To investigate vessel coagulation depth and tissue damage in therapy with the flashlamp-pumped pulsed dye laser (585 nm, 5 mm spot size, 450 microsecond pulse duration, 6-8 J/cm2), we used the nitroblue-tetrazolium chloride stain in 22 post-treatment biopsy specimens from patients with port wine stain. With this method, thermally damaged tissue can be easily differentiated from unchanged tissue to the level of single cells. The results showed that in superficial port wine stain vessels up to 150 microns in diameter, vessel coagulation was complete and selective without further dermal damage. With the increase of vessel diameter, strong superficial hemoglobin absorption led to only partial vessel-wall coagulation and, in some cases, to superficial dermal damage. Likewise, deeper vessels were not coagulated because of shadow effects by superficial vessel layers. Thus, the overall vessel-wall coagulation depth of the flashlamp-pumped dye laser was limited to a maximum of 0.65 mm (mean 0.37 mm). In addition, some degree of epidermal damage was present in most specimens, which significantly increased with epidermal melanin content and resulted in epidermal coagulation and blistering in pigmented skin. Our results explain the occurrence of crusting, hyperpigmentation, and hypopigmentation in therapy with the flashlamp-pumped dye laser and its limited effect on dark or hypertrophic port wine stains in adults featuring large vessel diameters or multiple vessel layers.

No abstract

Mouse models indicate that metastatic dissemination occurs extremely early; however, the timing in human cancers is unknown. We therefore determined the time point of metastatic seeding relative to tumour thickness and genomic alterations in melanoma. Here, we find that lymphatic dissemination occurs shortly after dermal invasion of the primary lesion at a median thickness of ~0.5 mm and that typical driver changes, including BRAF mutation and gained or lost regions comprising genes like MET or CDKNA2, are acquired within the lymph node at the time of colony formation. These changes define a colonisation signature that was linked to xenograft formation in immunodeficient mice and death from melanoma. Thus, melanoma cells leave primary tumours early and evolve at different sites in parallel. We propose a model of metastatic melanoma dormancy, evolution and colonisation that will inform direct monitoring of adjuvant therapy targets.

In the vast majority of the hemangiomas, it was possible to stop further progression or induce regression by FPDL treatment. Total regression could be achieved in nearly half of the small superficial hemangiomas. Because the treatment is fast, effective, and nearly without side effects, we recommend early laser treatment especially in superficial and small childhood hemangiomas.

No abstract