Germline Cancer Susceptibility in Individuals with Melanoma.

Cancer Predisposition DNA Repair Familial Melanoma Family History Genetic Testing Germline Homologous Repair Deficiency Inherited Cancer Syndromes Melanoma

Journal

Journal of the American Academy of Dermatology
ISSN: 1097-6787
Titre abrégé: J Am Acad Dermatol
Pays: United States
ID NLM: 7907132

Informations de publication

Date de publication:
19 Mar 2024
Historique:
received: 19 05 2023
revised: 05 11 2023
accepted: 27 11 2023
medline: 22 3 2024
pubmed: 22 3 2024
entrez: 21 3 2024
Statut: aheadofprint

Résumé

Prior studies have estimated a small number of individuals with melanoma (2-2.5%) have germline cancer predisposition, yet a recent twin study suggested melanoma has the highest hereditability among cancers. To determine the incidence of hereditary melanoma and characterize the spectrum of cancer predisposition genes that may increase the risk of melanoma. 400 individuals with melanoma and personal or family history of cancers underwent germline testing of >80 cancer predisposition genes. Comparative analysis of germline data was performed on 3 additional oncologic and dermatologic datasets. Germline pathogenic/likely pathogenic (P/LP) variants were identified in 15.3% (61) individuals with melanoma. Most variants (41, 67%) involved genes considered unrelated to melanoma (BLM, BRIP1, CHEK2, MLH1, MSH2, PMS2, RAD51C). A third (20, 33%) were in genes previously associated with familial melanoma (BAP1, BRCA2, CDKN2A, MITF, TP53). Nearly half (30, 46.9%) of P/LP variants were in HRD genes. Validation cohorts demonstrated P/LP rates of 10.6% from an unselected oncologic cohort, 15.8% from a selected commercial testing cohort and 14.5% from a highly selected dermatologic study. Cohorts with varying degrees of selection, some retrospective. Germline predisposition in individuals with melanoma is common, with clinically actionable findings diagnosed in 10.6% to 15.8%.

Sections du résumé

BACKGROUND BACKGROUND
Prior studies have estimated a small number of individuals with melanoma (2-2.5%) have germline cancer predisposition, yet a recent twin study suggested melanoma has the highest hereditability among cancers.
OBJECTIVE OBJECTIVE
To determine the incidence of hereditary melanoma and characterize the spectrum of cancer predisposition genes that may increase the risk of melanoma.
METHODS METHODS
400 individuals with melanoma and personal or family history of cancers underwent germline testing of >80 cancer predisposition genes. Comparative analysis of germline data was performed on 3 additional oncologic and dermatologic datasets.
RESULTS RESULTS
Germline pathogenic/likely pathogenic (P/LP) variants were identified in 15.3% (61) individuals with melanoma. Most variants (41, 67%) involved genes considered unrelated to melanoma (BLM, BRIP1, CHEK2, MLH1, MSH2, PMS2, RAD51C). A third (20, 33%) were in genes previously associated with familial melanoma (BAP1, BRCA2, CDKN2A, MITF, TP53). Nearly half (30, 46.9%) of P/LP variants were in HRD genes. Validation cohorts demonstrated P/LP rates of 10.6% from an unselected oncologic cohort, 15.8% from a selected commercial testing cohort and 14.5% from a highly selected dermatologic study.
LIMITATIONS CONCLUSIONS
Cohorts with varying degrees of selection, some retrospective.
CONCLUSION CONCLUSIONS
Germline predisposition in individuals with melanoma is common, with clinically actionable findings diagnosed in 10.6% to 15.8%.

Identifiants

pubmed: 38513832
pii: S0190-9622(24)00504-8
doi: 10.1016/j.jaad.2023.11.070
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Auteurs

P Funchain (P)

Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH, USA. Electronic address: funchap@stanford.edu.

Y Ni (Y)

Center for Immunotherapy & Precision Immuno-Oncology, Cleveland Clinic Foundation, Cleveland, OH, USA.

B Heald (B)

Genomic Medicine Institute, Cleveland Clinic Foundation, Cleveland, OH, USA; Invitae Corporation, South San Francisco, CA, USA.

B Bungo (B)

Medicine Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.

M Arbesman (M)

Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.

T R Behera (TR)

Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH, USA; Center for Immunotherapy & Precision Immuno-Oncology, Cleveland Clinic Foundation, Cleveland, OH, USA.

S McCormick (S)

Center Cancer Risk Assessment, Massachusetts General Hospital, Cambridge, MA, USA.

J M Song (JM)

Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH, USA; Department of Hematology/Oncology, MetroHealth, Cleveland, USA.

L B Kennedy (LB)

Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.

S M Nielsen (SM)

Invitae Corporation, South San Francisco, CA, USA.

E D Esplin (ED)

Invitae Corporation, South San Francisco, CA, USA.

E Nizialek (E)

Department of Medical Oncology, Johns Hopkins University, Baltimore, MD, USA.

J Ko (J)

Pathology and Laboratory Medicine Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.

C M Diaz-Montero (CM)

Center for Immunotherapy & Precision Immuno-Oncology, Cleveland Clinic Foundation, Cleveland, OH, USA.

B Gastman (B)

Dermatology and Plastic Surgery Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.

A J Stratigos (AJ)

A. Sygros Hospital Medical School, University of Athens, Athens, Greece.

M Artomov (M)

Broad Institute, Cambridge, MA, USA.

H Tsao (H)

Department of Dermatology, Massachusetts General Hospital, Cambridge, MA, USA.

J Arbesman (J)

Dermatology and Plastic Surgery Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.

Classifications MeSH