Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Spitz melanoma is a distinct subset of spitzoid melanoma

Abstract

Melanomas that have histopathologic features that overlap with those of Spitz nevus are referred to as spitzoid melanomas. However, the diagnostic concept is used inconsistently and genomic analyses suggest it is a heterogeneous category. Spitz tumors, the spectrum of melanocytic neoplasms extending from Spitz nevi to their malignant counterpart Spitz melanoma, are defined in the 2018 WHO classification of skin tumors by the presence of specific genetic alterations, such as kinase fusions or HRAS mutations. It is unclear what fraction of “spitzoid melanomas” defined solely by their histopathologic features belong to the category of Spitz melanoma or to other melanoma subtypes. We assembled a cohort of 25 spitzoid melanomas diagnosed at a single institution over an 8-year period and performed high-coverage DNA sequencing of 480 cancer related genes. Transcriptome wide RNA sequencing was performed for select cases. Only nine cases (36%) had genetic alterations characteristic of Spitz melanoma, including HRAS mutation or fusion involving BRAF, ALK, NTRK1, or MAP3K8. The remaining cases were divided into those with an MAPK activating mutation and those without an MAPK activating mutation. Both Spitz melanoma and spitzoid melanomas in which an MAPK-activating mutation could not be identified tended to occur in younger patients on skin with little solar elastosis, infrequently harbored TERT promoter mutations, and had a lower burden of pathogenic mutations than spitzoid melanomas with non-Spitz MAPK-activating mutations. The MAPK-activating mutations identified affected non-V600 residues of BRAF as well as NRAS, MAP2K1/2, NF1, and KIT, while BRAF V600 mutations, the most common mutations in melanomas of the WHO low-CSD category, were entirely absent. While the “spitzoid melanomas” comprising our cohort were enriched for bona fide Spitz melanomas, the majority of melanomas fell outside of the genetically defined category of Spitz melanomas, indicating that histomorphology is an unreliable predictor of Spitz lineage.

Access options

Rent or Buy article

Get time limited or full article access on ReadCube.

from$8.99

All prices are NET prices.

Fig. 1: Spitz melanomas with HRAS mutations share features with HRAS mutant Spitz nevi.
Fig. 2: Histopathology of Spitz melanomas with BRAF fusions.
Fig. 3: Spitz melanoma with ALK fusion.
Fig. 4: Rosette-like structures in Spitz melanoma with NTRK1 fusion.
Fig. 5: Spitzoid melanoma with a class 3 BRAF mutation.
Fig. 6: Spitzoid melanomas with NRAS mutation.
Fig. 7: Genetic alterations in spitzoid melanomas.

References

  1. 1.

    Barnhill RL. The Spitzoid lesion: rethinking Spitz tumors, atypical variants, “Spitzoid melanoma” and risk assessment. Mod Pathol. 2006;19 Suppl 2 :S21–33.

    PubMed  Article  Google Scholar 

  2. 2.

    Spitz S. Melanomas of childhood. Am J Pathol. 1948;24:591–609.

    CAS  PubMed  PubMed Central  Google Scholar 

  3. 3.

    Dika E, Fanti PA, Fiorentino M, Capizzi E, Neri I, Piraccini BM, et al. Spitzoid tumors in children and adults: a comparative clinical, pathological, and cytogenetic analysis. Melanoma Res. 2015;25:295–301.

    PubMed  Article  Google Scholar 

  4. 4.

    Gerami P, Busam K, Cochran A, Cook MG, Duncan LM, Elder DE, et al. Histomorphologic assessment and interobserver diagnostic reproducibility of atypical spitzoid melanocytic neoplasms with long-term follow-up. Am J Surg Pathol. 2014;38:934–40.

    PubMed  Article  Google Scholar 

  5. 5.

    Bastian BC, LeBoit PE, Pinkel D. Mutations and copy number increase of HRAS in Spitz nevi with distinctive histopathological features. Am J Pathol. 2000;157:967–72.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  6. 6.

    Botton T, Yeh I, Nelson T, Vemula SS, Sparatta A, Garrido MC, et al. Recurrent BRAF kinase fusions in melanocytic tumors offer an opportunity for targeted therapy. Pigment Cell Melanoma Res. 2013;26:845–51.

    CAS  PubMed  Article  Google Scholar 

  7. 7.

    Wiesner T, He J, Yelensky R, Esteve-Puig R, Botton T, Yeh I, et al. Kinase fusions are frequent in Spitz tumours and spitzoid melanomas. Nat Commun. 2014;5:3116.

    PubMed  PubMed Central  Article  CAS  Google Scholar 

  8. 8.

    Yeh I, Botton T, Talevich E, Shain AH, Sparatta AJ, de la Fouchardiere A, et al. Activating MET kinase rearrangements in melanoma and Spitz tumours. Nat Commun. 2015;6:7174.

    PubMed  PubMed Central  Article  Google Scholar 

  9. 9.

    Yeh I, Tee MK, Botton T, Shain AH, Sparatta AJ, Gagnon A, et al. NTRK3 kinase fusions in Spitz tumours. J Pathol. 2016;240:282–90.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  10. 10.

    Wang L, Busam KJ, Benayed R, Cimera R, Wang J, Denley R, et al. Identification of NTRK3 fusions in childhood melanocytic neoplasms. J Mol Diagn. 2017;19:387–96.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  11. 11.

    VandenBoom T, Quan VL, Zhang B, Garfield EM, Kong BY, Isales MC, et al. Genomic fusions in pigmented spindle cell nevus of reed: Am J Surg Pathol. 2018;42:1042–51.

  12. 12.

    Quan VL, Zhang B, Mohan LS, Shi K, Isales MC, Panah E, et al. Activating structural alterations in MAPK genes are distinct genetic drivers in a unique subgroup of spitzoid neoplasms. Am J Surg Pathol. 2019. https://doi.org/10.1097/PAS.0000000000001213.

  13. 13.

    Newman S, Fan L, Pribnow A, Silkov A, Rice SV, Lee S, et al. Clinical genome sequencing uncovers potentially targetable truncations and fusions of MAP3K8 in spitzoid and other melanomas. Nat Med. 2019;25:597–602.

  14. 14.

    Busam KJ, Kutzner H, Cerroni L, Wiesner T. Clinical and pathologic findings of Spitz nevi and atypical Spitz tumors with ALK fusions. Am J Surg Pathol. 2014;38:925–33.

    PubMed  PubMed Central  Article  Google Scholar 

  15. 15.

    Yeh I, de la Fouchardiere A, Pissaloux D, Mully TW, Garrido MC, Vemula SS, et al. Clinical, histopathologic, and genomic features of Spitz tumors with ALK fusions. Am J Surg Pathol. 2015;39:581–91.

    PubMed  PubMed Central  Article  Google Scholar 

  16. 16.

    Amin SM, Haugh AM, Lee CY, Zhang B, Bubley JA, Merkel EA, et al. A comparison of morphologic and molecular features of BRAF, ALK, and NTRK1 fusion spitzoid neoplasms. Am J Surg Pathol. 2017;41:491–8.

    PubMed  Article  Google Scholar 

  17. 17.

    Pollock PM, Harper UL, Hansen KS, Yudt LM, Stark M, Robbins CM, et al. High frequency of BRAF mutations in nevi. Nat Genet. 2003;33:19–20.

    CAS  PubMed  Article  Google Scholar 

  18. 18.

    Yeh I, von Deimling A, Bastian BC. Clonal BRAF mutations in melanocytic nevi and initiating role of BRAF in melanocytic neoplasia. J Natl Cancer Inst. 2013;105:917–9.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  19. 19.

    Ackerman AB. Spitz’s nevus: reassessment critical, revision radical. New York: Ardor Scribendi, 2007.

  20. 20.

    Wu G, Barnhill RL, Lee S, Li Y, Shao Y, Easton J, et al. The landscape of fusion transcripts in spitzoid melanoma and biologically indeterminate spitzoid tumors by RNA sequencing. Mod Pathol. 2016. https://doi.org/10.1038/modpathol.2016.37.

  21. 21.

    van Dijk MCRF, Bernsen MR, Ruiter DJ. Analysis of mutations in B-RAF, N-RAS, and H-RAS genes in the differential diagnosis of Spitz nevus and spitzoid melanoma. Am J Surg Pathol. 2005;29:1145–51.

    PubMed  Article  Google Scholar 

  22. 22.

    Fullen DR, Poynter JN, Lowe L, Su LD, Elder JT, Nair RP, et al. BRAF and NRAS mutations in spitzoid melanocytic lesions. Mod Pathol. 2006;19:1324–32.

    CAS  PubMed  Article  Google Scholar 

  23. 23.

    Da Forno PD, Pringle JH, Fletcher A, Bamford M, Su L, Potter L, et al. BRAF, NRAS and HRAS mutations in spitzoid tumours and their possible pathogenetic significance. Br J Dermatol. 2009;161:364–72.

    PubMed  Article  CAS  Google Scholar 

  24. 24.

    Lazova R, Pornputtapong N, Halaban R, Bosenberg M, Bai Y, Chai H, et al. Spitz nevi and Spitzoid melanomas: exome sequencing and comparison with conventional melanocytic nevi and melanomas. Mod Pathol. 2017. https://doi.org/10.1038/modpathol.2016.237.

  25. 25.

    Elder DE, Massi D, Scolyer R, Willemze R. WHO classification of skin tumours, 4th ed. Lyon, France: IARC Press; 2018.

  26. 26.

    Paradela S, Fonseca E, Pita-Fernández S, Prieto Vg. Spitzoid and non-spitzoid melanoma in children. A prognostic comparative study. J Eur Acad Dermatol Venereol. 2013;27:1214–21.

    CAS  PubMed  Google Scholar 

  27. 27.

    Viros A, Fridlyand J, Bauer J, Lasithiotakis K, Garbe C, Pinkel D, et al. Improving melanoma classification by integrating genetic and morphologic features. PLoS Med. 2008;5:e120.

    PubMed  PubMed Central  Article  CAS  Google Scholar 

  28. 28.

    Landi MT, Bauer J, Pfeiffer RM, Elder DE, Hulley B, Minghetti P, et al. MC1R germline variants confer risk for BRAF-mutant melanoma. Science. 2006;313:521–2.

    CAS  PubMed  Article  Google Scholar 

  29. 29.

    Li H, Durbin R. Fast and accurate short read alignment with Burrows-Wheeler transform. Bioinforma Oxf Engl. 2009;25:1754–60.

    CAS  Article  Google Scholar 

  30. 30.

    McKenna A, Hanna M, Banks E, Sivachenko A, Cibulskis K, Kernytsky A, et al. The genome analysis toolkit: a MapReduce framework for analyzing next-generation DNA sequencing data. Genome Res. 2010;20:1297–303.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  31. 31.

    Garrison, Erik M Gabor. Haplotype-based variant detection from short-read sequencing. 2012. https://arxiv.org/abs/1207.3907.

  32. 32.

    Broad Institute. Picard. Broad Institute. http://broadinstitute.github.io/picard/.

  33. 33.

    Wang K, Li M, Hakonarson H. ANNOVAR: functional annotation of genetic variants from high-throughput sequencing data. Nucleic Acids Res. 2010;38:e164–e164.

    PubMed  PubMed Central  Article  CAS  Google Scholar 

  34. 34.

    Rausch T, Zichner T, Schlattl A, Stütz AM, Benes V, Korbel JO. DELLY: structural variant discovery by integrated paired-end and split-read analysis. Bioinformatics. 2012;28:i333–i339.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  35. 35.

    Thorvaldsdóttir H, Robinson JT, Mesirov JP. Integrative genomics viewer (IGV): high-performance genomics data visualization and exploration. Brief Bioinform. 2013;14:178–92.

    PubMed  Article  CAS  Google Scholar 

  36. 36.

    Talevich E, Shain AH, Botton T, Bastian BC. CNVkit: genome-wide copy number detection and visualization from targeted dna sequencing. PLOS Comput Biol. 2016;12:e1004873.

    PubMed  PubMed Central  Article  CAS  Google Scholar 

  37. 37.

    Oesper L, Satas G, Raphael BJ. Quantifying tumor heterogeneity in whole-genome and whole-exome sequencing data. Bioinformatics. 2014;30:3532–40.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  38. 38.

    Landrum MJ, Lee JM, Benson M, Brown G, Chao C, Chitipiralla S, et al. ClinVar: public archive of interpretations of clinically relevant variants. Nucleic Acids Res. 2016;44:D862–868.

    CAS  PubMed  Article  Google Scholar 

  39. 39.

    NHLBI GO Exome Sequencing Project (ESP). Exome variant server. Seattle, WA. http://evs.gs.washington.edu/EVS/.

  40. 40.

    Consortium T 1000 GP. A global reference for human genetic variation. Nature. 2015;526:nature15393.

    Google Scholar 

  41. 41.

    Online Mendelian Inheritance in Man, OMM. McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University (Baltimore, MD). https://omim.org.

  42. 42.

    My Cancer Genome. https://www.mycancergenome.org.

  43. 43.

    Dobin A, Davis CA, Schlesinger F, Drenkow J, Zaleski C, Jha S, et al. STAR: ultrafast universal RNA-seq aligner. Bioinformatics. 2013;29:15–21.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  44. 44.

    Nicorici D, Şatalan M, Edgren H, Kangaspeska S, Murumägi A, Kallioniemi O, et al. FusionCatcher—a tool for finding somatic fusion genes in paired-end RNA-sequencing data. 2014. https://www.biorxiv.org/content/10.1101/011650v1.

  45. 45.

    Akbani R, Akdemir KC, Aksoy BA, Albert M, Ally A, Amin SB, et al. Genomic classification of cutaneous melanoma. Cell. 2015;161:1681–96.

    Article  CAS  Google Scholar 

  46. 46.

    Gao J, Aksoy BA, Dogrusoz U, Dresdner G, Gross B, Sumer SO, et al. Integrative analysis of complex cancer genomics and clinical profiles using the cBioPortal. Sci Signal. 2013;6:pl1–pl1.

    PubMed  PubMed Central  Article  CAS  Google Scholar 

  47. 47.

    Cerami E, Gao J, Dogrusoz U, Gross BE, Sumer SO, Aksoy BA, et al. The cBio cancer genomics portal: an open platform for exploring multidimensional cancer genomics data. Cancer Disco. 2012;2:401–4.

    Article  Google Scholar 

  48. 48.

    Stransky N, Cerami E, Schalm S, Kim JL, Lengauer C. The landscape of kinase fusions in cancer. Nat Commun. 2014;5. https://doi.org/10.1038/ncomms5846.

  49. 49.

    Lehmann BD, Shaver TM, Johnson DB, Li Z, Gonzalez-Ericsson PI, Sanchez V, et al. Identification of targetable recurrent MAP3K8 rearrangements in melanomas lacking known driver mutations. Mol Cancer Res. 2019. https://doi.org/10.1158/1541-7786.MCR-19-0257.

  50. 50.

    Chakraborty R, Hampton OA, Shen X, Simko SJ, Shih A, Abhyankar H, et al. Mutually exclusive recurrent somatic mutations in MAP2K1 and BRAF support a central role for ERK activation in LCH pathogenesis. Blood. 2014;124:3007–15.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  51. 51.

    Yeh I, Lang UE, Durieux E, Tee MK, Jorapur A, Shain AH, et al. Combined activation of MAP kinase pathway and β-catenin signaling cause deep penetrating nevi. Nat Commun. 2017;8:644.

    PubMed  PubMed Central  Article  CAS  Google Scholar 

  52. 52.

    Phillips JJ, Gong H, Chen K, Joseph NM, van Ziffle J, Jin L-W, et al. Activating NRF1-BRAF and ATG7-RAF1 fusions in anaplastic pleomorphic xanthoastrocytoma without BRAF p.V600E mutation. Acta Neuropathol. 2016;132:757–60.

    PubMed  PubMed Central  Article  Google Scholar 

  53. 53.

    Huang FW, Hodis E, Xu MJ, Kryukov GV, Chin L, Garraway LA. Highly recurrent TERT promoter mutations in human melanoma. Science. 2013;339:957–9.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  54. 54.

    Horn S, Figl A, Rachakonda PS, Fischer C, Sucker A, Gast A, et al. TERT promoter mutations in familial and sporadic melanoma. Science. 2013;339:959–61.

    CAS  PubMed  Article  Google Scholar 

  55. 55.

    Han S-Y, Kato H, Kato S, Suzuki T, Shibata H, Ishii S, et al. Functional evaluation of PTEN missense mutations using in vitro phosphoinositide phosphatase assay. Cancer Res. 2000;60:3147–51.

    CAS  PubMed  Google Scholar 

  56. 56.

    Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, et al. TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors. Nat Genet. 2015;47:1411–4.

    CAS  PubMed  Article  Google Scholar 

  57. 57.

    Yao Z, Yaeger R, Rodrik-Outmezguine VS, Tao A, Torres NM, Chang MT, et al. Tumours with class 3 BRAF mutants are sensitive to the inhibition of activated RAS. Nature. 2017;548:234.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  58. 58.

    Nyström A-M, Ekvall S, Berglund E, Björkqvist M, Braathen G, Duchen K, et al. Noonan and cardio-facio-cutaneous syndromes: two clinically and genetically overlapping disorders. J Med Genet. 2008;45:500–6.

    PubMed  Article  CAS  Google Scholar 

  59. 59.

    Senawong T, Phuchareon J, Ohara O, McCormick F, Rauen KA, Tetsu O. Germline mutations of MEK in cardio-facio-cutaneous syndrome are sensitive to MEK and RAF inhibition: implications for therapeutic options. Hum Mol Genet. 2008;17:419–30.

    CAS  PubMed  Article  Google Scholar 

  60. 60.

    Gos M, Smigiel R, Kaczan T, Landowska A, Abramowicz A, Sasiadek M, et al. MAP2K2 mutation as a cause of cardio-facio-cutaneous syndrome in an infant with a severe and fatal course of the disease. Am J Med Genet A. 2018;176:1670–4.

    CAS  PubMed  Article  Google Scholar 

  61. 61.

    Souroullas GP, Jeck WR, Parker JS, Simon JM, Liu J-Y, Paulk J, et al. An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation. Nat Med. 2016;22:632–40.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  62. 62.

    Parsons DW, Jones S, Zhang X, Lin JC-H, Leary RJ, Angenendt P, et al. An integrated genomic analysis of human glioblastoma multiforme. Science. 2008;321:1807–12.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  63. 63.

    Zhao S, Lin Y, Xu W, Jiang W, Zha Z, Wang P, et al. Glioma-derived mutations in IDH1 dominantly inhibit IDH1 catalytic activity and induce HIF-1alpha. Science. 2009;324:261–5.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  64. 64.

    Shain AH, Garrido M, Botton T, Talevich E, Yeh I, Sanborn JZ, et al. Exome sequencing of desmoplastic melanoma identifies recurrent NFKBIE promoter mutations and diverse activating mutations in the MAPK pathway. Nat Genet. 2015;47:1194–9.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  65. 65.

    Curtin JA, Busam K, Pinkel D, Bastian BC. Somatic activation of KIT in distinct subtypes of melanoma. J Clin Oncol. 2006;24: 4340–6.

    CAS  PubMed  Article  Google Scholar 

  66. 66.

    Nikolaev SI, Rimoldi D, Iseli C, Valsesia A, Robyr D, Gehrig C, et al. Exome sequencing identifies recurrent somatic MAP2K1 and MAP2K2 mutations in melanoma. Nat Genet. 2012;44:133–9.

    CAS  Article  Google Scholar 

  67. 67.

    Cellier L, Perron E, Pissaloux D, Karanian M, Haddad V, Alberti L, et al. Cutaneous melanocytoma With CRTC1-TRIM11 fusion: report of 5 cases resembling clear cell sarcoma. Am J Surg Pathol. 2018;42:382–91.

    PubMed  Article  Google Scholar 

  68. 68.

    Lee S, Barnhill RL, Dummer R, Dalton J, Wu J, Pappo A, et al. TERT promoter mutations are predictive of aggressive clinical behavior in patients with spitzoid melanocytic neoplasms. Sci Rep. 2015;5:11200.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  69. 69.

    Griewank KG, Murali R, Puig-Butille JA, Schilling B, Livingstone E, Potrony M, et al. TERT promoter mutation status as an independent prognostic factor in cutaneous melanoma. J Natl Cancer Inst. 2014;106:dju246.

    PubMed  PubMed Central  Article  CAS  Google Scholar 

  70. 70.

    Gerami P, Scolyer RA, Xu X, Elder DE, Abraham RM, Fullen D, et al. Risk assessment for atypical spitzoid melanocytic neoplasms using FISH to identify chromosomal copy number aberrations. Am J Surg Pathol. 2013;37:676–84.

    PubMed  Article  Google Scholar 

  71. 71.

    Dubruc E, Balme B, Dijoud F, Disant F, Thomas L, Wang Q, 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. J Cutan Pathol. 2014;41:866–72.

    PubMed  Article  Google Scholar 

  72. 72.

    Wiesner T, Murali R, Fried I, Cerroni L, Busam K, Kutzner H, et al. A distinct subset of atypical Spitz tumors is characterized by BRAF mutation and loss of BAP1 expression. Am J Surg Pathol. 2012;36:818–30.

    PubMed  PubMed Central  Article  Google Scholar 

  73. 73.

    Busam KJ, Sung J, Wiesner T, von Deimling A, Jungbluth A. Combined BRAF(V600E)-positive melanocytic lesions with large epithelioid cells lacking BAP1 expression and conventional nevomelanocytes. Am J Surg Pathol. 2013;37:193–9.

    PubMed  Article  Google Scholar 

  74. 74.

    Yeh I, Mully TW, Wiesner T, Vemula SS, Mirza SA, Sparatta AJ, et al. Ambiguous melanocytic tumors with loss of 3p21. Am J Surg Pathol. 2014;38:1088–95.

    PubMed  PubMed Central  Article  Google Scholar 

  75. 75.

    Vilain RE, McCarthy SW, Thompson JF, Scolyer RA. BAP1-inactivated spitzoid naevi. Am J Surg Pathol. 2015;39:722.

    PubMed  Article  Google Scholar 

  76. 76.

    Cohen JN, Joseph NM, North JP, Onodera C, Zembowicz A, LeBoit PE. Genomic analysis of pigmented epithelioid melanocytomas reveals recurrent alterations in PRKAR1A, and PRKCA genes. Am J Surg Pathol. 2017;41:1333–46.

    PubMed  Article  Google Scholar 

  77. 77.

    LaFave LM, Béguelin W, Koche R, Teater M, Spitzer B, Chramiec A, et al. Loss of BAP1 function leads to EZH2-dependent transformation. Nat Med. 2015;21:1344–9.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

Download references

Acknowledgements

We thank Connie Jang and Yvonne Lee for their assistance in organizing and obtaining the cases. SR was funded in part by the American Society of Dermatopathology Mentorship Award, and Sandra Peternel was supported by a grant from the European Academy of Dermatology and Venereology (RF-2017-17). This work was supported by the National Cancer Institute at the National Institutes of Health (grant number 1R35CA220481).

Author information

Affiliations

Authors

Corresponding author

Correspondence to Iwei Yeh.

Ethics declarations

Conflict of interest

The authors declare that they have no conflict of interest.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary information

Rights and permissions

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Raghavan, S.S., Peternel, S., Mully, T.W. et al. Spitz melanoma is a distinct subset of spitzoid melanoma. Mod Pathol 33, 1122–1134 (2020). https://doi.org/10.1038/s41379-019-0445-z

Download citation

Further reading

Search

Quick links