Precision medicine for patients with gastro-oesophageal cancer: A subset analysis of the ProfiLER program.

CGH Gastric cancer Molecular alterations, molecular-targeted agents NGS Oesophageal cancer

Journal

Translational oncology
ISSN: 1936-5233
Titre abrégé: Transl Oncol
Pays: United States
ID NLM: 101472619

Informations de publication

Date de publication:
Jan 2022
Historique:
received: 13 09 2021
revised: 24 10 2021
accepted: 04 11 2021
pubmed: 19 11 2021
medline: 19 11 2021
entrez: 18 11 2021
Statut: ppublish

Résumé

Chemotherapy, anti-HER2 and PD-1 antibodies are standard treatments but only a minority of patients derive long-term benefit from these agents. In this report we describe the mutational landscape and outcome of patients with gastroesophageal cancers enroled in the ProfiLER program. Adenocarcinoma (n = 86, 59%), signet-cell (n = 37, 25%) and squamous-cell (n = 21, 14%) were the dominant histology amongst 147 patients. Genomic analyses could be performed for 114 (78%) patients. The most common genomic alterations involved ERBB2 (15%), KRAS (12%), CCND1 (7%), FGFR1-3 (8%), EGFR (5%) and MET (3%), TP53 (51%) and CDKN2A/B (10%). ERBB2, MET and FGFR alterations were found exclusively in the adenocarcinoma and signet-cell subtypes, while CCND1 amplification, TP53 mutations and CDKN2A/B loss were found in both adenocarcinoma and squamous-cell subtypes. Nine patients (8%) received therapy matched to their genomic alteration, with 5 of them achieving disease control. In an exploratory analysis, patients with stage IV disease at diagnosis who had an actionable alteration had longer overall survival compared to those without. Genomic profiling for patients with advanced gastroesophageal cancers allows the identification of actionable alterations in large proportion of patients. Increased accessibility to molecularly matched therapy may improve survival in this disease.

Sections du résumé

BACKGROUND BACKGROUND
Chemotherapy, anti-HER2 and PD-1 antibodies are standard treatments but only a minority of patients derive long-term benefit from these agents.
METHODS METHODS
In this report we describe the mutational landscape and outcome of patients with gastroesophageal cancers enroled in the ProfiLER program.
RESULTS RESULTS
Adenocarcinoma (n = 86, 59%), signet-cell (n = 37, 25%) and squamous-cell (n = 21, 14%) were the dominant histology amongst 147 patients. Genomic analyses could be performed for 114 (78%) patients. The most common genomic alterations involved ERBB2 (15%), KRAS (12%), CCND1 (7%), FGFR1-3 (8%), EGFR (5%) and MET (3%), TP53 (51%) and CDKN2A/B (10%). ERBB2, MET and FGFR alterations were found exclusively in the adenocarcinoma and signet-cell subtypes, while CCND1 amplification, TP53 mutations and CDKN2A/B loss were found in both adenocarcinoma and squamous-cell subtypes. Nine patients (8%) received therapy matched to their genomic alteration, with 5 of them achieving disease control. In an exploratory analysis, patients with stage IV disease at diagnosis who had an actionable alteration had longer overall survival compared to those without.
CONCLUSION CONCLUSIONS
Genomic profiling for patients with advanced gastroesophageal cancers allows the identification of actionable alterations in large proportion of patients. Increased accessibility to molecularly matched therapy may improve survival in this disease.

Identifiants

pubmed: 34794033
pii: S1936-5233(21)00257-6
doi: 10.1016/j.tranon.2021.101266
pmc: PMC8605190
pii:
doi:

Types de publication

Journal Article

Langues

eng

Pagination

101266

Informations de copyright

Copyright © 2021. Published by Elsevier Inc.

Auteurs

Philippe A Cassier (PA)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France. Electronic address: philippe.cassier@lyon.unicancer.fr.

Clémentine Peyramaure (C)

Service d'Oncologie, Centre Hospitalier Universitaire de Limoges, Limoges, France.

Valery Attignon (V)

Département de la Recherche Translationelle et de l'Innovation, Centre Léon Bérard, Lyon, France.

Lauriane Eberst (L)

Institut de Cancérologie de Strasbourg, Strasbourg, France.

Camille Pacaud (C)

Service d'Onco-Hémato Pédiatrie, Hôpital Hautepierre, Centre Hospitalier Universitaire de Strasbourg, Strasbourg, France.

Sandrine Boyault (S)

Département de la Recherche Translationelle et de l'Innovation, Centre Léon Bérard, Lyon, France.

Françoise Desseigne (F)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France.

Mathieu Sarabi (M)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France.

Pierre Guibert (P)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France.

Pauline Rochefort (P)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France.

Nathalie Marques (N)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France.

Michel Rivoire (M)

Département de Chirurgie, Centre Léon Bérard, Lyon, France.

Aurélien Dupré (A)

Département de Chirurgie, Centre Léon Bérard, Lyon, France.

Patrice Peyrat (P)

Département de Chirurgie, Centre Léon Bérard, Lyon, France.

Catherine Terret (C)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France.

Isabelle Ray-Coquard (I)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France; Université Claude Bernard Lyon I, Lyon, France.

Clélia Coutzac (C)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France.

David Pérol (D)

Direction de la Recherche Clinique et de l'Innovation, Centre Léon Bérard, Lyon, France.

Jean-Yves Blay (JY)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France; Université Claude Bernard Lyon I, Lyon, France; Unicancer, Paris, France.

Olivier Trédan (O)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France.

Christelle de la Fouchardière (C)

Département de Cancérologie Médicale, Centre Léon Bérard, 28 rue Laennec, Lyon 69008, France.

Classifications MeSH