Spitz Melanoma is a Distinct Subset of Spitzoid Melanoma

[1]  Douglas B. Johnson,et al.  Identification of Targetable Recurrent MAP3K8 Rearrangements in Melanomas Lacking Known Driver Mutations , 2019, Molecular Cancer Research.

[2]  K. White,et al.  Activating Structural Alterations in MAPK Genes Are Distinct Genetic Drivers in a Unique Subgroup Of Spitzoid Neoplasms , 2019, The American journal of surgical pathology.

[3]  Heather L. Mulder,et al.  Clinical genome sequencing uncovers potentially targetable truncations and fusions of MAP3K8 in spitzoid and other melanomas , 2019, Nature Medicine.

[4]  K. White,et al.  Genomic Fusions in Pigmented Spindle Cell Nevus of Reed , 2018, The American journal of surgical pathology.

[5]  R. Śmigiel,et al.  MAP2K2 mutation as a cause of cardio‐facio‐cutaneous syndrome in an infant with a severe and fatal course of the disease , 2018, American journal of medical genetics. Part A.

[6]  D. Pissaloux,et al.  Cutaneous Melanocytoma With CRTC1-TRIM11 Fusion: Report of 5 Cases Resembling Clear Cell Sarcoma , 2017, The American journal of surgical pathology.

[7]  C. Onodera,et al.  Genomic Analysis of Pigmented Epithelioid Melanocytomas Reveals Recurrent Alterations in PRKAR1A, and PRKCA Genes , 2017, The American journal of surgical pathology.

[8]  Robert L. Judson,et al.  Combined activation of MAP kinase pathway and β-catenin signaling cause deep penetrating nevi , 2017, Nature Communications.

[9]  B. Taylor,et al.  Tumours with class 3 BRAF mutants are sensitive to the inhibition of activated RAS , 2017, Nature.

[10]  M. Ladanyi,et al.  Identification of NTRK3 Fusions in Childhood Melanocytic Neoplasms. , 2017, The Journal of molecular diagnostics : JMD.

[11]  Robert L. Judson,et al.  148 Combined activation of MAP kinase and beta-catenin signaling define deep penetrating nevi , 2017 .

[12]  Pedram Gerami,et al.  A Comparison of Morphologic and Molecular Features of BRAF, ALK, and NTRK1 Fusion Spitzoid Neoplasms , 2017, The American journal of surgical pathology.

[13]  R. Halaban,et al.  Spitz nevi and Spitzoid melanomas - Exome sequencing and comparison to conventional melanocytic nevi and melanomas , 2016, Modern Pathology.

[14]  I. Yeh,et al.  NTRK3 kinase fusions in Spitz tumours , 2016, The Journal of pathology.

[15]  A. Bollen,et al.  Activating NRF1-BRAF and ATG7-RAF1 fusions in anaplastic pleomorphic xanthoastrocytoma without BRAF p.V600E mutation , 2016, Acta Neuropathologica.

[16]  J. Parker,et al.  An oncogenic Ezh2 mutation cooperates with particular genetic alterations to induce tumors in mice and redistributes H3K27 trimethylation throughout the genome , 2016, Nature Medicine.

[17]  J. Parker,et al.  An oncogenic Ezh2 mutation cooperates with particular genetic alterations to induce tumors in mice and redistributes H3K27 trimethylation throughout the genome , 2016, Nature medicine.

[18]  Eric Talevich,et al.  CNVkit: Genome-Wide Copy Number Detection and Visualization from Targeted DNA Sequencing , 2016, PLoS Comput. Biol..

[19]  J. Easton,et al.  The landscape of fusion transcripts in spitzoid melanoma and biologically indeterminate spitzoid tumors by RNA sequencing , 2016, Modern Pathology.

[20]  Ricardo Villamarín-Salomón,et al.  ClinVar: public archive of interpretations of clinically relevant variants , 2015, Nucleic Acids Res..

[21]  D. Zwijnenburg,et al.  Abstract PR06: TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors , 2016 .

[22]  Gabor T. Marth,et al.  A global reference for human genetic variation , 2015, Nature.

[23]  S. Armstrong,et al.  Loss of BAP1 function leads to EZH2-dependent transformation , 2015, Nature Medicine.

[24]  B. Piraccini,et al.  Spitzoid tumors in children and adults: a comparative clinical, pathological, and cytogenetic analysis , 2015, Melanoma research.

[25]  Nam Huh,et al.  Exome sequencing of desmoplastic melanoma identifies recurrent NFKBIE promoter mutations and diverse activating mutations in the MAPK pathway , 2015, Nature Genetics.

[26]  Steven J. M. Jones,et al.  Genomic Classification of Cutaneous Melanoma , 2015, Cell.

[27]  R. Dummer,et al.  TERT Promoter Mutations Are Predictive of Aggressive Clinical Behavior in Patients with Spitzoid Melanocytic Neoplasms , 2015, Scientific Reports.

[28]  R. Scolyer,et al.  BAP1-inactivated spitzoid naevi. , 2015, The American journal of surgical pathology.

[29]  I. Yeh,et al.  Clinical, Histopathologic, and Genomic Features of Spitz Tumors With ALK Fusions , 2015, The American journal of surgical pathology.

[30]  I. Yeh,et al.  Activating MET Kinase Rearrangements in Melanoma and Spitz Tumors , 2015, Nature Communications.

[31]  Benjamin J. Raphael,et al.  Quantifying tumor heterogeneity in whole-genome and whole-exome sequencing data , 2014, Bioinform..

[32]  O. Kallioniemi,et al.  FusionCatcher – a tool for finding somatic fusion genes in paired-end RNA-sequencing data , 2014, bioRxiv.

[33]  D. Muzny,et al.  Mutually exclusive recurrent somatic mutations in MAP2K1 and BRAF support a central role for ERK activation in LCH pathogenesis. , 2014, Blood.

[34]  L. Thomas,et al.  Mutated and amplified NRAS in a subset of cutaneous melanocytic lesions with dermal spitzoid morphology: report of two pediatric cases located on the ear , 2014, Journal of cutaneous pathology.

[35]  Nicolas Stransky,et al.  The landscape of kinase fusions in cancer , 2014, Nature Communications.

[36]  D. Schadendorf,et al.  TERT promoter mutation status as an independent prognostic factor in cutaneous melanoma. , 2014, Journal of the National Cancer Institute.

[37]  I. Yeh,et al.  Ambiguous Melanocytic Tumors With Loss of 3p21 , 2014, The American journal of surgical pathology.

[38]  L. Cerroni,et al.  Clinical and Pathologic Findings of Spitz Nevi and Atypical Spitz Tumors With ALK Fusions , 2014, The American journal of surgical pathology.

[39]  B. B. Weitner,et al.  Histomorphologic Assessment and Interobserver Diagnostic Reproducibility of Atypical Spitzoid Melanocytic Neoplasms With Long-term Follow-up , 2014, The American journal of surgical pathology.

[40]  Iwei Yeh,et al.  Kinase fusions are frequent in Spitz tumours and spitzoid melanomas , 2014, Nature Communications.

[41]  Iwei Yeh,et al.  Recurrent BRAF kinase fusions in melanocytic tumors offer an opportunity for targeted therapy , 2013, Pigment cell & melanoma research.

[42]  I. Yeh,et al.  Clonal BRAF mutations in melanocytic nevi and initiating role of BRAF in melanocytic neoplasia. , 2013, Journal of the National Cancer Institute.

[43]  D. Elder,et al.  Risk Assessment for Atypical Spitzoid Melanocytic Neoplasms Using FISH to Identify Chromosomal Copy Number Aberrations , 2013, The American journal of surgical pathology.

[44]  Benjamin E. Gross,et al.  Integrative Analysis of Complex Cancer Genomics and Clinical Profiles Using the cBioPortal , 2013, Science Signaling.

[45]  Lynda Chin,et al.  Highly Recurrent TERT Promoter Mutations in Human Melanoma , 2013, Science.

[46]  D. Schadendorf,et al.  TERT Promoter Mutations in Familial and Sporadic Melanoma , 2013, Science.

[47]  A. von Deimling,et al.  Combined BRAFV600E-positive Melanocytic Lesions With Large Epithelioid Cells Lacking BAP1 Expression and Conventional Nevomelanocytes , 2013, The American journal of surgical pathology.

[48]  V. Beneš,et al.  DELLY: structural variant discovery by integrated paired-end and split-read analysis , 2012, Bioinform..

[49]  S. Pita-Fernández,et al.  Spitzoid and non‐spitzoid melanoma in children. A prognostic comparative study , 2012, Journal of the European Academy of Dermatology and Venereology : JEADV.

[50]  Gabor T. Marth,et al.  Haplotype-based variant detection from short-read sequencing , 2012, 1207.3907.

[51]  L. Cerroni,et al.  A Distinct Subset of Atypical Spitz Tumors is Characterized by BRAF Mutation and Loss of BAP1 Expression , 2012, The American journal of surgical pathology.

[52]  Benjamin E. Gross,et al.  The cBio cancer genomics portal: an open platform for exploring multidimensional cancer genomics data. , 2012, Cancer discovery.

[53]  Helga Thorvaldsdóttir,et al.  Integrative Genomics Viewer (IGV): high-performance genomics data visualization and exploration , 2012, Briefings Bioinform..

[54]  C. V. Jongeneel,et al.  Exome sequencing identifies recurrent somatic MAP2K1 and MAP2K2 mutations in melanoma , 2011, Nature Genetics.

[55]  M. DePristo,et al.  The Genome Analysis Toolkit: a MapReduce framework for analyzing next-generation DNA sequencing data. , 2010, Genome research.

[56]  H. Hakonarson,et al.  ANNOVAR: functional annotation of genetic variants from high-throughput sequencing data , 2010, Nucleic acids research.

[57]  G. Saldanha,et al.  BRAF, NRAS and HRAS mutations in spitzoid tumours and their possible pathogenetic significance , 2009, The British journal of dermatology.

[58]  D. Louis,et al.  Faculty Opinions recommendation of Glioma-derived mutations in IDH1 dominantly inhibit IDH1 catalytic activity and induce HIF-1alpha. , 2009 .

[59]  Kun-Liang Guan,et al.  Glioma-Derived Mutations in IDH1 Dominantly Inhibit IDH1 Catalytic Activity and Induce HIF-1α , 2009, Science.

[60]  D. Busam,et al.  An Integrated Genomic Analysis of Human Glioblastoma Multiforme , 2008, Science.

[61]  S. Ekvall,et al.  Noonan and cardio-facio-cutaneous syndromes: two clinically and genetically overlapping disorders , 2008, Journal of Medical Genetics.

[62]  Frank McCormick,et al.  Germline mutations of MEK in cardio-facio-cutaneous syndrome are sensitive to MEK and RAF inhibition: implications for therapeutic options. , 2007, Human molecular genetics.

[63]  S. Macht.  ???Spitz??s Nevus???: Reassessment Critical, Revision Radical , 2007 .

[64]  James T. Elder,et al.  BRAF and NRAS mutations in spitzoid melanocytic lesions , 2006, Modern Pathology.

[65]  D. Pinkel,et al.  Somatic activation of KIT in distinct subtypes of melanoma. , 2006, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[66]  D. Pinkel,et al.  MC1R Germline Variants Confer Risk for BRAF-Mutant Melanoma , 2006, Science.

[67]  R. Barnhill.  The Spitzoid lesion: rethinking Spitz tumors, atypical variants, ‘Spitzoid melanoma’ and risk assessment , 2006, Modern Pathology.

[68]  D. Ruiter,et al.  Analysis of Mutations in B-RAF, N-RAS, and H-RAS Genes in the Differential Diagnosis of Spitz Nevus and Spitzoid Melanoma , 2005, The American journal of surgical pathology.

[69]  D. Pinkel,et al.  Mutations and copy number increase of HRAS in Spitz nevi with distinctive histopathological features. , 2000, The American journal of pathology.

[70]  S Matsuno,et al.  Functional evaluation of PTEN missense mutations using in vitro phosphoinositide phosphatase assay. , 2000, Cancer research.

[71]  S SPITZ,et al.  Melanomas of childhood. , 1948, The American journal of pathology.

[72]  D. Elder,et al.  WHO classification of skin tumours , 2018 .

[73]  Thomas R. Gingeras,et al.  STAR: ultrafast universal RNA-seq aligner , 2013, Bioinform..

[74]  Claude-Alain H. Roten,et al.  Fast and accurate short read alignment with Burrows–Wheeler transform , 2009, Bioinform..

[75]  Jane Fridlyand,et al.  Improving Melanoma Classification by Integrating Genetic and Morphologic Features , 2008, PLoS medicine.

[76]  P. Meltzer,et al.  High frequency of BRAF mutations in nevi , 2003, Nature Genetics.