This study demonstrates increased tumour angiogenesis in NMSC in RTRs, and suggests a role for VEGF-A-positive peritumoural leukocytes in suppressing NMSC development.
We present a series of 5 intravenous drug users (4 male, age range 24–47 years) with glomerular deposition of a lipid-like material. Three patients presented with the nephrotic syndrome, 1 with acute renal failure and 1 with hypertension and an active urinary sediment. All were continuing to use opiates intravenously (mixed with lemon juice or acetic anhydride and sodium bicarbonate). Investigations: plasma creatinine 0.10–0.30 mmol/l, urinary protein excretion 1.0–6.75 g/24 h, hepatitis C antibody positive (4), all seronegative for hepatitis B and HIV. Renal biopsy showed large vacuolated areas consistent with heavy deposition of lipid-like material in all glomerular cells and infiltrating macrophages. Two showed ATN and another FGS. We suggest that these changes are due to the pattern of illicit drug availability and preparation peculiar to these users.
Melanoma, the most aggressive skin cancer type, is responsible for 75% of skin cancer related deaths worldwide. Given that New Zealand (NZ) has the world's highest melanoma incidence, we sought to determine the frequency of mutations in NZ melanomas in recurrently mutated genes. NZ melanomas were from localities distributed between North (35°S-42°S) and South Islands (41°S-47°S). A total of 529 melanomas were analyzed for BRAF exon 15 mutations by Sanger sequencing, and also by Sequenom MelaCarta MassARRAY. While, a relatively low incidence of BRAFV600E mutations (23.4%) was observed overall in NZ melanomas, the incidence of NRAS mutations in South Island melanomas was high compared to North Island melanomas (38.3% vs. 21.9%, P=0.0005), and to The Cancer Genome Atlas database (TCGA) (38.3% vs. 22%, P=0.0004). In contrast, the incidence of EPHB6G404S mutations was 0% in South Island melanomas, and was 7.8% in North Island (P=0.0002). Overall, these data suggest that melanomas from geographically different regions in NZ have markedly different mutation frequencies, in particular in the NRAS and EPHB6 genes, when compared to TCGA or other populations. These data have implications for the causation and treatment of malignant melanoma in NZ.
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