One of Nick’s key early achievements at QIMR was to establish a twin study on melanoma risk factors. The Brisbane Twin Nevus Study (BTNS) had an initial focus on nevus (mole) count in adolescents but, reflecting Nick’s broad interests, expanded in scope enormously over the decades. In the skin cancer arena, BTNS was essential to genetic discoveries in melanoma, eye color and pigmentation. Later studies amassed data on thousands of phenotypes, ranging from molecular phenotypes such as gene expression to studies where gene mapping findings in adolescents turned out to have translational potential in late-onset diseases. Nick’s twin data have formed the basis for an enormous range of discoveries, with Nick and his colleagues continuing to capitalize on these data.

Local chemotherapy with biocompatible drug-delivery systems prolongs survival in patients. Due to the biocompatibility and high loading capacity, bentonite nanoclay is a good candidate for the fabrication of drug-delivery vehicles. In this study, doxorubicin-bentonite nanoclay complex (DOX-Bent complex) was prepared for the first time as a sustained-release drug-delivery system for intratumoural chemotherapy of melanoma. An efficient loading of DOX on 1 mg of bentonite nanoclay as high as 994.45 ± 4.9 µg was obtained at a 30:1 DOX:bentonite nanoclay mass ratio. The DOX-Bent complex showed a low initial burst release of DOX in the first 24 h of release, followed by a sustained-release pattern for 21 days. The cumulative in vitro release of DOX from the DOX-Bent complex at pHs 6.5 and 7.4 revealed that the DOX-Bent complex can distinguish between tumour and normal tissues and express specific drug release at the tumour site. The results of cytotoxicity experiments indicated that the release pattern of DOX can supply sufficient DOX to inhibit growth of the melanoma cancer cell with an IC50 of 0.29 ± 0.07 µg/mL. It is thus suggested that the DOX-Bent complex be introduced as a drug-delivery system for effective local cancer therapy.

Skin self-examination (SSE) is a crucial preventive health behaviour in melanoma survivors, as it facilitates early detection. Physician endorsement of SSE is important for the initiation and maintenance of this behaviour. This study focussed on the preliminary validation of a new nine-item measure assessing physician support of SSE in melanoma patients. English and French versions of this measure were administered to 188 patients diagnosed with melanoma in the context of a longitudinal study investigating predictors and facilitators of SSE. Structural validity was investigated using exploratory factor analysis conducted in Mplus and convergent and divergent validity was assessed using bivariate correlations conducted in spss. Results suggest that the scale is a unidimensional and reliable measure of physician support for SSE. Given the uncertainty regarding the optimal frequency of SSE for at-risk individuals, we recommend that future psychometric evaluations of this scale consider tailoring items according to the most up-to-date research on SSE effectiveness.

Glycaemic index (GI) and glycaemic load (GL) are indicators of dietary carbohydrate quantity and quality and have been associated with increased risk of certain cancers and type 2 diabetes. Insulin resistance has been associated with increased melanoma risk. However, GI and GL have not been investigated for melanoma. We present the first study to examine the possible association of GI and GL with melanoma risk. We carried out a population-based, case–control study involving 380 incident cases of cutaneous melanoma and 719 age- and sex-matched controls in a northern Italian region. Dietary GI and GL were computed for each subject using data from a self-administered, semi-quantitative food frequency questionnaire. We computed the odds ratio (OR) for melanoma according to quintiles of distribution of GL and GL among controls. A direct association between melanoma risk and GL emerged in females (OR 2·38; 95 % CI 1·25, 4·52 for the highest v. the lowest quintile of GL score, Pfor trend 0·070) but not in males. The association in females persisted in the multivariable analysis after adjusting for several potential confounders. There was no evidence of an association between GI and melanoma risk. GL might be associated with melanoma risk in females.

Sinclair swine develop an aggressive form of melanoma, which, in many cases, spontaneously regresses after a complete metastatic phase. We used Affymetrix GeneChip® Porcine Genome Arrays consisting of 24 123 probe sets to compare gene expression in white blood cells (WBCs) and various tissues including the liver, lungs, inguinal lymph nodes and spleen harvested from a Sinclair piglet afflicted by melanoma at birth and exhibiting metastatic lesions at weaning (6 weeks) with those from a full-sibling piglet that showed no incidence of melanoma at birth and weaning. The highest number (3489; ∼14%) of significantly upregulated transcripts (fold change in gene expression ⩾2.0 and t-test P-value ≤0.05) was observed in the liver, while the spleen exhibited the lowest number of upregulated transcripts (528; ∼2%). Among significantly downregulated genes, the highest numbers were observed in the inguinal lymph nodes (3651; ∼15%) and the least in WBCs (730; ∼3%). Differentially expressed transcripts included genes involved in melanoma pathogenesis including SILV, TYR and RAB28. SILV was over-expressed 784-, 430- and 164-fold, while TYR was over-expressed 138-, 81- and 28-fold in the liver, lungs and inguinal lymph nodes, respectively. Quantitative real-time RT-PCR (qRT-PCR) confirmed the microarray data of 12 selected differentially expressed sequences. These results suggest that significant changes in gene expression occur during metastasis of malignant melanoma in the Sinclair swine model. In addition, qRT-PCR analysis of the above 12 differentially expressed sequences was carried out on liver samples collected from 22 pigs (12 of which had melanoma during the first 6 weeks of life), and an ANOVA test contrasting absolute RNA expression between pigs with regressing, progressing and without tumors was significant for TYR, TACSTD1, MATP, GPNMB and CYP4A22, with P-values of 0.034, 0.015, 0.007, 0.050 and 0.022, respectively.

Stratospheric ozone depletion threatens to increase exposure to ultraviolet (UV) radiation which is known to be a factor in a number of diseases. There is little doubt that cumulative exposure to UV radiation is important in the aetiology of non-melanoma skin cancers. Evidence is also strong for a link with cutaneous malignant melanoma, although here it appears to be intermittent intense exposure that is most damaging. More controversial is the view that exposure to solar radiation is a significant factor in ocular damage, particularly in the formation of cataracts. Earlier studies pointing to such an effect have been criticized and alternative aetiological hypotheses have been proposed. However, other studies do show an effect of UV exposure on cortical cataract. Concern is also growing that UV may be capable of activating viruses and have immunological effects that might exacerbate infectious disease. Very worrying is the possibility that UV exposure can activate the human immunodeficiency virus which might accelerate the onset of AIDS. Any such health effects that have been observed in human populations are the result of exposure to existing, naturally occurring levels of UV radiation. There is, therefore, great concern about the possible exacerbation of these impacts as a result of increased exposure to UV radiation associated with stratospheric ozone depletion. However, any assessment of the nature and scale of such impacts on human health has to deal with several major problems and these are the focus of this paper. There are uncertainties about recent trends in stratospheric ozone and problems in the prediction of future changes. Following on from this are the difficulties of estimating what effects these changes will have on UV flux at ground level in populated areas. Further problems arise in the prediction of changes in biologically significant doses to humans which might be affected by changes in behaviour as well as by changes in the environment. Finally, the limitations of existing epidemiological knowledge of the effects of UV exposure are a constraint on our ability to predict what the health effects of any changed UV doses might be.

The study objective was to examine the association, among older persons with cutaneous melanoma, between areal socioeconomic status (SES) and receiving chemotherapy. SEER-Medicare-linked database (1,239 white men and women aged ≥ 66, with invasive melanoma [regional and distant stages]; 1991–1999) was used. SES was measured by census tract poverty level (average of 1990 and 2000 Census data). Covariates were sociodemographics, tumor characteristics, and comorbidity index. Residing in poorer SES areas was associated with a lower likelihood for receiving chemotherapy among patients in the overall sample (adjusted odds ratios = OR 0.97, 95% confidence interval = CI 0.95–0.99), and those with regional stage at diagnosis (OR 0.97, 95% CI 0.94–0.98). These findings reflect socioeconomic disparities in chemotherapy use for melanoma among older white patients in the United States.

Status epilepticus (SE), both convulsive and nonconvulsive, is a rare adverse effect of electroconvulsive therapy (ECT). This case report describes SE post-ECT associated with central nervous system (CNS) metastatic melanoma and reviews pertinent literature. The authors recommend that when CNS pathology is suspected, pre-ECT neurology consultation, neuroimaging, and EEG all may be indicated. This is especially important for patients with histories of primary cancers, such as melanoma, that metastasise to the brain.

This review examines the mechanisms involved in anti-tumor immunity and how peptides present in many tumor types (tumor-associated antigens) are recognized by T cells from tumor-bearing cancer patients. Tumor-associated antigens are derived from proteins that are also expressed in normal cells. It is predicted that immune responses to such peptides will be compromised by self-tolerance or that stimulation of effective immune responses will be accompanied by autoimmunity. We also consider that the immunity induced against two autoantigens, which are highly conserved in vertebrates, involve qualitatively different mechanisms, such as the production of antibodies and cell-mediated immune responses. However, both pathways lead to tumor immunity and identical phenotypic manifestations of autoimmunity. Appropriate selection of the optimal tumor antigen is critical for the induction of an anti-tumor immune response. Thus, we stress that the methods for antigen presentation using dendritic cells play a critical role in the development of tumor vaccines, to break immune tolerance and induce a strong immune response against them. The viability and feasibility of expansion of canine dendritic cells from bone marrow and peripheral blood ex vivo for the treatment of spontaneous cancers in dogs is also discussed.