Refining the selection of patients with metastatic colorectal cancer for treatment with temozolomide using proteomic analysis of O6-methylguanine-DNA-methyltransferase.


Journal

European journal of cancer (Oxford, England : 1990)
ISSN: 1879-0852
Titre abrégé: Eur J Cancer
Pays: England
ID NLM: 9005373

Informations de publication

Date de publication:
01 2019
Historique:
received: 29 08 2018
revised: 08 11 2018
accepted: 11 11 2018
pubmed: 24 12 2018
medline: 6 5 2020
entrez: 23 12 2018
Statut: ppublish

Résumé

The repair enzyme O6-methylguanine-DNA-methyltransferase (MGMT) is a validated predictor of benefit from temozolomide (TMZ) in glioblastoma. However, only 10% of patients with MGMT-methylated metastatic colorectal cancer (mCRC) respond to TMZ. Archived tumour samples (N = 41) from three phase II TMZ trials carried out in MGMT-methylated mCRC (assessed by methylation-specific polymerase chain reaction [PCR]) were stratified by MGMT status as assessed by three different methods: mass spectrometry, PCR/methyl-BEAMing and RNA-seq. The performance of each method was assessed in relation to overall response rate, progression-free survival (PFS) and overall survival (OS). Overall, 9 of 41 patients responded to TMZ. Overall response rates were 50% (9/18), 50% (6/12) and 35% (8/23) among patients determined likely to respond to TMZ by mass spectrometry, methyl-BEAMing and RNA-seq, respectively. Low/negative MGMT protein expressors by mass spectrometry had longer PFS than high MGMT expressors (3.7 vs 1.8 months; HR = 0.50, P = 0.014). Results for OS were similar but statistically non-significant (8.7 vs. 7.4 months; HR = 0.55, P = 0.077). No significant association between survival and MGMT status by methyl-BEAMing or RNA-seq could be demonstrated as comparable subgroups survival could not be confirmed/excluded. Specifically, the association of high versus low methyl-BEAMing MGMT hypermethylation with survival was HR = 0.783, P = 0.46 for PFS and 0.591, P = 0.126 for OS, while association of low versus high RNA-seq MGMT level with survival was HR = 0.697, P = 0.159 for PFS and HR = 0.697, P = 0.266 for OS. Quantitative proteomic analysis of MGMT may be useful for refining the selection of patients eligible for salvage treatment with single-agent TMZ.

Sections du résumé

BACKGROUND
The repair enzyme O6-methylguanine-DNA-methyltransferase (MGMT) is a validated predictor of benefit from temozolomide (TMZ) in glioblastoma. However, only 10% of patients with MGMT-methylated metastatic colorectal cancer (mCRC) respond to TMZ.
METHODS
Archived tumour samples (N = 41) from three phase II TMZ trials carried out in MGMT-methylated mCRC (assessed by methylation-specific polymerase chain reaction [PCR]) were stratified by MGMT status as assessed by three different methods: mass spectrometry, PCR/methyl-BEAMing and RNA-seq. The performance of each method was assessed in relation to overall response rate, progression-free survival (PFS) and overall survival (OS).
RESULTS
Overall, 9 of 41 patients responded to TMZ. Overall response rates were 50% (9/18), 50% (6/12) and 35% (8/23) among patients determined likely to respond to TMZ by mass spectrometry, methyl-BEAMing and RNA-seq, respectively. Low/negative MGMT protein expressors by mass spectrometry had longer PFS than high MGMT expressors (3.7 vs 1.8 months; HR = 0.50, P = 0.014). Results for OS were similar but statistically non-significant (8.7 vs. 7.4 months; HR = 0.55, P = 0.077). No significant association between survival and MGMT status by methyl-BEAMing or RNA-seq could be demonstrated as comparable subgroups survival could not be confirmed/excluded. Specifically, the association of high versus low methyl-BEAMing MGMT hypermethylation with survival was HR = 0.783, P = 0.46 for PFS and 0.591, P = 0.126 for OS, while association of low versus high RNA-seq MGMT level with survival was HR = 0.697, P = 0.159 for PFS and HR = 0.697, P = 0.266 for OS.
CONCLUSIONS
Quantitative proteomic analysis of MGMT may be useful for refining the selection of patients eligible for salvage treatment with single-agent TMZ.

Identifiants

pubmed: 30579113
pii: S0959-8049(18)31514-4
doi: 10.1016/j.ejca.2018.11.016
pii:
doi:

Substances chimiques

Antineoplastic Agents, Alkylating 0
Biomarkers, Tumor 0
Proteome 0
Tumor Suppressor Proteins 0
DNA Modification Methylases EC 2.1.1.-
MGMT protein, human EC 2.1.1.63
DNA Repair Enzymes EC 6.5.1.-
Temozolomide YF1K15M17Y

Types de publication

Clinical Trial, Phase II Journal Article Multicenter Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

164-174

Informations de copyright

Copyright © 2018 Elsevier Ltd. All rights reserved.

Auteurs

Sarit Schwartz (S)

NantOmics, LLC, Rockville, MD, USA.

Chris Szeto (C)

NantOmics, LLC, Santa Cruz, CA, USA.

Yuan Tian (Y)

NantOmics, LLC, Rockville, MD, USA.

Fabiola Cecchi (F)

NantOmics, LLC, Rockville, MD, USA.

Salvatore Corallo (S)

Medical Oncology Department, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Maria Alessandra Calegari (MA)

Medical Oncology Unit, Fondazione Policlinico Universitario Agostino Gemelli, Rome, Italy.

Maria Di Bartolomeo (M)

Medical Oncology Department, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Federica Morano (F)

Medical Oncology Department, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Alessandra Raimondi (A)

Medical Oncology Department, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Giovanni Fucà (G)

Medical Oncology Department, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Antonia Martinetti (A)

Medical Oncology Department, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Ivana De Pascalis (I)

Institute of Pathology, Università Cattolica Del Sacro Cuore, Rome, Italy.

Maurizio Martini (M)

Institute of Pathology, Università Cattolica Del Sacro Cuore, Rome, Italy.

Antonino Belfiore (A)

Department of Pathology and Laboratory Medicine, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Massimo Milione (M)

Department of Pathology and Laboratory Medicine, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Armando Orlandi (A)

Medical Oncology Unit, Fondazione Policlinico Universitario Agostino Gemelli, Rome, Italy.

Ludovic Barault (L)

Department of Oncology, Candiolo Cancer Institute IRCC, University of Turin, Candiolo, Turin, Italy; Candiolo Cancer Institute, FPO-IRCCS, Candiolo, Turin, Italy.

Carlo Barone (C)

Medical Oncology Unit, Fondazione Policlinico Universitario Agostino Gemelli, Rome, Italy.

Filippo de Braud (F)

Medical Oncology Department, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy; Department of Oncology and Hemato-oncology, University of Milan, Milan, Italy.

Federica Di Nicolantonio (F)

Department of Oncology, Candiolo Cancer Institute IRCC, University of Turin, Candiolo, Turin, Italy; Candiolo Cancer Institute, FPO-IRCCS, Candiolo, Turin, Italy.

Steve Benz (S)

NantOmics, LLC, Santa Cruz, CA, USA.

Todd Hembrough (T)

NantOmics, LLC, Rockville, MD, USA. Electronic address: Todd.Hembrough@nantomics.com.

Filippo Pietrantonio (F)

Medical Oncology Department, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy; Department of Oncology and Hemato-oncology, University of Milan, Milan, Italy. Electronic address: filippo.pietrantonio@istitutotumori.mi.it.

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