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Acral Compound Nevus SJ Yun S Korea

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Acral Compound Nevus SJ Yun S Korea University of Pennsylvania, Founded by Ben Franklin in 1740 Disclosures Consultant for Myriad Genetics and for SciBase (might try to sell you a book, as well) Multidimensional Pathway Classification of Melanocytic Tumors WHO 4th Edition, 2018 Epidemiologic, Clinical, Histologic and Genomic Aspects of Melanoma David E. Elder, MB ChB, FRCPA University of Pennsylvania, Philadelphia, PA, USA Napa, May, 2018 3rd Edition, 2006 Malignant Melanoma • A malignant tumor of melanocytes • Not all melanomas are the same – variation in: – Epidemiology – risk factors, populations – Cell/Site of origin – Precursors – Clinical morphology – Microscopic morphology – Simulants – Genomic abnormalities Incidence of Melanoma D.M. Parkin et al. CSD/Site-Related Classification • Bastian’s CSD/Site-Related Classification (Taxonomy) of Melanoma – “The guiding principles for distinguishing taxa are genetic alterations that arise early during progression; clinical or histologic features of the primary tumor; characteristics of the host, such as age of onset, ethnicity, and skin type; and the role of environmental factors such as UV radiation.” Bastian 2015 Epithelium associated Site High UV Low UV Glabrous Mucosa Benign Acquired Spitz nevus nevus Atypical Dysplastic Spitz Borderline nevus tumor High Desmopl. Low-CSD Spitzoid Acral Mucosal Malignant CSD melanoma melanoma melanoma melanoma melanoma 105 Point mutations 103 Structural Rearrangements 2018 WHO Classification of Melanoma • Integrates Epidemiologic, Genomic, Clinical and Histopathologic Features • Assists in sensitivity, specificity and reproducibility of diagnosis by providing a conceptual morphologic framework • Provides a context for selection of therapy: – Targeted therapy directed against oncogenes – Immune therapy directed against neoantigens Fourth Edition WHO Classification • 4e WHO Classification, to be published in 2018, defines 9 “Pathways” to melanoma • “Pathway” concept is based on epidemiologic, clinical, histological, and genomic attributes of the lesions • Term attributable to Whiteman et al (Brisbane, AU) - distinguished two pathways for common cutaneous melanomas: – “Prevalences of nevi and solar keratoses differ markedly between patients with head and neck melanomas or LMM and patients with melanomas of the trunk (i.e. SSM). Cutaneous melanomas may arise through two pathways, one associated with melanocyte proliferation and the other with chronic exposure to sunlight. Whiteman DC, Watt P, Purdie DM, Hughes MC, Hayward NK, Green AC. Melanocytic nevi, solar keratoses, and divergent pathways to cutaneous melanoma. J.Natl.Cancer Inst. 2003;95:806-12. Pathways in Melanoma • The pathways reflect evolution of melanomas from benign precursor lesions through intermediate or dysplastic lesions to radial (low risk) and vertical growth phase melanomas, all in particular epidemiologic and genomic contexts: – e.g. Junctional Nevus- Dysplastic Nevus - RGP Melanoma - VGP Melanoma – Low CSD - BRAF/NRAS – Blue nevus – Cellular Blue Nevus (CBN) – Melanoma in Blue Nevus (MBN) – No or Variable CSD - GNAQ/GNA11 driver oncogenes Tumor Progression in Melanoma Most of the histopathologic • Precursor Nevus “classifiers” for melanoma are • Radial Growth attributes of the radial growth phase – Phase (RGP)/MIS . Pagetoid proliferation • Vertical Growth . Lentiginous proliferation Phase (VGP) • Not obligate • Steps can be skipped The Genetic Evolution of Melanoma from Precursor Lesions. Shain et al., NEJM 2015. • Precursor lesions initiated by mutations of genes that activate MAP kinase pathway. • Unequivocally benign precursors had BRAF V600E mutations exclusively • “Intermediate” lesions were enriched for NRAS and additional driver mutations. • TERT promoter mutations were present in intermediate lesions and melanomas in situ. • Biallelic inactivation of CDKN2A exclusively found in invasive melanomas. • The study identified an intermediate category of melanocytic neoplasia, characterized by the presence of more than one pathogenic genetic alteration and distinctive histopathological features. New Classification • The new classification incorporates benign, intermediate or “borderline” and malignant lesions • The benign lesions have a single genomic abnormality (e.g. BRAF V600E) • The intermediate lesions typically have two genomic abnormalities – e.g. hemizygous loss of CDKN2A, TERT promoter mutations, BAP1 loss • They have architectural and cytological features different from benign lesions (architectural disorder and cytological atypia – e.g. dysplastic nevi, deep penetrating nevus (DPN), Pigmented Epithelioid Melanocytoma (PEM), BAP1 deficiency “Melanocytomas” Classification of Melanoma WHO, 2018 • Pathway I. Low CSD Melanoma/Superficial Spreading Melanoma (SSM) • Pathway II. High CSD Melanoma/Lentigo Maligna Melanoma (LMM) • Pathway III. Desmoplastic Melanoma • Pathway IV. Malignant Spitz Tumor • Pathway V. Acral Melanoma • Pathway VI. Mucosal Melanoma • Pathway VII. Melanoma in Congenital Nevus (MCN) • Pathway VIII. Melanoma in Blue Nevus (MBN) • Pathway IX. Uveal Melanoma • Variable Pathways: Nodular Melanoma Table 1. Classification of Melanocytic Tumors by Epidemiologic, Clinical, Histopathologic and Genomic Attributes Role of UV: Low UV High UV Low to No (or Variable) CSD Pathway: I II III IV V VI VII VIII IX High-CSD Melanoma in Low-CSD Melanoma Desmoplastic Spitz Acral Mucosal Melanoma Uveal Melanoma Congenital Melanoma Melanoma Melanoma Melanoma In Blue Nevus Melanoma Superficial Spreading Melanoma (LMM) Nevus Congenital Nevus ? IAMP ? IAMP Spitz Nevus ?IAMP Melanosis Blue Nevus ? Benign Nevus (CN) Atypical Nodular Borderline Low Grade Atypical Spitz Atypical Cellular Blue Bap-1 ? IAMP ? IAMP melanocytic proliferation in Uveal nevus Dysplasia DPN PEM nevus melanosis Nevus Low Deficiency proliferation CN Melanocytoma Melanocytoma Melanocytoma /MELTUMP /MELTUMP Borderline High Grade /MELTUMP Lentigo Melanoma in IAMPUS/ Melanoma in situ STUMP ? MIS in CN Atypical CBN ? High Dysplasia maligna situ SAMPUS Superficial Lentigo Acral Mucosal Melanoma in Melanoma in Melanoma in Desmoplastic Malignant Spitz Melanoma in Melanoma ex Uveal Spreading Maligna lentiginous lentiginous Malignant BPDM (rare) DPN (rare) PEM (rare) Melanoma Tumor CN Blue Nevus melanoma Melanoma Melanoma melanoma melanoma BRAF V600E, (BRAF or (BRAF, MEK1, (BRAF+PRKAR1 NRAS, NF1, ERBB2, MAP2K1, HRAS, ALK, KIT, NRAS, KIT, NRAS, NRAS, BRAF GNAQ, GNA11, GNAQ, GNA11, NRAS NRAS)+BAP1 or NRAS) A) or PRKCA BRAFnon- MAP3K1, BRAF, EGFR, ROS1, RET, BRAF, HRAS, KRAS, or BRAF, V600E (small CYSLTR2, CYSLTR2, or +(CBNN1 or V600E, KIT, NF1MET, NTRK1, NTRK3, KRAS, NTRK3, lesions), BRAF PLCB4 APC) BRAF,MET, ALK, NF1 Common TERT, CDKN2A, TERT, CDKN2A, TERT, NFKBIE, NRAS CDKN2A CDKN2A, TERT NF1, CDKN2A BAP1, EIF1AX SF3B1, EIF1AX, mutations TP53, PTEN, TP53, PTEN, PIK3CA PTPN11 CCND1, GAB2 SF3B1, CCND1, SF3B1 BAP1 RAC1 CDK4, MDM2 Low UV Pathway I Lentiginous junctional Low-CSD Melanoma Supertpficial Spreading Melanoma nevus Banal Acquired Nevus (junctional, compound, dermal) Low Grade Deep Pigmented Dysplasia Bap-1 penetrating Epithelioid Compound Deficiency nevus (DPN)/ Melanocytoma Melanocytoma dysplastic High Grade Melanocytoma (PEM) Dysplasia nevus Superficial Melanoma in Melanoma in Melanoma in Spreading BPDM (rare) DPN (rare) PEM (rare) Melanoma BRAF V600E, (BRAF or (BRAF, MEK1, (BRAF+PRKAR1 NRAS NRAS)+BAP1 or NRAS) A) or PRKCA +(CBNN1 or APC) Superficial spreading or TERT, CDKN2A, “pagetoid” TP53, PTEN melanoma WHO classification of skin tumours / edited by David E. Elder, Daniela Massi, Richard A. Scolyer, Rein Willemze. – 4th edition. High UV Pathway II Pathway III High-CSD Desmoplastic Melanoma Melanoma (LMM) ? IMP ? IMP ? IAMP ? IAMP Lentigo maligna Melanoma in situ melanoma in situ Lentigo Maligna Desmoplastic Melanoma Melanoma NRAS, BRAFnon- NF1, ERBB2, MAP2K1, V600E, KIT, NF1 MAP3K1, BRAF, EGFR, MET, TERT, CDKN2A, TERT, NFKBIE, NRAS PIK3CA TP53, PTEN, RAC1 PTPN11 WHO classification of skin tumours / edited by David E. Elder, Daniela Massi, Richard A. Scolyer, Rein Willemze. – 4th edition. Pathway IV Fatal Malignant Spitz No UV Malignant Spitz Tumor tumor (vs Spitzoid melanoma) in a 12 y.o. Spitz Nevus girl Atypical Spitz nevus STUMP Malignant Spitz Tumor (vs. Malignant Spitzoid Tumor, vs. “Melanoma with Spitzoid Features”) HRAS, ALK, ROS1, RET, NTRK1, NTRK3, BRAF, MET, CDKN2A • Younger patients/ children • Fusion genes WHO classification of skin tumours / edited by David E. Elder, Daniela Massi, Richard A. Scolyer, Rein Willemze. – 4th edition. Pathway V No UV Acral Melanoma Atypical melanocytic proliferation Melanoma in situ Acral lentiginous melanoma KIT, NRAS, SJ Yun BRAF, HRAS, KRAS, NTRK3, ALK, NF1 CDKN2A, TERT CCND1, GAB2 2018 Proposed Classification of Melanoma, Precursors and Simulants 2 Melanocytic Tumours 2-4 Melanoma in acral skin and simulants/precursors 2-5A Acral melanoma 2-5B Acral naevus Next Case Your Diagnosis Nevus? Melanoma? 5 years later … Local recurrences are relatively common in acral melanomas Compared to SSM e.g. of the trunk 11q amplification (Cyclin D) (red probe) in acral melanoma. Bastian et al, Cancer Res 2000 Field Effect in ALM Pathway V • Genomically abnormal No UV melanocytes extending Acral Melanoma as much as 1 cm from detectable border Atypical melanocytic proliferation • May partly explain Melanoma in situ propensity of these Acral lentiginous melanoma lesions for local KIT, NRAS, BRAF, HRAS, KRAS, recurrences NTRK3, ALK, NF1 • (Bastian et al, Cancer CDKN2A, TERT CCND1, GAB2 Research, 2000) Acral
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