*A pproximately 50% of melanomas are BRAF positive, specifically NRAS mutations are present in ~20% of melanomas CDKN2A/RB1 pathway – CDKN2A encodes the p16 and p14ARF proteins, both of which act as tumour suppressors by regulating the cell cycle (specifically, by blocking transition from the G1 to S-phase) mutation to CDKN2A can result in unregulated cell growth and neoplastic progression.MAPK pathway – mutations to proto-oncogenes, such as BRAF and NRAS, which normally promote cell proliferation and survival, result in activation of MAPK pathway, which causes uncontrolled cell proliferation*.Genetic mutations may also increase the susceptibility to carcinogenic effects of UV radiation two main mutations include:
#Wle left lower extermity mass sentinel lymph node biopsy skin
Specifically, UVB radiation (315–280nm wavelength light) from the sun is absorbed by the skin and causes direct DNA damage (through the creation of cyclobutane pyrimidine dimers). The definite pathophysiology of melanoma remains unclear, however the main contributor is ultraviolet (UV) radiation exposure. Table 1 – Main subtypes of skin melanoma Pathophysiology Variable pigmentation, often present with appearance of a stain, typically large size at presentation Large flat pigmented lesions, often in the older population Rapidly growing, pigmented, bleeding, or ulcerated nodule, typically in those >50yrs Large, flat, and irregularly pigmented lesion, typically in those aged 30-50yrs *Lentigo maligna is a macular lesion containing an increased number of abnormal melanocytes, confined to epidermis (aka melanoma in situ), whilst lentigo maligna melanoma are when these abnormal melanocytes invade the dermis Melanin itself is produced in response to UV radiation exposure and acts to protect against DNA damage by dissipating >99.9% of absorbed radiation. The four main histological subtypes of melanoma are superficial spreading, nodular, lentigo maligna melanoma*, and acral lentiginous (Table 1). They metastasise early (relative to other tumour types), partly due to their vertical growth (as opposed to radially) and can spread to nearly every tissue and organ in the body In the UK, melanoma has an incidence of approximately 00 people, most commonly on the trunk or legs, with incidence rising with age. Melanoma commonly arises from melanocytes in the stratum basale of the epidermis, but can also arise from melanocytes at other sites. Journal compilation © Blackwell Verlag GmbH, Berlin.Melanoma is a malignant tumour of melanocytes, the melanin-producing neural crest-derived cells of the body.Obesity, location of the primary melanoma at a distal site on the leg, a wide safety margin, and seromas are associated with postoperative leg swelling. More than two-thirds of patients did not have any swelling. Age, sex, the number of sentinel lymph nodes, the drainage fluid volume, and the time since SLNE were non-significant.īoth inguinal SLNE and primary melanoma excision may contribute to minimal fluid accumulation in the leg. Wider excision margins around a primary melanoma on the thigh were also associated with a significant increase in volume. Obesity, primary melanoma location on the lower leg, and inguinal seromas were identified as significant risk factors for postoperative swelling. Both the lower leg and the thigh increased in volume. Following inguinal SLNE, there was a mean volume increase of 1.5% in the operated leg. Perceived swelling, clinically diagnosed swelling, and manifest edema occurred in 31%, 15%, and 7% of patients respectively. We prospectively studied three parameters in 105 subjects: 1) subjectively perceived swelling, 2) clinically diagnosed swelling and 3) photo-optical measurement of volume differences between both legs. Risk-factors for leg swelling following primary melanoma excision and inguinal sentinel lymphadenectomy (SLNE) have not been sufficiently investigated.
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