevent nucleic acid contamination, we analyzed these tissues for the presence of 51 mucosotropic human alpha-papillomaviruses by two sensitive, broad-spectrum genotyping methods, and for the markers of HPV-transformed phenotype: (i) HPV16/18 viral loads by quantitative real-time PCR, (ii) type-specific viral mRNA by E6*I/E6 full-length RT-PCR assays and (iii) expression of cellular protein p16(INK4a). Of 118 analyzable ESCC tissues, 10 (8%) were positive for DNA of HPV types: 16 (4 tumors); 33, 35, 45 (1 tumor each); 11 (2 tumors) and 16, 70 double infection (1 tumor). Inconsistent HPV DNA+ findings by two genotyping methods and negativity in qPCR indicated very low viral loads. A single HPV16 DNA+ tumor additionally harbored HPV16 E6*I mRNA but was p16(INK4a) negative (HPV16 E1 seropositive patient). Another HPV16 DNA+ tumor from an HPV16 E6 seropositive patient showed p16(INK4a) upregulation but no HPV16 mRNA. In the tumor tissues of these serologically preselected ESCC patients, we did not find consistent presence of HPV DNA, HPV mRNA or p16(INK4a) upregulation. These results were supported by a meta-analysis of 14 other similar studies regarding HPV-transformation of ESCC. Our study does not support the etiological role of the 51 analyzed mucosotropic HPV types in the ESCC carcinogenesis.

Randomised controlled trials and large-scale observational studies have found that current use of menopausal hormone therapy (MHT) is associated with an increased risk of breast cancer; this risk is higher for oestrogen-progestagen combination therapy than for oestrogen-only therapy. Our study was designed to estimate MHT-associated breast cancer risk in a population of Australian women. Data were analysed for postmenopausal women with self-reported incident invasive breast cancer (n = 1,236) and cancer-free controls (n = 862), recruited between 2006 and 2014 into a large case-control study for all cancer types, the NSW CLEAR study. Information on past and current MHT use was collected from all participants, along with other lifestyle and demographic factors, using a self-administered questionnaire. Unmatched multivariable logistic regression was performed, adjusting for socio-demographic, reproductive and health behaviour variables, body mass index and breast screening history. Compared to never users of MHT, the adjusted odds ratio (aOR) for breast cancer in current users of any type of MHT was 2.09 (95% CI: 1.57-2.78; p < 0.0001) and for past users of any type of MHT was 1.03 (0.82-1.28; p = 0.8243). For current users of oestrogen-only and oestrogen-progestagen therapy, aORs were 1.80 (1.21-2.68; p = 0.0039) and 2.62 (1.56-4.38; p = 0.0003), respectively. These findings are consistent with those from other international observational studies, that current, but not past, use of MHT is associated with a substantially increased risk of breast cancer.

Background Continued smoking following a cancer diagnosis has adverse impacts on cancer treatment and puts individuals at risk of secondary cancers. Data on the prevalence and correlates of smoking among cancer patients are critical for successfully targeting smoking cessation interventions. Aims To explore among a sample of medical oncology outpatients (a) the prevalence of self-reported current smoking and (b) the demographic and psychosocial factors associated with self-reported smoking. Methods A heterogeneous sample of cancer patients aged 18 years or over was recruited from 1 of 11 medical oncology treatment centres across Australia. Patients completed a survey assessing the following: smoking status; socio-demographic, disease and treatment characteristics; time since diagnosis; anxiety; and depression. Factors associated with self-reported smoking were examined using a univariate and multivariate mixed-effects logistic regression. Results A total of 1379 patients returned surveys and 1338 were included in the analysis. The prevalence of current smoking was 10.9% (n = 146). After adjusting for treatment centre, patients aged 65 years and older and those without health concession cards were significantly less likely to smoke. Patients diagnosed with lung cancer and those without private health insurance were more likely to smoke. Discussion A minority of cancer patients reported continued smoking at an average time of 13 months post-diagnosis. Patients, who are younger, have been diagnosed with lung cancer and have lower socioeconomic status are at-risk groups and represent important targets for smoking cessation advice and intervention. Copyright © 2015 John Wiley & Sons, Ltd.

Background Australia commenced a publically-funded, National Human Papillomavirus (HPV) Vaccination Program in 2007 with a two year catch-up phase for females aged 12–26 years. Objective To identify the factors associated with the uptake of the HPV vaccine (which has a recommended 3-dose schedule in Australia) by young adult women vaccinated by general practitioners and community-based programs within the catch-up phase. Methods 1139 women who were eligible to receive the free HPV vaccine during the catch-up period were recruited in 2008–2009 (age 20–29 years at recruitment), in New South Wales, after having a normal (negative) cervical smear result recorded on the NSW Pap Test Register. Participants completed a self-administered questionnaire providing information on vaccination status, and sociodemographic and other factors. Results Overall, 880 (77%) women reported receiving ≥1 dose of the vaccine and 777 women (68%) reported receiving ≥2 doses. In multivariable analysis (adjusting for the period for which each woman was eligible for free HPV vaccination), uptake of ≥1 dose of the vaccine was significantly associated with being born in Australia (p < 0.01), being single (p = 0.02), being nulliparous (p < 0.01), living in a higher socioeconomic status area (p-trend = 0.03), living in more remote areas (p = 0.03), drinking alcohol (p < 0.01) and using hormonal contraceptives (p < 0.01). Although vaccinated women were more likely to have fewer sexual partners than unvaccinated women (p-trend = 0.02), they were also more likely to report a prior sexually transmitted infection (STI) (p = 0.03). Similar factors were associated with receiving ≥2 doses. Conclusions In this group, women living in higher socioeconomic status areas were more likely to be vaccinated against HPV in the catch-up phase of the national program. Although vaccinated women tended to have fewer sexual partners, they also reported prior STIs, which may be a marker of increased risk of prior exposure to HPV. The findings of this study reinforce the continuing need to prioritise equitable delivery of vaccination to various population subgroups. The study was funded by the National Health and Medical Research Council Australia (NHMRC Project Grant ID 387701) and by Cancer Council NSW.

Barrett's esophagus (BE), a common condition, is the only known precursor to esophageal adenocarcinoma (EAC). There is uncertainty about the best way to manage BE as most people with BE never develop EAC and most patients diagnosed with EAC have no preceding diagnosis of BE. Moreover, there have been recent advances in knowledge and practice about the management of BE and early EAC. To aid clinical decision making in this rapidly moving field, Cancer Council Australia convened an expert working party to identify pertinent clinical questions. The questions covered a wide range of topics including endoscopic and histological definitions of BE and early EAC; prevalence, incidence, natural history, and risk factors for BE; and methods for managing BE and early EAC. The latter considered modification of lifestyle factors; screening and surveillance strategies; and medical, endoscopic, and surgical interventions. To answer each question, the working party systematically reviewed the literature and developed a set of recommendations through consensus. Evidence underpinning each recommendation was rated according to quality and applicability.

Background Human papillomavirus (HPV) vaccines protect against HPV types 16/18, but do not eliminate the need to detect pre-cancerous lesions. Australian women vaccinated as teenage girls are now entering their mid-thirties. Since other oncogenic HPV types have been shown to be more prevalent in women ≥30 years old, understanding high grade cervical lesions in older women is still important. Hormonal contraceptives (HC) and smoking are recognised cofactors for the development of pre-malignant lesions. Methods 886 cases with cervical intraepithelial neoplasia (CIN) 2/3 and 3636 controls with normal cytology were recruited from the Pap Test Register of NSW, Australia. All women were aged 30–44 years. Conditional logistic regression was used to quantify the relationship of HC and smoking to CIN 2/3 adjusted for various factors. Results Current-users of HC were at higher risk for CIN 2/3 than never-users [odds ratio (OR) = 1.50, 95%CI = 1.03–2.17] and risk increased with increasing duration of use [ORs:1.13 (0.73–1.75), 1.51 (1.00–2.72), 1.82 (1.22–2.72) for

Background Older people represent increasing proportions of the population with cancer. To understand the representivity of cancer treatments in older people, we performed a systematic literature review using PRISMA guidelines of the age distribution of clinical trial participants for three leading cancer types, namely breast, prostate, and lung. Methods We used PubMed to identify articles detailing meta or pooled-analyses of phase III, randomised controlled trials (RCTs) of survival for breast, prostate and lung cancer, published ≤5 years from 2016. We compared the age distribution of participants to that of these cancers for “More developed regions”. Results 4993 potential papers were identified, but only three papers on breast cancer, three on lung cancer, and none on prostate cancer presented the age distribution of their participants. Except for one paper of breast cancer, participants ≥70 years in all other papers were underrepresented. Conclusions We recommend the age distribution of patients be clearly reported in all clinical trials, as per guidelines. Clinical trials ought to be more representative of the populations most affected by the disease for which treatments are being tested. This should lead to better knowledge of effectiveness of treatments and better translation of trial results to optimal care of older cancer patients.

A multicenter hospital-based case-control study comprising 670 incident cases of esophageal cancer (EC) and 1188 controls, frequency-matched for age and sex, was conducted to evaluate the role of diet on EC development in the Eastern Cape Province, South Africa. A locally relevant lifestyle and dietary questionnaire was used. Adjusted odds ratios (OR) and 95% confidence intervals (CI) were computed using unconditional multivariable logistic regression. Individually, maize or sorghum consumption vs. never or rare consumption were not associated with EC (P > 0.1). Males and females consuming green leafy vegetables 5-7 days/wk had 38% (P = 0.04) and 50% (P = 0.007) reduced odds of developing EC, respectively, compared with consumption

IntroductionData on the association between HIV infection and deaths from underlying medical conditions are needed to understand and assess the impact of HIV on mortality. We present data on mortality in the Chris Hani Baragwanath Hospital (CHBH) South Africa and analyse the relationship between each cause of death and HIV.MethodsFrom 2006 to 2009 data were collected on 15,725 deaths including age, sex, day of admittance and of death, HIV status, ART initiation and CD4+ cell counts. Causes of death associated with HIV were cases, causes of death not associated with HIV were controls. We calculate the odds-ratios (ORs) for being HIV-positive and for each AIDS related condition the disease-attributable fraction (DAF) and the population-attributable fraction (PAF) due to HIV for cases relative to controls.ResultsAmong those that died, the prevalence of HIV was 61% and of acquired immune deficiency syndrome (AIDS) related conditions was 69%. The HIV-attributable fraction was 36% in the whole sample and 60% in those that were HIV-positive. Cryptococcosis, Kaposi's sarcoma and Pneumocystis jirovecii, TB, gastroenteritis and anaemia were highly predictive of HIV with odds ratios for being HIV-positive ranging from 8 to 124, while genito-urinary conditions, meningitis, other respiratory conditions and sepsis, lymphoma and conditions of skin and bone were significantly associated with HIV with odds ratios for being HIV-positive ranging from 3 to 8. Most of the deaths attributable to HIV were among those dying of TB or of other respiratory conditions.ConclusionsThe high prevalence of HIV among those that died, peaking at 70% in those aged 30 years but still 7% in those aged 80 years, demonstrates the impact of the HIV epidemic on adult mortality and on hospital services and the extent to which early anti-retroviral treatment would have reduced the burden of both. These data make it possible to better assess mortality and morbidity due to HIV in this still high prevalence setting and, in particular, to identify those causes of death that are most strongly associated with HIV.

Background: Serologic testing for antibodies against epitopes from pathogens is a valuable tool for investigating the relationship between infection and disease. This study comprehensively evaluates the impact of preanalytic variation on antibody seropositivities to a selected set of antigens arising from delays in processing of blood samples, preprocessing storage temperature, and vacutainer type. Methods: We assessed peripheral blood collected from 29 volunteers in four different Vacutainer types [ethylenediaminoetetraacetic acid (EDTA), acid-citrate-dextrose (ACD), lithium heparin (LH), serum separator tubes (SST)], and stored at 4°C or room temperature for 0, 1, 2, 3, 4, 5, and 6 days before processing. Multiplex serology was used to determine antibody reactivity against 35 antigens derived from human papillomaviruses, human polyomaviruses, Epstein–Barr virus, and Helicobacter pylori. Cohen's κ statistic was used to measure agreement on seropositivity status between samples exposed to standard and nonstandard clinical practice conditions. Results: For samples processed without delay, κ was not associated with storage-temperature (P value range 0.23 to 0.95) or vacutainer type (P value range, 0.35–0.89). Kappa did not significantly decline with increasing delays in processing for any vacutainer-type storage temperature combination (P slope range, 0.06–1.00). Conclusions: Antibodies to epitopes from various pathogenic infectious agents can be measured reliably from samples stored in SST, EDTA, ACD, or LH vacutainers at either room temperature or 4°C for up to 6 days before processing. Impact: Serologic testing is robust to several preanalytic options. These findings are particularly important for epidemiologic studies recruiting participants from remote settings where sample exposure to preanalytic conditions can vary considerably. Cancer Epidemiol Biomarkers Prev; 26(8); 1337–44. ©2017 AACR.

Sun exposure is the main cause of squamous (SCC) and basal cell carcinoma (BCC) although pattern and amount differ by cancer type, and sun sensitivity is the major host risk factor. Our study investigated risk factors and residential ambient UV in a population-based sample of Australian 45 and Up Study participants: 916 BCC cases, 433 SCC cases, 1224 controls. Unconditional logistic regression models adjusting for key covariates demonstrated 60% increased BCC risk and two-fold increased SCC risk with sun sensitivity, and three- and four-fold increased risk, respectively, with solar keratoses. BCC but not SCC risk increased with higher early-life residential UV in all participants (odds ratio (OR) = 1.54; 95% CI 1.22-1.96 for intermediate; OR = 1.31; 95% CI 1.03-1.68 for high UV at birthplace) and similarly in Australian-born participants (P-values < 0.05). Risk of SCC but not BCC increased with long-term cumulative sun exposure assessed by self-reported outdoor work (OR 1.74, 95% CI 1.21-2.49). In conclusion, sun sensitivity is important for both cancers, early-life UV but not cumulative UV appears to increase BCC risk, the former an apparently novel finding, and SCC risk appears only to be related to long-term cumulative sun exposure.

Response from the authors to correspondence related to ‘Has the incidence of brain cancer risen in Australia since the introduction of mobile phones 29 years ago?’

Prostate cancer (PC) is the most common non-cutaneous cancer in men worldwide. The relationships between PC and possible risk factors for PC cases (n = 1,181) and male controls (n = 875) from the New South Wales (NSW) Cancer, Lifestyle and Evaluation of Risk Study (CLEAR) were examined in this study. The associations between PC risk and paternal history of PC, body mass index (BMI), medical conditions, sexual behaviour, balding pattern and puberty, after adjusting for age, income, region of birth, place of residence, and PSA testing, were examined. Adjusted risk of PC was higher for men with a paternal history of PC (OR = 2.31; 95%CI: 1.70-3.14), personal history of prostatitis (OR = 2.30; 95%CI: 1.44-3.70), benign prostatic hyperplasia (OR = 2.29; 95%CI: 1.79-2.93), being overweight (vs. normal; OR = 1.24; 95%CI: 0.99-1.55) or obese (vs. normal; OR = 1.44; 95%CI: 1.09-1.89), having reported more than seven sexual partners in a lifetime (vs. 3 partners; OR = 2.00; 95%CI: 1.49-2.68), and having reported more than 5 orgasms a month prior to PC diagnosis (vs. ≤3 orgasms; OR = 1.59; 95%CI: 1.18-2.15). PC risk was lower for men whose timing of puberty was later than their peers (vs. same as peers; OR = 0.75; 95%CI: 0.59-0.97), and a smaller risk reduction of was observed in men whose timing of puberty was earlier than their peers (vs. same as peers; OR = 0.85; 95%CI: 0.61-1.17). No associations were found between PC risk and vertex balding, erectile function, acne, circumcision, vasectomy, asthma or diabetes. These results support a role for adult body size, sexual activity, and adolescent sexual development in PC development.

Introduction and Aims.Approximately 25% of the Australian population was born abroad, yet there has been very little tobacco control aimed at culturally and linguistically diverse communities and limited data exist on smoking among Australian migrants. The aim of this study was to compare smoking characteristics of Australian migrants (in terms of place of birth and age migrated) to those of Australian-born residents. Design and Methods.A cross-sectional analysis of self-reported questionnaire data from 53 207 women and 48 777 men aged 45 years or over in The 45 and Up Study in Australia (2006–2008) was performed. Results.52.6% (95% confidence intervals 52.1–53.0) of men and 35.5% (35.1–35.9) of women reported ever being a regular smoker and 7.6% (7.4–7.8) and 7.3% (7.1–7.5) reported current smoking, respectively. Compared with Australian-born men, a higher proportion of men born in Europe, North Africa and the Middle East were current smokers, with odds ratios adjusted for age, income, education and place of residence (OR; 95% confidence intervals) ranging from 1.30 (1.16–1.45) to 1.96 (1.49–2.58). Compared with Australian-born women, a lower proportion of women from East (0.21; 0.12–0.36) and Southeast Asia (0.38; 0.26–0.54) were current smokers and a higher proportion of women from New Zealand (1.45; 1.17–1.79) and the UK/Ireland (1.25; 1.12–1.40) were current smokers. Among women born in Asia, the risk of smoking increased significantly the younger they migrated to Australia. Duration smoked and amount smoked per day were primarily lower among migrants than Australian-born. Conclusions.Smoking prevalence varies substantially across cultural subgroups. Understanding smoking dynamics across diverse cultural groups will assist in better targeting of tobacco control programs. [Weber WF, Banks E, Sitas F. Smoking in migrants in New South Wales, Australia: Report on data from over 100 000 participants in the 45 and Up Study. Drug Alcohol Rev 2010;30:597–605]

Objectives To provide a more accurate estimate of early smoking-attributable mortality and potential years of life lost using data from a representative study of 103 study areas in China. Methods Two datasets were employed as follows. Firstly, retrospective national mortality survey data, which included a population of 67 million in 103 study areas, and about 1 million adults who died in 1986–1988; secondly, nationally representative case-control comparative data was extracted from the survey data to measure the effect of smoking on age trends in smoking-attributable mortality. Potential years of life lost, and sex differences in life expectancy in smokers and non-smokers in the total population aged 35 and over were also estimated. Results Tobacco caused 11.2% (16.0% of men and 3.7% of women) of total deaths in 1987, and more than two-thirds of these excess deaths occurred between the ages of 50 and 74 years, but only less than 5% excess deaths occurred at ages under 50. Although life expectancies varied with region or sex differences, the years of life lost attributable to smoking was almost the same. Smokers at age 35 lost about 3 years of life expectancy in comparison with never smokers. The study also confirmed that more than 50% of the sex difference in life expectancy was accounted for by smoking. Conclusion Fully understanding the consequences of smoking in relation to mortality can clarify its effects on the health and longevity of the entire population.

Objective To compare the characteristics of people who utilize colorectal cancer screening tests with those who do not. Setting Self-reported questionnaire data from 15,900 women and 14,953 men aged 50 or over who had never had colorectal cancer were taken from the 45 and Up Study cohort in Australia in 2006. Methods A cross-sectional analysis of colorectal cancer test behaviour within the last five years by faecal occult blood test (FOBT), or by any test (FOBT, sigmoidoscopy or colonoscopy) was performed. Results A total of 36.2% of participants reported colorectal cancer testing and 17.9% reported having a FOBT. Both FOBT and any testing were reduced significantly in groups with the following attributes compared with the remaining population; ages 50–59 and 80+; female; no family history of colorectal cancer; lower education; lower income; not speaking English at home; lack of private health insurance; not being retired; not living with a partner and not having other screening tests. Compared with other participants, test uptake was particularly low among current smokers (relative risk 0.76, 95% CI 0.71–0.80), sedentary participants (0.71, 95% CI 0.66–0.77), those without fruit (0.77, 95% CI 0.71–0.84) or vegetables (0.79, 95% CI 0.69–0.90) in their daily diet and those with a disability (0.91, 95% CI 0.85–0.97). Compared with participants from major cities, outer regional area participants were significantly more likely to report a FOBT (1.31, 95% CI 1.23–1.39) however participants in remote areas were significantly less likely to have had any colorectal cancer test (0.75, 95% CI 0.67–0.85). Conclusion Subgroups of the Australian population may require targeted intervention to ensure equity in colorectal cancer screening.

BACKGROUND: The Eastern Cape Province of South Africa, which includes the former Transkei has high rates of squamous cell oesophageal cancer (OC), thought to be caused mainly by nutritional deficiencies and fungal contamination of staple maize. A hospital-based case-control study was conducted at three of the major referral hospitals in this region to measure, among other suspected risk factors, the relative importance of tobacco smoking and alcohol consumption for the disease in this population. METHODS: Incident cases (n=670) of OC and controls (n=1188) were interviewed using a structured questionnaire which included questions on tobacco and alcohol-related consumption. Odds ratios (ORs) with 95% confidence intervals for each of the risk factors were calculated using unconditional multiple logistic regression models. RESULTS: A monotonic dose-response was observed across the categories of each tobacco-related variable in both sexes. Males and females currently smoking a total of >14g of tobacco per day were observed to have over 4-times the odds of developing OC (males OR=4.36, 95% CI 2.24-8.48; females OR=4.56, 95% CI 1.46-14.30), with pipe smoking showing the strongest effect. Similar trends were observed for the alcohol-related variables. The quantity of ethanol consumed was the most important factor in OC development rather than any individual type of alcoholic beverage, especially in smokers. Males and females consuming >53g of ethanol per day had approximately 5-times greater odds in comparison to non-drinkers (males OR=4.72, 95% CI 2.64-8.41; females OR=5.24, 95% CI 3.34-8.23) and 8.5 greater odds in those who smoked >14g tobacco daily. The attributable fractions for smoking and alcohol consumption were 58% and 48% respectively, 64% for both factors combined. CONCLUSION: Tobacco and alcohol use are major risk factors for OC development in this region. IMPACT: This study provides evidence for further reinforcement of cessation of smoking and alcohol consumption to curb OC development. South African Medical Research Council, The Rockefeller Foundation, Cancer Council NSW and UICC are acknowledged for their financial support of this study.

BACKGROUND: Mobile phone use in Australia has increased rapidly since its introduction in 1987 with whole population usage being 94% by 2014. We explored the popularly hypothesised association between brain cancer incidence and mobile phone use. STUDY METHODS: Using national cancer registration data, we examined age and gender specific incidence rates of 19,858 male and 14,222 females diagnosed with brain cancer in Australia between 1982 and 2012, and mobile phone usage data from 1987 to 2012. We modelled expected age specific rates (20-39, 40-59, 60-69, 70-84 years), based on published reports of relative risks (RR) of 1.5 in ever-users of mobile phones, and RR of 2.5 in a proportion of 'heavy users' (19% of all users), assuming a 10-year lag period between use and incidence. SUMMARY ANSWERS: Age adjusted brain cancer incidence rates (20-84 years, per 100,000) have risen slightly in males (p0.05) and are higher in males 8.7 (CI=8.1-9.3) than in females, 5.8 (CI=5.3-6.3). Assuming a causal RR of 1.5 and 10-year lag period, the expected incidence rate in males in 2012 would be 11.7 (11-12.4) and in females 7.7 (CI=7.2-8.3), both p

Menopausal Hormone Therapy (MHT) use in Australia fell by 55% from 2001 to 2005, following the release of large-scale findings on its risks and benefits. Comprehensive national data, including information on overall prevalence of MHT use as well as information on duration of use in Australia have not been reported since the 2004–5 National Health Survey, when 11% of women aged 45+ years were estimated to be current MHT users. No national data are available on prevalence of use of “bioidentical” hormone therapy (BHT). The objective of this study was to determine recent prevalence of MHT and BHT use. A cross-sectional, national, age-stratified, population survey was conducted in 2013. Eligible women, aged 50–69 years, resident in Australia were randomly sampled in 5-year age groups from the Medicare enrolment database (Australia’s universal health scheme). The response rate was 22% based on return of completed questionnaires, and analyses were restricted to 4,389 women within the specified age range. The estimated population-weighted prevalence of current use of MHT was 13% (95%CI 12–14), which was broadly similar to the previously reported national figures in 2004–5, suggesting that the use of MHT in Australia has largely stabilised over the past decade. A total of 39% and 20% of current-users with an intact uterus reported use of oestrogen-progestagen MHT and oestrogen-only MHT, respectively, whereas 77% of hysterectomised current-users used oestrogen-only MHT. Almost three-quarters of current-users [population-weighted prevalence 9% (95%CI 8–10)] had used MHT for 5 years. In regard to BHT, estimated population-weighted prevalence of ever use was 6% (95%CI 6–7) and 2% (95%CI 2–3) for current use. The populationweighted prevalence of MHT and BHT combined, in current users in their fifties and sixties was 15% (95%CI 14–16). These data provide a recent national “snapshot” of Australian women’s use of both conventional MHT and of BHT. The study was funded by Cancer Council NSW. The funding source had no involvement in the study design, analysis, and interpretation of results, writing of the manuscript or the decision to submit for publication. KC and EB receive salary support from the National Medical Research Council Australia (APP1082989 and APP1042717, respectively)

The objective was to assess whether Kaposi sarcoma--associated herpesvirus (KSHV) with or without HIV coinfection in South African mothers is associated with higher KSHV seropositivity in their children. We tested sera from 1287 South African children and 1179 mothers using assays for KSHV lytic K8.1 and latent ORF73 antigens. We computed odds ratios (ORs) and 95% confidence intervals (CIs) to assess associations between KSHV serostatus and risk factors. KSHV seroprevalence was 15.9% (204 of 1287 subjects) in children and 29.7% (350 of 1179 subjects) in mothers. The risk of KSHV seropositivity was significantly higher in children of KSHV-seropositive mothers compared with those of KSHV--seronegative mothers. The HIV status of mothers was marginally associated with an increased risk of KSHV seropositivity in their children (OR = 1.6 95% CI: 1.0 to 2.6; P = 0.07). KSHV seroprevalence was significantly higher in HIV-infected subjects (P = 0.0005) and HIV-infected subjects had significantly higher lytic and latent KSHV antibody levels than HIV-negative subjects. The risk of acquisition of KSHV was higher among children of KSHV-seropositive mothers. Although KSHV seroprevalence was significantly higher in children and mothers who were infected with HIV the HIV status of the mother was only marginally associated with an increased risk of KSHV seropositivity in the child. (authors)

Human papillomavirus (HPV) types causing anogenital lesions and cancer are accepted as being sexually transmitted. The methods whereby children acquire these anogenital type HPV infections are unclear. The present study determined the prevalence of anti-HPV-16, HPV-11 and HPV-18 IgG antibodies in mothers and their children in an attempt to identify evidence of HPV transmission from mother to child. HPV virus-like particles (VLP) VLP-16, VLP-11 and VLP-18 were used in enzyme-linked immunosorbent assay to identify IgG antibodies in serum from 100 mothers and their 111 children. Antibodies to VLP-16, VLP-11 and VLP-18 were found in serum from 17%, 21% and 16% of mothers, respectively and seroprevalences were 9%, 11.7% and 9.9%, respectively amongst the children. Of the 111 children, 23 (20.7%) showed antibodies to one or more of the three HPV types tested. Seven of these (30.4%) HPV IgG positive children had the same antibodies to one or more HPV types as their mothers. The prevalence of HPV-11 was similar in children of seropositive compared with seronegative mothers (14% and 11%, respectively). The prevalence of HPV-16 and HPV-18 was higher in children of seropositive mothers compared with seronegative mothers (for HPV-16, 18% and 7%, respectively, P = 0.1, for HPV-18, 19% and 8%, respectively, P = 0.2). None of these differences were statistically significant indicating a lack of correlation between antibodies in mothers and children and no evidence to support vertical or horizontal mother to child transmission of HPV infection. Indications were of multiple sources of HPV infection in the children. J. Med. Virol. 79:1370–1374, 2007. © 2007 Wiley-Liss, Inc.

Stomach cancer is one of the leading causes of cancer death worldwide, despite its incidence and mortality falling in many places. The discovery in 1984 that a bacterial infection with Helicobacter pylori could cause stomach and duodenal ulcers prompted work in its role in causing gastritis, and led to the first prospective study in 1991 by Forman et al., showing that infection with H.pylori increased the risk of stomach cancer in those infected by almost three-fold. Prior to then, it was hypothesized that stomach was caused by poor diets. While diets may still play a role, the falls in stomach cancer incidence have been associated with reductions in population prevalence of H. pylori. Discovery of the link was accelerated by the use of stored sera from other unrelated studies, and the use of serological assays. Since those discoveries the treatment landscape of gastric disorders has changed significantly, with a rapid uptake of antibiotic and proton pump inhibitors (triple) therapies in those who are H. pylori positive. Over time we have seen falls in gastric cancer, peptic and duodenal ulcers and in many of the procedures previously used to cure peptic ulcer disease, such as vagotomies and gastrectomies. Further still, an oral vaccine against H. pylori, first trialled in China, holds much promise of being the third vaccine against a cancer causing infection. If successful this would lead to a further reduction in H. pylori related conditions, and ultimately gastric cancer, an otherwise lethal disease.

Background In 2013, about 32 % of the Australian population over 15 years of age was born overseas. Previous cancer-related immigrant health studies identified differences in mortality and incidence between immigrants and Australian-born people. To identify groups that may require targeted interventions, we describe by region of birth: 1. the highest cancer incidence and mortality rates for NSW residents, Australia’s most populous state; and 2. mortality to incidence ratios (MIR) for all cancers. Methods Cancer incidence and mortality data were obtained from NSW residents for 2004–2008 (averaged) by sex, region of birth and 10 year age groups. Age standardised incidence and mortality rates were calculated with 95 % confidence intervals (per 100,000), using the world standard population. In the place of 5-year survival rates, we used age standardised MIRs (=M/I) as a simple proxy indicator of cancer survival. Results All-cancer incidence only exceeded Australian born people (308.5) for New Zealand born (322). The highest reported incidence rates for cancers from all regions were prostate and breast cancers. All-cancer mortality exceeded Australian-born (105.3) in people born in Western Europe (110.9), Oceania (108.2) and UK and Ireland (106.4). For Australian-born residents, the MIR was 34 cancer deaths per 100 cases compared to residents from Central Europe at 38 deaths per 100 cases and lowest at 28 deaths per 100 cases for residents from Central and Southern Asia. Conclusion Some disparities between Australian-born NSW residents and immigrants were identified in prostate, breast and lung cancer mortality rates. While on average most immigrant groups have similar cancer characteristics for the top cancers, areas for improvement to inform strategies to alleviate cancer disparities are required. This analysis suggests that NSW residents could benefit from specific prevention programmes on healthy eating and smoking cessation, especially people from Central Europe, UK and Ireland and Western Europe. Rising immigration rates encourage us to continue to address the areas indicated for improvement. Electronic supplementary material The online version of this article (doi:10.1186/s12889-015-2141-3) contains supplementary material, which is available to authorized users.

PURPOSE: Limited research has examined smoking amongst recent cancer survivors or the relative contribution of factors on smoking behaviour. This study aimed to describe amongst recent Australian cancer survivors (i) prevalence of smoking by cancer type, (ii) characteristics associated with continued smoking following diagnosis, (iii) intention to quit among those who continue to smoke and (iv) characteristics associated with quitting following diagnosis. METHOD: Cross-sectional data were analysed from 1299 cancer survivors diagnosed with their first primary cancer recruited from two Australian cancer registries in Australia between 2006 and 2008. RESULTS: Of participants, 8.6 % reported current smoking. Participants who were younger and single or widowed reported higher odds of current smoking. Participants who had a certificate/diploma or tertiary education reported lower odds of smoking. Among current smokers, 53 % intended to quit in the future. Lung cancer survivors reported more than four times the odds of quitting smoking since diagnosis compared to other cancer types. CONCLUSION: Of recent Australian cancer survivors, 14 % report continued smoking. IMPLICATIONS FOR CANCER SURVIVORS: Smoking following a cancer diagnosis is associated with increased risk of mortality and further morbidity. There is a need to target cessation efforts towards survivors who are younger, without a partner and with a low level of education.