Melanoma is staged using the TNM classification the clinical TNM (cTNM) stage is then updated with information after surgery to give the pathological stage (pTNM). Typically this involves a CT chest-abdomen-pelvis and MRI brain, or whole body PET-CT with additional imaging of the brain. Imaging should be performed in patients with stage IIc melanoma who have not had SLNB, or stage III and IV melanoma. If the lymph nodes are clinically or radiologically suspicious, then fine needle aspiration cytology (FNAC) should be performed. SLNB has a high sensitivity and specificity for subclinical regional lymph node involvement, and can give prognostic information. Sentinel lymph node biopsy (SNLB) aims to identify whether or not there is any melanoma in the primary draining lymph node(s) within a regional lymph node basin, when the nodes are not clinically or radiologically suspicious.Ĭurrent NICE guidelines recommend offering SLNB to patients with melanoma with a Breslow thickness >1 mm, without clinically apparent nodal or metastatic disease. Mitotic rate (number of mitotic figures per square millimeter).Immunohistocytochemistry (to identify any genetic markers, such as BRAF status, present).Breslow thickness (distance between the stratum granulosum and the deepest point of the melanoma).Key histopathological features that can be identified following biopsy for a suspected melanoma, which can determine both management or prognosis, include: *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: 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. Melanoma is a malignant tumour of melanocytes, the melanin-producing neural crest-derived cells of the body.
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