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Background: People at high risk of developing melanoma are usually identified by pigmentary and naevus phenotypes. Objective: We examined whether associations of these phenotypes with melanoma risk differed by ambient sun exposure or participant characteristics in two population‐based, case–control studies with comparable ancestry but different ambient sun exposure. Methods: Data were analysed from 616 cases and 496 controls from the Australian Melanoma Family Study and 2012 cases and 504 controls from the Leeds (UK) case–control study. Questionnaire, interview and dermatological skin examination data were collected using the same measurement protocols. Relative risks were estimated as odds ratios using unconditional logistic regression, adjusted for potential confounders. Results: Hair and skin colour were the strongest pigmentary phenotype risk factors. All associations of pigmentary phenotype with melanoma risk were similar across countries. The median number of clinically assessed naevi was approximately three times higher in Australia than Leeds, but the relative risks for melanoma associated with each additional common or dysplastic naevus were higher for Leeds than Australia, especially for naevi on the upper and lower limbs. Higher naevus counts on the head and neck were associated with a stronger relative risk for melanoma for women than men. The two countries had similar relative risks for melanoma based on self‐reported naevus density categories, but personal perceptions of naevus number differed by country. There was no consistent evidence of interactions between phenotypes on risk. Conclusions: Classifying people at high risk of melanoma based on their number of naevi should ideally take into account their country of residence, type of counts (clinical or self‐reported), body site on which the naevus counts are measured and sex. The presence of naevi may be a stronger indicator of a genetic predisposition in the UK than in Australia based on less opportunity for sun exposure to influence naevus development. [ABSTRACT FROM AUTHOR]

The epidemiology of androgenetic alopecia (AGA) is not fully understood. Although a strong genetic basis has long been identified, little is known of its non-genetic causes. To estimate the prevalence of and to determine risk factors for AGA in men aged 40–69 years in Australia. Men ( n = 1390) were recruited at random from the electoral rolls to serve as controls in a population-based case–control study of prostate cancer. All were interviewed in person and direct observations of AGA were made. Men were grouped into the following categories; no AGA, frontal AGA, vertex AGA and full AGA (frontal and vertex AGA). Epidemiological data collected from these men were used for an analysis of risk factors for each AGA category using unconditional logistic regression with AGA category as the response variable adjusting for age, education and country of birth. The prevalence of vertex and full AGA increased with age from 31% (age 40–55 years) to 53% (age 65–69 years). Conversely, the proportion of men with only frontal AGA was very similar across all age groups (31–33%). No associations were found between pubertal growth spurt or acne, reports of adult body size at time of interview, urinary symptom score, marital status, or current smoking status or duration of smoking and the risk of any form of AGA. The consumption of alcohol was associated with a significant increase in risk of frontal and vertex AGA but not full AGA. Men with vertex AGA had fewer female sexual partners but average ejaculatory frequency did not differ between men in different AGA categories. Reported weight and lean body mass at reaching maturity at about 21 years of age were negatively associated with vertex balding ( P for trend < 0·05) but not with frontal AGA or full AGA. Evidence for environmental influences on AGA remains very slight. Our study failed to confirm previously reported or hypothesized associations with smoking and benign prostatic hypertrophy. The associations that we found with alcohol consumption and with lean body mass at age 21 years would be worthy of further research if they were able to be replicated in other studies. [ABSTRACT FROM AUTHOR]

Summary: Melanoma is a cancer that develops in the melanocytes, the pigment cells of the skin. Melanoma incidence rates, which show how common it is, have been increasing in people with fair skin, with the highest rates in Australia, New Zealand, North America and Europe. In Australia, one in 14 men and one in 24 women will be diagnosed with melanoma during their lifetime. Risk factors for melanoma include sun exposure, sunbed use, the number of moles on the skin, the skin's sensitivity to the sun, the number of freckles, skin colour, eye colour, hair colour, family history and a number of susceptibility genes (genes that place you at higher risk). Melanoma risk prediction models, which combine many individual melanoma risk factors into an overall risk, may be useful in the prevention of melanoma by matching prevention strategies (interventions) to the patient's melanoma risk levels. Many melanoma risk prediction models use self‐assessed risk factors because it is quicker and less costly compared to the clinical (medical) assessment of risk factors, but many people underestimate the number of moles they have. This study aims to derive a melanoma risk prediction model, which includes the number of moles on the body and solar lentigines (darker skin patches caused by the sun) as clinically‐assessed risk factors, and pigmentation (skin colour) characteristics, sun exposure, family history and history of skin cancer as self‐assessed risk factors. The number of moles is the strongest risk factor in the model. The model performs well on discrimination, the model's ability to distinguish between individuals with and without melanoma. In a clinical setting, this model may help clinicians identify patients for targeted prevention strategies based on the patient's melanoma risk. This is a summary of the study: Development and external validation study of a melanoma risk prediction model incorporating clinically assessed naevi and solar lentigines Linked Article: Vuong et al. Br J Dermatol 2020; 182:1262–1268 [ABSTRACT FROM AUTHOR]

We used data from 765 cases and 564 controls in the population-based Australian Breast Cancer Family Study to investigate whether, in women under the age of 40, the profile of risk factors differed between breast cancer subtypes defined by joint oestrogen and progesterone receptor status. As hypothesised, no significant differences were found. [ABSTRACT FROM AUTHOR]

Background Whether BRCA1 and BRCA2 mutation carriers have a clinically relevant elevated risk of uterine cancer has implications for risk-reducing surgery. Aim This multicentre, prospective cohort study assessed uterine cancer risk for mutation carriers compared with the general population. Methods Eligible mutation carriers were enrolled in the Kathleen Cuningham Foundation Consortium for Research into Familial Breast Cancer (kConFab) cohort study, had a uterus present and no history of uterine cancer at cohort entry. Epidemiological, lifestyle and clinical data were collected at cohort entry and updated three-yearly. Cancer events were verified using pathology reports. Follow-up was censored at death or last contact. Relative risk of uterine cancer was estimated using the standardised incidence ratio (SIR), with the expected number of cases determined using population-based data for Australia. Results Of 1,111 mutation carriers in kConFab, 283 were excluded due to prior hysterectomy ( N = 278), prior uterine cancer ( N = 2) or being non-residents ( N = 3). After a median follow-up of 9.0 years, five incident uterine cancers were reported in the 828 eligible women (419 had prior breast cancer and 160 had prior tamoxifen use), compared to 2.04 expected (SIR = 2.45; 95% confidence interval [CI]: 0.80–5.72; P = 0.11). In 438 BRCA1 mutation carriers and 390 BRCA2 mutation carriers, three and two incident cases of uterine cancer were reported, respectively, compared to 1.04 expected (SIR = 2.87; 95% CI: 0.59–8.43; P = 0.18) and 0.99 expected (SIR = 2.01; 95% CI: 0.24–7.30; P = 0.52), respectively. All cases were endometrioid subtype, International Federation of Gynaecology and Obstetrics stage I–II disease. No serous uterine cancers were reported. Conclusions Our findings are consistent with those from most other reports and do not support routine risk-reducing hysterectomy for BRCA1 and BRCA2 mutation carriers. [ABSTRACT FROM AUTHOR]