Validation of a 40-gene expression profile test to predict metastatic risk in localized high-risk cutaneous squamous cell carcinoma.


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:
Feb 2021
Historique:
received: 20 01 2020
revised: 22 03 2020
accepted: 15 04 2020
pubmed: 29 4 2020
medline: 30 7 2021
entrez: 29 4 2020
Statut: ppublish

Résumé

Current staging systems for cutaneous squamous cell carcinoma (cSCC) have limited positive predictive value for identifying patients who will experience metastasis. To develop and validate a gene expression profile (GEP) test for predicting risk for metastasis in localized, high-risk cSCC with the goal of improving risk-directed patient management. Archival formalin-fixed paraffin-embedded primary cSCC tissue and clinicopathologic data (n = 586) were collected from 23 independent centers in a prospectively designed study. A GEP signature was developed using a discovery cohort (n = 202) and validated in a separate, nonoverlapping, independent cohort (n = 324). A prognostic 40-GEP test was developed and validated, stratifying patients with high-risk cSCC into classes based on metastasis risk: class 1 (low risk), class 2A (high risk), and class 2B (highest risk). For the validation cohort, 3-year metastasis-free survival rates were 91.4%, 80.6%, and 44.0%, respectively. A positive predictive value of 60% was achieved for the highest-risk group (class 2B), an improvement over staging systems, and negative predictive value, sensitivity, and specificity were comparable to staging systems. Potential understaging of cases could affect metastasis rate accuracy. The 40-GEP test is an independent predictor of metastatic risk that can complement current staging systems for patients with high-risk cSCC.

Sections du résumé

BACKGROUND BACKGROUND
Current staging systems for cutaneous squamous cell carcinoma (cSCC) have limited positive predictive value for identifying patients who will experience metastasis.
OBJECTIVE OBJECTIVE
To develop and validate a gene expression profile (GEP) test for predicting risk for metastasis in localized, high-risk cSCC with the goal of improving risk-directed patient management.
METHODS METHODS
Archival formalin-fixed paraffin-embedded primary cSCC tissue and clinicopathologic data (n = 586) were collected from 23 independent centers in a prospectively designed study. A GEP signature was developed using a discovery cohort (n = 202) and validated in a separate, nonoverlapping, independent cohort (n = 324).
RESULTS RESULTS
A prognostic 40-GEP test was developed and validated, stratifying patients with high-risk cSCC into classes based on metastasis risk: class 1 (low risk), class 2A (high risk), and class 2B (highest risk). For the validation cohort, 3-year metastasis-free survival rates were 91.4%, 80.6%, and 44.0%, respectively. A positive predictive value of 60% was achieved for the highest-risk group (class 2B), an improvement over staging systems, and negative predictive value, sensitivity, and specificity were comparable to staging systems.
LIMITATIONS CONCLUSIONS
Potential understaging of cases could affect metastasis rate accuracy.
CONCLUSION CONCLUSIONS
The 40-GEP test is an independent predictor of metastatic risk that can complement current staging systems for patients with high-risk cSCC.

Identifiants

pubmed: 32344066
pii: S0190-9622(20)30704-0
doi: 10.1016/j.jaad.2020.04.088
pii:
doi:

Substances chimiques

Biomarkers, Tumor 0

Types de publication

Journal Article Multicenter Study Validation Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

361-369

Commentaires et corrections

Type : ErratumIn

Informations de copyright

Copyright © 2020 American Academy of Dermatology, Inc. All rights reserved.

Auteurs

Ashley Wysong (A)

University of Nebraska Medical Center, Omaha, Nebraska.

Jason G Newman (JG)

University of Pennsylvania, Philadelphia, Pennsylvania.

Kyle R Covington (KR)

Castle Biosciences, Inc, Friendswood, Texas.

Sarah J Kurley (SJ)

Castle Biosciences, Inc, Friendswood, Texas.

Sherrif F Ibrahim (SF)

University of Rochester, Rochester, New York.

Aaron S Farberg (AS)

Icahn School of Medicine at Mount Sinai, New York, New York; Arkansas Dermatology Skin Cancer Center, Little Rock, Arkansas.

Anna Bar (A)

Oregon Health & Science University, Portland, Oregon.

Nathan J Cleaver (NJ)

Cleaver Dermatology, Kirksville, Missouri.

Ally-Khan Somani (AK)

Indiana University School of Medicine, Indianapolis, Indiana.

David Panther (D)

Zitelli and Brodland, P.C. Skin Cancer Center, Pittsburgh, Pennsylvania.

David G Brodland (DG)

Zitelli and Brodland, P.C. Skin Cancer Center, Pittsburgh, Pennsylvania.

John Zitelli (J)

Zitelli and Brodland, P.C. Skin Cancer Center, Pittsburgh, Pennsylvania.

Jennifer Toyohara (J)

Adult & Pediatric Dermatology, Concord, Massachusetts.

Ian A Maher (IA)

University of Minnesota, Minneapolis, Minnesota.

Yang Xia (Y)

Brooke Army Medical Center, San Antonio, Texas.

Kristin Bibee (K)

University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.

Robert Griego (R)

Skin Cancer Specialists, Ltd, Mesa, Arizona.

Darrell S Rigel (DS)

New York University School of Medicine, New York, New York.

Kristen Meldi Plasseraud (K)

Castle Biosciences, Inc, Friendswood, Texas.

Sarah Estrada (S)

Castle Biosciences, Inc, Phoenix, Arizona; Affiliated Dermatology, Scottsdale, Arizona.

Lauren Meldi Sholl (LM)

Castle Biosciences, Inc, Phoenix, Arizona.

Clare Johnson (C)

Castle Biosciences, Inc, Phoenix, Arizona.

Robert W Cook (RW)

Castle Biosciences, Inc, Friendswood, Texas. Electronic address: rcook@castlebiosciences.com.

Chrysalyne D Schmults (CD)

Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.

Sarah T Arron (ST)

University of California San Francisco, San Francisco, California. Electronic address: sarah.arron@ucsf.edu.

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