Prediction and monitoring of relapse in stage III melanoma using circulating tumor DNA.


Journal

Annals of oncology : official journal of the European Society for Medical Oncology
ISSN: 1569-8041
Titre abrégé: Ann Oncol
Pays: England
ID NLM: 9007735

Informations de publication

Date de publication:
01 05 2019
Historique:
pubmed: 7 3 2019
medline: 13 6 2020
entrez: 7 3 2019
Statut: ppublish

Résumé

The advent of effective adjuvant therapies for patients with resected melanoma has highlighted the need to stratify patients based on risk of relapse given the cost and toxicities associated with treatment. Here we assessed circulating tumor DNA (ctDNA) to predict and monitor relapse in resected stage III melanoma. Somatic mutations were identified in 99/133 (74%) patients through tumor tissue sequencing. Personalized droplet digital PCR (ddPCR) assays were used to detect known mutations in 315 prospectively collected plasma samples from mutation-positive patients. External validation was performed in a prospective independent cohort (n = 29). ctDNA was detected in 37 of 99 (37%) individuals. In 81 patients who did not receive adjuvant therapy, 90% of patients with ctDNA detected at baseline and 100% of patients with ctDNA detected at the postoperative timepoint relapsed at a median follow up of 20 months. ctDNA detection predicted patients at high risk of relapse at baseline [relapse-free survival (RFS) hazard ratio (HR) 2.9; 95% confidence interval (CI) 1.5-5.6; P = 0.002] and postoperatively (HR 10; 95% CI 4.3-24; P < 0.001). ctDNA detection at baseline [HR 2.9; 95% CI 1.3-5.7; P = 0.003 and postoperatively (HR 11; 95% CI 4.3-27; P < 0.001] was also associated with inferior distant metastasis-free survival (DMFS). These findings were validated in the independent cohort. ctDNA detection remained an independent predictor of RFS and DMFS in multivariate analyses after adjustment for disease stage and BRAF mutation status. Baseline and postoperative ctDNA detection in two independent prospective cohorts identified stage III melanoma patients at highest risk of relapse and has potential to inform adjuvant therapy decisions.

Sections du résumé

BACKGROUND
The advent of effective adjuvant therapies for patients with resected melanoma has highlighted the need to stratify patients based on risk of relapse given the cost and toxicities associated with treatment. Here we assessed circulating tumor DNA (ctDNA) to predict and monitor relapse in resected stage III melanoma.
PATIENTS AND METHODS
Somatic mutations were identified in 99/133 (74%) patients through tumor tissue sequencing. Personalized droplet digital PCR (ddPCR) assays were used to detect known mutations in 315 prospectively collected plasma samples from mutation-positive patients. External validation was performed in a prospective independent cohort (n = 29).
RESULTS
ctDNA was detected in 37 of 99 (37%) individuals. In 81 patients who did not receive adjuvant therapy, 90% of patients with ctDNA detected at baseline and 100% of patients with ctDNA detected at the postoperative timepoint relapsed at a median follow up of 20 months. ctDNA detection predicted patients at high risk of relapse at baseline [relapse-free survival (RFS) hazard ratio (HR) 2.9; 95% confidence interval (CI) 1.5-5.6; P = 0.002] and postoperatively (HR 10; 95% CI 4.3-24; P < 0.001). ctDNA detection at baseline [HR 2.9; 95% CI 1.3-5.7; P = 0.003 and postoperatively (HR 11; 95% CI 4.3-27; P < 0.001] was also associated with inferior distant metastasis-free survival (DMFS). These findings were validated in the independent cohort. ctDNA detection remained an independent predictor of RFS and DMFS in multivariate analyses after adjustment for disease stage and BRAF mutation status.
CONCLUSION
Baseline and postoperative ctDNA detection in two independent prospective cohorts identified stage III melanoma patients at highest risk of relapse and has potential to inform adjuvant therapy decisions.

Identifiants

pubmed: 30838379
pii: S0923-7534(19)31155-X
doi: 10.1093/annonc/mdz048
pmc: PMC6551451
pii:
doi:

Substances chimiques

Biomarkers, Tumor 0
Circulating Tumor DNA 0
Membrane Proteins 0
BRAF protein, human EC 2.7.11.1
Proto-Oncogene Proteins B-raf EC 2.7.11.1
GTP Phosphohydrolases EC 3.6.1.-
NRAS protein, human EC 3.6.1.-

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

804-814

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Cancer Research UK
ID : C5759/A20971
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 100282/Z/12/Z
Pays : United Kingdom

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

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Auteurs

L Tan (L)

Peter MacCallum Cancer Centre, Melbourne; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Australia.

S Sandhu (S)

Peter MacCallum Cancer Centre, Melbourne; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Australia.

R J Lee (RJ)

Molecular Oncology Group, Cancer Research UK Manchester Institute, Manchester; Faculty of Biology, Medicine and Health, The University of Manchester, Manchester.

J Li (J)

Peter MacCallum Cancer Centre, Melbourne; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Australia.

J Callahan (J)

Peter MacCallum Cancer Centre, Melbourne.

S Ftouni (S)

Peter MacCallum Cancer Centre, Melbourne.

N Dhomen (N)

Molecular Oncology Group, Cancer Research UK Manchester Institute, Manchester.

P Middlehurst (P)

Molecular Oncology Group, Cancer Research UK Manchester Institute, Manchester.

A Wallace (A)

Genomic Diagnostics Laboratory, Manchester Centre for Genomic Medicine, Manchester, UK.

J Raleigh (J)

Peter MacCallum Cancer Centre, Melbourne.

A Hatzimihalis (A)

Peter MacCallum Cancer Centre, Melbourne.

M A Henderson (MA)

Peter MacCallum Cancer Centre, Melbourne; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Australia.

M Shackleton (M)

The Alfred Hospital, Melbourne.

A Haydon (A)

The Alfred Hospital, Melbourne.

V Mar (V)

The Alfred Hospital, Melbourne.

D E Gyorki (DE)

Peter MacCallum Cancer Centre, Melbourne; Department of Surgery, The University of Melbourne, Melbourne, Australia.

D Oudit (D)

Faculty of Biology, Medicine and Health, The University of Manchester, Manchester; The Christie NHS Foundation Trust, Manchester, UK.

M A Dawson (MA)

Peter MacCallum Cancer Centre, Melbourne; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Australia; Centre for Cancer Research, The University of Melbourne, Melbourne, Australia.

R J Hicks (RJ)

Peter MacCallum Cancer Centre, Melbourne; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Australia.

P Lorigan (P)

Faculty of Biology, Medicine and Health, The University of Manchester, Manchester; The Christie NHS Foundation Trust, Manchester, UK.

G A McArthur (GA)

Peter MacCallum Cancer Centre, Melbourne; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Australia.

R Marais (R)

Molecular Oncology Group, Cancer Research UK Manchester Institute, Manchester; Faculty of Biology, Medicine and Health, The University of Manchester, Manchester.

S Q Wong (SQ)

Peter MacCallum Cancer Centre, Melbourne.

S-J Dawson (SJ)

Peter MacCallum Cancer Centre, Melbourne; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Australia; Centre for Cancer Research, The University of Melbourne, Melbourne, Australia. Electronic address: sarah-jane.dawson@petermac.org.

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Classifications MeSH