Clinicopathologic and genetic characterization of invasive melanoma with BRAF V600K mutation: A study of 16 cases.


Journal

Journal of cutaneous pathology
ISSN: 1600-0560
Titre abrégé: J Cutan Pathol
Pays: United States
ID NLM: 0425124

Informations de publication

Date de publication:
Aug 2023
Historique:
revised: 28 04 2023
received: 24 02 2023
accepted: 07 05 2023
medline: 14 7 2023
pubmed: 25 5 2023
entrez: 25 5 2023
Statut: ppublish

Résumé

The clinicopathologic and genetic features of cutaneous melanoma with a BRAF V600K mutation are not well-known. We aimed to evaluate these characteristics in comparison with those associated with BRAF V600E. Real-time polymerase chain reaction (PCR) and/or the MassARRAY® system were used to detect BRAF V600K in 16 invasive melanomas and confirm BRAF V600E in another 60 cases. Immunohistochemistry and panel next-generation sequencing were used to evaluate protein expression and tumor mutation burden, respectively. The median age of melanoma patients harboring the BRAF V600K mutation (72.5 years) was higher than those with the BRAF V600E (58.5 years). The two groups also differed in sex (13/16 [81.3%] male in the V600K group vs. 23/60 [38.3%] in V600E) and in the frequency of scalp involvement (8/16 [50.0%] in V600K vs. 1/60 [1.6%] in V600E). The clinical appearance was similar to a superficial spreading melanoma. Histopathologically, non-nested lentiginous intraepidermal spread and subtle solar elastosis were observed. One patient (1/13, 7.7%) had a pre-existing intradermal nevus. Diffuse PRAME immunoexpression was seen in only one (14.3%) of seven tested cases. Loss of p16 expression was observed in all 12 cases (100%) analyzed. The tumor mutation burden was 8 and 6 mutations/Mb in the two tested cases. Melanoma carrying the BRAF V600K mutation showed the predominance on the scalp of elderly men, lentiginous intraepidermal growth, subtle solar elastosis, possible existence of intradermal nevus component, frequent loss of p16 immunoexpression, limited immunoreactivity for PRAME, and intermediate tumor mutation burden.

Sections du résumé

BACKGROUND BACKGROUND
The clinicopathologic and genetic features of cutaneous melanoma with a BRAF V600K mutation are not well-known. We aimed to evaluate these characteristics in comparison with those associated with BRAF V600E.
METHODS METHODS
Real-time polymerase chain reaction (PCR) and/or the MassARRAY® system were used to detect BRAF V600K in 16 invasive melanomas and confirm BRAF V600E in another 60 cases. Immunohistochemistry and panel next-generation sequencing were used to evaluate protein expression and tumor mutation burden, respectively.
RESULTS RESULTS
The median age of melanoma patients harboring the BRAF V600K mutation (72.5 years) was higher than those with the BRAF V600E (58.5 years). The two groups also differed in sex (13/16 [81.3%] male in the V600K group vs. 23/60 [38.3%] in V600E) and in the frequency of scalp involvement (8/16 [50.0%] in V600K vs. 1/60 [1.6%] in V600E). The clinical appearance was similar to a superficial spreading melanoma. Histopathologically, non-nested lentiginous intraepidermal spread and subtle solar elastosis were observed. One patient (1/13, 7.7%) had a pre-existing intradermal nevus. Diffuse PRAME immunoexpression was seen in only one (14.3%) of seven tested cases. Loss of p16 expression was observed in all 12 cases (100%) analyzed. The tumor mutation burden was 8 and 6 mutations/Mb in the two tested cases.
CONCLUSIONS CONCLUSIONS
Melanoma carrying the BRAF V600K mutation showed the predominance on the scalp of elderly men, lentiginous intraepidermal growth, subtle solar elastosis, possible existence of intradermal nevus component, frequent loss of p16 immunoexpression, limited immunoreactivity for PRAME, and intermediate tumor mutation burden.

Identifiants

pubmed: 37226844
doi: 10.1111/cup.14470
doi:

Substances chimiques

Proto-Oncogene Proteins B-raf EC 2.7.11.1
BRAF protein, human EC 2.7.11.1
PRAME protein, human 0
Antigens, Neoplasm 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

739-747

Subventions

Organisme : JSPS KAKENHI
ID : JP22K06994

Informations de copyright

© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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Auteurs

Keisuke Goto (K)

Department of Diagnostic Pathology, Shizuoka Cancer Center Hospital, Sunto, Japan.
Department of Dermatology, Hyogo Cancer Center, Akashi, Japan.
Department of Diagnostic Pathology and Cytology, Osaka International Cancer Institute, Osaka, Japan.
Department of Pathology, Tokyo Metropolitan Cancer and Infectious Disease Center Komagome Hospital, Tokyo, Japan.
Department of Pathology, Itabashi Central Clinical Laboratory, Tokyo, Japan.
Department of Anatomic Pathology, Tokyo Medical University, Tokyo, Japan.
Department of Diagnostic Pathology, Chutoen General Medical Center, Kakegawa, Japan.
Department of Clinical Laboratory and Diagnostic Pathology, Osaka National Hospital, Osaka, Japan.
Department of Dermato-Oncology/Dermatology, National Hospital Organization Kagoshima Medical Center, Kagoshima, Japan.

Shusuke Yoshikawa (S)

Department of Dermatology, Shizuoka Cancer Center Hospital, Sunto, Japan.

Toshihiro Takai (T)

Department of Dermatology, Hyogo Cancer Center, Akashi, Japan.

Kota Tachibana (K)

Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Melanoma Center, Okayama University Hospital, Okayama, Japan.

Keiichiro Honma (K)

Department of Diagnostic Pathology and Cytology, Osaka International Cancer Institute, Osaka, Japan.

Taiki Isei (T)

Department of Dermatologic Oncology, Osaka International Cancer Institute, Osaka, Japan.

Yoji Kukita (Y)

Laboratory of Genomic Pathology, Research Center, Osaka International Cancer Institute, Osaka, Japan.

Takuma Oishi (T)

Department of Diagnostic Pathology, Shizuoka Cancer Center Hospital, Sunto, Japan.

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