Simultaneous two organ metastases of the giant basal cell carcinoma of the skin

BACKGROUND: Basal Cell Carcinoma (BCC) is the most common carcinoma in humans. It accounts for 20% of carcinomas in men and 10-15% of carcinomas in women. Despite its high incidence, metastatic events are exceedingly rare. The reported frequency of metastatic dissemination is estimated at 0.0028-0.5 percent. Once metastasis is detected, there is a high mortality rate of 50% within 8 months. METHODS: In this study, we present a case of simultaneous lung and parotid metastases of giant BCC primary located on the right medial canthus of a 62 year old female. RESULTS: Examination of the tumor located on the medial canthus obtained showed "adenoid BCC". Computed tomography (CT) was performed to evaluate parotid region for evaluation of parotid gland and chest. Parotid and lung metastasis were detected in CT. Routine labarotory tests and radiological investigations were done. There was no abnormal finding. We also investigated this patient with a bone scan (normal), abdominal and cranial CT scans (also normal). CONCLUSION: Although metastasis of BCC is a very rare condition, this study reports a case of simultaneous parotid gland and lung metastasis originating from a giant BCC primary that was located on the right inner canthus of a 62 year old female.     

Journey to the skin

The peripheral axons of vertebrate tactile somatosensory neurons travel long distances from ganglia just outside the central nervous system to the skin. Once in the skin these axons form elaborate terminals whose organization must be regionally patterned to detect and accurately localize different kinds of touch stimuli. This review describes key studies that identified choice points for somatosensory axon growth cones and the extrinsic molecular cues that function at each of those steps. While much has been learned in the past 20 years about the guidance of these axons, there is still much to be learned about how the peripheral axons of different kinds of somatosensory neurons adopt different trajectories and form specific terminal structures.     

Use of the in vivo skin comet assay to evaluate the DNA-damaging potential of chemicals applied to the skin

The aim of the present study was to evaluate both sensitivity and specificity of an in vivo skin comet assay using chemically treated, hairless mouse dorsal skin as a model. N-methyl-N'-nitro-N-nitrosoguanidine (MNNG, 0.0125-0.2%), 4-nitroquinoline-1-oxide (4NQO, 0.01-0.25%), mitomycin C (MMC, 0.0125-0.05%), benzo[a]pyrene (B[a]P, 0.25-2%), and 7,12-dimethylbenz[a]anthracene (DMBA, 0.25-1%) were each applied once to the dorsal skin of hairless male mice; after 3h, epidermal skin cells were isolated, and the alkaline comet assay was performed. The assay was performed after 24h for only the B[a]P and DMBA. Furthermore, B[a]P and DMBA were evaluated by alkaline comet assay using liver cells after both 3 and 24h. The mean percent of DNA (%DNA) in tail in the 0.05-0.2% MNNG and 0.1-0.25% 4NQO treatment groups was markedly higher than in the control group at 3h post-application. Although the mean %DNA values in the tail in the B[a]P and DMBA groups were the same as the controls at 3h post-application, the 2% B[a]P and 1% DMBA groups showed significantly higher values versus controls 24h after application. No significant increases in the mean %DNA in the tail were observed in the MMC group. No clear increases in %DNA in the tail were observed in the B[a]P and DMBA groups at 3 or 24h after application in the liver. These results suggest that the in vivo skin comet assay is able to accurately identify DNA-damaging potential with a skin-specific response and is a useful method to detect the DNA-damaging potential of genotoxic chemicals on the skin.     

Ultraviolet light induced alteration to the skin

Solar light is the primary source of UV radiation for all living systems. UV photons can mediate damage through two different mechanisms, either by direct absorption of UV via cellular chromophores, resulting in excited states formation and subsequent chemical reaction, or by phosensitization mechanisms, where the UV light is absorbed by endogenous (or exogenous) sensitizers that are excited and their further reactions lead to formation of reactive oxygen species (ROS). These highly reactive species can interact with cellular macromolecules such as DNA, proteins, fatty acids and saccharides causing oxidative damage. Direct and indirect injuries result in a number of harmful effects such as disrupted cell metabolism, morphological and ultrastructural changes, attack on the regulation pathways and, alterations in the differentiation, proliferation and apoptosis of skin cells. Processes like these can lead to erythema, sunburn, inflammation, immunosuppression, photoaging, gene mutation, and development of cutaneous malignancies. The endogenous and exogenous mechanisms of skin photoprotection are discussed.