Clinical Outcomes After Progression on First-Line Therapies in IDH1 Mutated Versus Wild-Type Intrahepatic Cholangiocarcinoma Patients.


Journal

Targeted oncology
ISSN: 1776-260X
Titre abrégé: Target Oncol
Pays: France
ID NLM: 101270595

Informations de publication

Date de publication:
01 2023
Historique:
accepted: 04 11 2022
pubmed: 24 1 2023
medline: 17 2 2023
entrez: 23 1 2023
Statut: ppublish

Résumé

Isocitrate dehydrogenase-1 (IDH1) mutations occur in a significant proportion of intrahepatic cholangiocarcinomas (iCCAs). No data are available regarding the prognostic impact of IDH1 mutations in advanced iCCA patients after progression on first-line therapies. We investigated the role of IDH1 mutation in advanced iCCA after progression on first-line therapies. After progression on first-line therapies for advanced iCCA, consecutive patients were retrospectively collected. The IDH1 status was tested at baseline. This analysis aimed to examine the association between the presence of IDH1 missense mutations and survival outcomes in patients with advanced iCCA treated with a second-line therapy. The analysis included 119 patients; 56/119 (47%) were IDH1 mutated (IDH1m) and 63/119 (53%) were IDH1 wild type (IDH1 WT). At univariate analysis for overall survival (OS), the presence of IDH1 mutation was associated with a worse median OS (mOS; 8.2 vs. 14.1 months; hazard ratio [HR] 1.9, 95% confidence interval [CI] 1.2-3.0, p = 0.0047). Patients harboring IDH1 mutations showed a worse objective response rate (ORR) compared with patients without IDH1 mutation, whereas no significant differences in disease control rate (DCR) were found. Multivariate analysis confirmed IDH1 mutations as an independent negative prognostic factor for OS (HR 1.7, 95% CI 1.1-2.7, p = 0.0256). By evaluating only patients receiving FOLFOX as second-line therapy, no statistically significant differences were found in terms of both OS and PFS between IDH1m and IDH1 WT patients. In this subset of patients, those harboring an IDH1 mutation showed a worse ORR and DCR compared with those without. Finally, at univariate analysis for OS from third-line treatment, the presence of an IDH1 mutation was associated with a trend toward a worse mOS (6.0 vs. 11.9 months; HR 1.6, 95% CI 0.8-3.2, p = 0.25). The present analysis constitutes the first evidence of a negative prognostic impact of IDH1 mutations in a cohort of patients treated after progression on first-line therapies in contrast to IDH1 inhibitors.

Sections du résumé

BACKGROUND
Isocitrate dehydrogenase-1 (IDH1) mutations occur in a significant proportion of intrahepatic cholangiocarcinomas (iCCAs). No data are available regarding the prognostic impact of IDH1 mutations in advanced iCCA patients after progression on first-line therapies.
OBJECTIVE
We investigated the role of IDH1 mutation in advanced iCCA after progression on first-line therapies.
PATIENTS AND METHODS
After progression on first-line therapies for advanced iCCA, consecutive patients were retrospectively collected. The IDH1 status was tested at baseline. This analysis aimed to examine the association between the presence of IDH1 missense mutations and survival outcomes in patients with advanced iCCA treated with a second-line therapy.
RESULTS
The analysis included 119 patients; 56/119 (47%) were IDH1 mutated (IDH1m) and 63/119 (53%) were IDH1 wild type (IDH1 WT). At univariate analysis for overall survival (OS), the presence of IDH1 mutation was associated with a worse median OS (mOS; 8.2 vs. 14.1 months; hazard ratio [HR] 1.9, 95% confidence interval [CI] 1.2-3.0, p = 0.0047). Patients harboring IDH1 mutations showed a worse objective response rate (ORR) compared with patients without IDH1 mutation, whereas no significant differences in disease control rate (DCR) were found. Multivariate analysis confirmed IDH1 mutations as an independent negative prognostic factor for OS (HR 1.7, 95% CI 1.1-2.7, p = 0.0256). By evaluating only patients receiving FOLFOX as second-line therapy, no statistically significant differences were found in terms of both OS and PFS between IDH1m and IDH1 WT patients. In this subset of patients, those harboring an IDH1 mutation showed a worse ORR and DCR compared with those without. Finally, at univariate analysis for OS from third-line treatment, the presence of an IDH1 mutation was associated with a trend toward a worse mOS (6.0 vs. 11.9 months; HR 1.6, 95% CI 0.8-3.2, p = 0.25).
CONCLUSION
The present analysis constitutes the first evidence of a negative prognostic impact of IDH1 mutations in a cohort of patients treated after progression on first-line therapies in contrast to IDH1 inhibitors.

Identifiants

pubmed: 36689074
doi: 10.1007/s11523-022-00933-7
pii: 10.1007/s11523-022-00933-7
doi:

Substances chimiques

Isocitrate Dehydrogenase EC 1.1.1.41
IDH1 protein, human EC 1.1.1.42.

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

139-145

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.

Références

Rimini M, Puzzoni M, Pedica F, Silvestris N, Fornaro L, Aprile G, et al. Cholangiocarcinoma: new perspectives for new horizons. Expert Rev Gastroenterol Hepatol. 2021;15(12):1367–83.
pubmed: 34669536
Sia D, Villanueva A, Friedman SL, Llovet JM. Liver cancer cell of origin, molecular class, and effects on patient prognosis. Gastroenterology. 2017;152:745–61.
pubmed: 28043904
Howlader N, Noone AM, Krapcho M, et al. (eds). SEER Cancer Statistics Review, 1975–2013, National Cancer Institute. Bethesda, MD. Based on November 2015 SEER Data Submission, Posted to the SEER Web Site; April 2016. http://seer.cancer.gov/csr/1975_2013/ . Accessed 10 Dec 2016.
Lowery MA, Ptashkin R, Jordan E, Berger MF, Zehir A, Capanu M, et al. Comprehensive molecular profiling of intra-hepatic and extrahepatic cholangiocarcinomas: potential targets for intervention. Clin Cancer Res. 2018;24:4154–61. Acessed Nov 2 2022
pubmed: 29848569 pmcid: 6642361
Nakamura H, Arai Y, Totoki Y, Shirota T, Elzawahry A, Kato M, et al. Genomic spectra of biliary tract cancer. Nat Genet. 2015;47(9):1003–10.
pubmed: 26258846
Simbolo M, Fassan M, Ruzzenente A, Mafficini A, Wood LD, Corbo V, et al. Multigene mutational profiling of cholangiocarcinomas identifies actionable molecular subgroups. Oncotarget. 2014;5:2839–52.
pubmed: 24867389 pmcid: 4058049
Boerner T, Drill E, Pak LM, Nguyen B, Sigel CS, Doussot A, et al. Genetic determinants of outcome in intrahepatic cholangiocarcinoma. Hepatology. 2021;74(3):1429–44.
pubmed: 33765338
Rimini M, Macarulla T, Burgio V, Lonardi S, Niger M, Scartozzi M, et al. Gene mutational profile of BRCAness and clinical implication in predicting response to platinum-based chemotherapy in patients with intrahepatic cholangiocarcinoma. Eur J Cancer. 2022;171:232–41.
pubmed: 35749808
Rimini M, Loi E, Fabregat-Franco C, Burgio V, Lonardi S, Niger M, et al. Next-generation sequencing analysis of cholangiocarcinoma identifies distinct IDH1-mutated clusters. Eur J Cancer. 2022;175:299–310.
pubmed: 36182816
Boscoe AN, Rolland C, Kelley RK. Frequency and prognostic significance of isocitrate dehydrogenase 1 mutations in cholangiocarcinoma: a systematic literature review. J Gastrointest Oncol. 2019;10:751–65.
pubmed: 31392056 pmcid: 6657309
Abou-Alfa GK, Macarulla T, Javle MM, Kelley RK, Lubner SJ, Adeva J, et al. Ivosidenib in IDH1-mutant, chemotherapy-refractory cholangiocarcinoma (ClarIDHy): a multicentre, randomised, double-blind, placebo-controlled, phase 3 study. Lancet Oncol. 2020;21(6):796–807.
pubmed: 32416072 pmcid: 7523268
Rimini M, Burgio V, Antonuzzo L, Rimassa L, Oneda E, Lavacchi D, et al. Real-world data on ivosidenib in patients with previously treated isocitrate dehydrogenase 1-mutated intrahepatic cholangiocarcinomas: an early exploratory analysis. Target Oncol. 2022;17(5):591–6.
pubmed: 36114954
Niger M, Nichetti F, Casadei-Gardini A, Rizzato MD, Pircher C, Bini M, et al. Platinum sensitivity in patients with IDH1/2 mutated vs wild-type intrahepatic cholangiocarcinoma: a propensity score-based study. Int J Cancer. 2022;151(8):1310–20.
pubmed: 35723131
Lamarca A, Palmer DH, Wasan HS, Ross PJ, Ma YT, Arora A, et al. Advanced Biliary Cancer Working Group. Second-line FOLFOX chemotherapy versus active symptom control for advanced biliary tract cancer (ABC-06): a phase 3, open-label, randomised, controlled trial. Lancet Oncol. 2021;22(5):690–701.
pubmed: 33798493 pmcid: 8082275
Goyal L, Govindan A, Sheth RA, Nardi V, Blaszkowsky LS, Faris J, et al. Prognosis and clinicopathologic features of patients with advanced stage isocitrate dehydrogenase (IDH) mutant and IDH wild-type intrahepatic cholangiocarcinoma. Oncologist. 2015;20:1019–27.
pubmed: 26245674 pmcid: 4571807
Jiao Y, Pawlik TM, Anders RA, Selaru FM, Streppel MM, Lucas DJ, et al. Exome sequencing identifies frequent inactivating mutations in BAP1, ARID1A and PBRM1 in intrahepatic cholangiocarcinomas. Nat Genet. 2013;45:1470–3.
pubmed: 24185509 pmcid: 4013720
Wang P, Dong Q, Zhang C, Kuan PF, Liu Y, Jeck WR, et al. Mutations in isocitrate dehydrogenase 1 and 2 occur frequently in intrahepatic cholangiocarcinomas and share hypermethylation targets with glioblastomas. Oncogene. 2013;32(25):3091–100.
pubmed: 22824796
Ma B, Meng H, Tian Y, Wang Y, Song T, Zhang T, et al. Distinct clinical and prognostic implication of IDH1/2 mutation and other most frequent mutations in large duct and small duct subtypes of intrahepatic cholangiocarcinoma. BMC Cancer. 2020;20(1):318.
pubmed: 32293336 pmcid: 7161164
Wintheiser G, Zemla T, Shi Q, Tran N, Prasai K, Tella SH, et al. Isocitrate dehydrogenase-mutated cholangiocarcinoma: natural history and clinical outcomes. JCO Precis Oncol. 2022;6: e2100156.
pubmed: 35005992

Auteurs

Margherita Rimini (M)

IRCCS San Raffaele Scientific Institute Hospital, Department of Oncology, Vita-Salute San Raffaele University, Milan, Italy. margherita.rimini@gmail.com.

Carles Fabregat-Franco (C)

Gastrointestinal Cancer Unit, Vall d'Hebron University Hospital & Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain.

Mara Persano (M)

Medical Oncology, University and University Hospital, Cagliari, Italy.

Valentina Burgio (V)

IRCCS San Raffaele Scientific Institute Hospital, Department of Oncology, Vita-Salute San Raffaele University, Milan, Italy.

Francesca Bergamo (F)

Oncology Unit 1, Veneto Institute of Oncology - IRCCS, Padua, Italy.

Monica Niger (M)

Medical Oncology Department, Fondazione IRCCS Istituto Nazionale dei Tumori di Milano, Milan, Italy.

Mario Scartozzi (M)

Medical Oncology, University and University Hospital, Cagliari, Italy.

Ilario Giovanni Rapposelli (IG)

Department of Medical Oncology, IRCCS Istituto Romagnolo per lo Studio dei Tumori (IRST) "Dino Amadori", 47014, Meldola, Italy.

Giuseppe Aprile (G)

Department of Oncology, San Bortolo General Hospital, Azienda ULSS8 Berica, Vicenza, Italy.

Francesca Ratti (F)

Hepatobiliary Surgery Division, Liver Center, Vita-Salute San Raffaele University, IRCCS San Raffaele Scientific Institute, 20132, Milan, Italy.

Federica Pedica (F)

Department of Experimental Oncology, Pathology Unit, IRCCS San Raffaele Scientific Institute, 20132, Milan, Italy.

Helena Verdaguer (H)

Gastrointestinal Cancer Unit, Vall d'Hebron University Hospital & Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain.

Mario Rizzato (M)

Oncology Unit 1, Veneto Institute of Oncology - IRCCS, Padua, Italy.

Federico Nichetti (F)

Medical Oncology Department, Fondazione IRCCS Istituto Nazionale dei Tumori di Milano, Milan, Italy.

Eleonora Lai (E)

Medical Oncology, University and University Hospital, Cagliari, Italy.

Alessandro Cappetta (A)

Department of Oncology, San Bortolo General Hospital, Azienda ULSS8 Berica, Vicenza, Italy.

Teresa Macarulla (T)

Gastrointestinal Cancer Unit, Vall d'Hebron University Hospital & Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain.

Matteo Fassan (M)

Oncology Unit 1, Veneto Institute of Oncology - IRCCS, Padua, Italy.

Filippo De Braud (F)

Medical Oncology Department, Fondazione IRCCS Istituto Nazionale dei Tumori di Milano, Milan, Italy.

Andrea Pretta (A)

Medical Oncology, University and University Hospital, Cagliari, Italy.

Francesca Simionato (F)

Department of Oncology, San Bortolo General Hospital, Azienda ULSS8 Berica, Vicenza, Italy.

Francesco De Cobelli (F)

School of Medicine, Vita-Salute San Raffaele University, 20132, Milan, Italy.

Luca Aldrighetti (L)

Hepatobiliary Surgery Division, Liver Center, Vita-Salute San Raffaele University, IRCCS San Raffaele Scientific Institute, 20132, Milan, Italy.

Lorenzo Fornaro (L)

Medical oncology, University Hospital of Pisa, Pisa, Italy.

Stefano Cascinu (S)

School of Medicine, Vita-Salute San Raffaele University, 20132, Milan, Italy.

Andrea Casadei-Gardini (A)

School of Medicine, Vita-Salute San Raffaele University, 20132, Milan, Italy.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH