Ebook Manual of clinical oncology (8/E): Part 2
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Ebook Manual of clinical oncology (8/E): Part 2
1 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melano Ebook Manual of clinical oncology (8/E): Part 2oma accounts for about 2% of all skin cancers, but it is responsible for 80% of deaths. The incidence of melanoma in the United States has been rising for the last 40 years. Before the age of 45, women have a higher risk than men, but after the age of 60, the risk for men is twice as high as for wom Ebook Manual of clinical oncology (8/E): Part 2en. The estimated number of new cases in the United States in 2016 is 76,380, and 10,130 patients would die of melanoma.The incidence of melanoma roseEbook Manual of clinical oncology (8/E): Part 2
rapidly in the 1970s at about 6% per year; it continues to rise but at a lower rate of 2.7% per year from 2006 to 2010. White people have a 2.4% life1 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melano Ebook Manual of clinical oncology (8/E): Part 2tors for melanoma are a family history of melanoma, multiple benign or atypical nevi, and a previous melanoma. The list of additional risk factors includes immunosuppression, sun sensitivity, and exposure to ultraviolet (UV) radiation.1Familial factors. Approximately 10% of melanomas are familial. T Ebook Manual of clinical oncology (8/E): Part 2he higher risk of melanoma in these families may be attributed to both shared susceptibility genes and shared environment.a. High-penetrance susceptibEbook Manual of clinical oncology (8/E): Part 2
ility genes. Two genes, CDKN2A and CDK4, are associated with high-penetrance susceptibility. Mutated CDKN2A is the most prevalent gene in families wit1 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melano Ebook Manual of clinical oncology (8/E): Part 2, which is one of the binding partners of pl6INK4a. Mutations in CDK4 arc found much less frequently than in CDKFI2A. Other less common high-penetrance genes are BAP/, TERT, XP (various genes mutated in individuals with xeroderma pigmentosum).rhe higher the number of family members with melanoma, th Ebook Manual of clinical oncology (8/E): Part 2e higher the probability of carrying a high-penetrance gene. Mutated CDKN2A was found in 14% families with 2 cases of melanoma, in 67% families with 6Ebook Manual of clinical oncology (8/E): Part 2
to 7 cases, and 100% families with 7 to 10 cases. Overall, between 20% (in Australia) and 57% (in Europe) of the cases of familial melanoma are assoc1 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melano Ebook Manual of clinical oncology (8/E): Part 2mong families with melanoma. The list includes BRCA2, MC1R, MITF E318K, shelterin complex genes (POTI, ACD, TERF2IP).c.Familial atypical multiple mole melanoma (FAMMM) syndrome, also known as the familial dysplastic nevus syndrome, was described in 1978 in families whose members suffered from melano Ebook Manual of clinical oncology (8/E): Part 2ma and had multiple (usually >100) large moles of variable size and color (reddish brown to bright red) with pigmentary leakage, rhe median age of theEbook Manual of clinical oncology (8/E): Part 2
development of melanoma in persons with this syndrome is 33 years, and 9% of affected people develop it before the age of 20. The syndrome is transmi1 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melano Ebook Manual of clinical oncology (8/E): Part 2.2Nevi. Typical nevi are frequently precursors of melanoma, but more importantly, they arc markers of increased risk. High common nevus counts (50 or more common novi) account for 27% of melanoma cases, whereas individuals with few common nevi (0 to 10) account for only 4% of melanoma cases.Congenit Ebook Manual of clinical oncology (8/E): Part 2al nevi are benign neoplasms that are present at birth and composed of nevomelanocytes. The malignant potential of giant congenital nevi varies betweeEbook Manual of clinical oncology (8/E): Part 2
n different types. Pigmented giant nevi have especially high risk for malignant transformation. Nevus642sebaceous is associated with the development o1 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melano Ebook Manual of clinical oncology (8/E): Part 2 cutaneous melanoma is 6% to 7%; the risk is higher among patients who initially presented with melanoma in situ than in those with invasive melanoma. The greatest risk is within the first 2 years, but it remains elevated for at least 20 years. Males, elderly patients, and individuals with the first Ebook Manual of clinical oncology (8/E): Part 2 melanoma on the face, the neck, and the trunk are at especially high risk. The incidence of a third primary melanoma from the time of second primaryEbook Manual of clinical oncology (8/E): Part 2
melanoma is 16% at 1 year and 31% at 5 years.4Immunosuppression. Among organ allograft recipients, melanoma constituted 5% of skin cancers and was sig1 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melano Ebook Manual of clinical oncology (8/E): Part 2lanocortin receptor gene (MC1R) that results in a decreased melanin production after exposure to ƯV radiation and in an increased risk of melanoma.6Exposure to sun and to uv radiation. It is known that uv radiation causes genetic changes in the skin, impairs cutaneous immune function, increases the Ebook Manual of clinical oncology (8/E): Part 2local production of growth factors, and induces the formation of DNA-damaging reactive oxygen species that affect keratinocyles and melanocytes. EpideEbook Manual of clinical oncology (8/E): Part 2
miologic studies revealed that intermittent sun exposure and frequent sunburns, especially during childhood, increase (he risk of melanoma. Chronic lo1 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melano Ebook Manual of clinical oncology (8/E): Part 2ng non-Hispanic White individuals. In addition, exposure to uv light from recreational tanning salons is an important risk factor for melanoma.7Occupational exposure. Exposure to coal tar, pilch, creosote, arsenic compounds, or radium increases the risk of melanoma development.8Other. An increased r Ebook Manual of clinical oncology (8/E): Part 2ate of melanoma was seen in patients with Parkinson disease, prostate cancer, and endometriosis and patients treated with voriconazole, sildenafil, anEbook Manual of clinical oncology (8/E): Part 2
d tumor necrosis factor (TNF) inhibitors.643IL PREVENTIONAvoidance of exposure to the sun during the midday hours, wearing skinprotecting clothing, su1 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melano Ebook Manual of clinical oncology (8/E): Part 2y prevention. It is unclear if dietary vitamin D has any impact on development of melanoma. Patients with a family or personal history of melanoma should undergo at least one annual skin examination performed by a dermatologist as a secondary prevention.III. PATHOLOGY AND NATURALHISTORYA.Pathology. Ebook Manual of clinical oncology (8/E): Part 2Melanoma originates from melanocytes, the neural crest-derived cells that migrate into the epidermis during embryogenesis to reside in the basal layerEbook Manual of clinical oncology (8/E): Part 2
of the epidermis. The overwhelming majority of melanomas originate in the skin, but some melanomas may arise from other primary sites. Potential extr1 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melano Ebook Manual of clinical oncology (8/E): Part 2), gastrointestinal (GI) tract (most frequently, the anus), and genitourinary tract (most frequently, the vagina).Several steps occur in the process of their malignant transformation. According to the Clark model, initially normal melanocytes proliferate and form a benign nevus. In the next phase, a Ebook Manual of clinical oncology (8/E): Part 2bnormal growth appears in the form of a dysplastic nevus. Melanoma may originate from a benign nevus, but it can also start from scattered melanocytesEbook Manual of clinical oncology (8/E): Part 2
present in the normal skin. Next, in the radial growth phase, the cells acquire the ability to grow intraepidermally and have all the features of can1 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melano Ebook Manual of clinical oncology (8/E): Part 2. Not all melanomas pass through each of these individual phases, however.B.Molecular events in the pathogenesis of melanoma. Several molecular alterations have known pathogenic effects in the transformation of melanocytes and the evolution of melanoma.1. Alterations in signal transduction pathways. Ebook Manual of clinical oncology (8/E): Part 2 Mutually exclusive somatic activating point mutations in NRAS (15% to 20% of melanomas) and BRAF (40% to 50% of melanomas), two members6441 *7 Skin CancersBartosz Chmielowski, Richard F.Wagner Jr, and Antoni RibasMalignant MelanomaI. EPIDEMIOLOGY AND ETIOLOGYA.Incidence. Malignant melanoGọi ngay
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