Larotrectinib efficacy and safety in adult patients with tropomyosin receptor kinase fusion sarcomas.


Journal

Cancer
ISSN: 1097-0142
Titre abrégé: Cancer
Pays: United States
ID NLM: 0374236

Informations de publication

Date de publication:
01 12 2023
Historique:
revised: 14 04 2023
received: 02 03 2023
accepted: 17 04 2023
medline: 6 11 2023
pubmed: 28 9 2023
entrez: 28 9 2023
Statut: ppublish

Résumé

Larotrectinib, a first-in-class, highly selective tropomyosin receptor kinase (TRK) inhibitor, has demonstrated efficacy in adult and pediatric patients with various solid tumors harboring NTRK gene fusions. This subset analysis focuses on the efficacy and safety of larotrectinib in an expanded cohort of adult patients with TRK fusion sarcomas. Patients (≥18 years old) with sarcomas harboring NTRK gene fusions were identified from three clinical trials. Patients received larotrectinib 100 mg orally twice daily. Response was investigator-assessed per RECIST v1.1. Data cutoff was July 20, 2021. At the data cutoff, 36 adult patients with TRK fusion sarcomas had initiated larotrectinib therapy: two (6%) patients had bone sarcomas, four (11%) had gastrointestinal stromal tumors, and 30 (83%) had soft tissue sarcomas. All patients were evaluable for response and demonstrated an objective response rate of 58% (95% confidence interval, 41-74). Patients responded well to larotrectinib regardless of number of prior lines of therapy. Adverse events (AEs) were mostly grade 1/2. Grade 3 treatment-emergent AEs (TEAEs) occurred in 15 (42%) patients. There were no grade 4 TEAEs. Two grade 5 TEAEs were reported, neither of which were considered related to larotrectinib. Four (11%) patients permanently discontinued treatment due to TEAEs. Larotrectinib demonstrated robust and durable responses, extended survival benefit, and a favorable safety profile in adult patients with TRK fusion sarcomas with longer follow-up. These results continue to demonstrate that testing for NTRK gene fusions should be incorporated into the clinical management of adult patients with various types of sarcomas. Tropomyosin receptor kinase (TRK) fusion proteins result from translocations involving the NTRK gene and cause cancer in a range of tumor types. Larotrectinib is an agent that specifically targets TRK fusion proteins and is approved for the treatment of patients with TRK fusion cancer. This study looked at how well larotrectinib worked in adult patients with sarcomas caused by TRK fusion proteins. Over half of patients had a durable response to larotrectinib, with no unexpected side effects. These results show that larotrectinib is safe and effective in adult patients with TRK fusion sarcomas.

Sections du résumé

BACKGROUND
Larotrectinib, a first-in-class, highly selective tropomyosin receptor kinase (TRK) inhibitor, has demonstrated efficacy in adult and pediatric patients with various solid tumors harboring NTRK gene fusions. This subset analysis focuses on the efficacy and safety of larotrectinib in an expanded cohort of adult patients with TRK fusion sarcomas.
METHODS
Patients (≥18 years old) with sarcomas harboring NTRK gene fusions were identified from three clinical trials. Patients received larotrectinib 100 mg orally twice daily. Response was investigator-assessed per RECIST v1.1. Data cutoff was July 20, 2021.
RESULTS
At the data cutoff, 36 adult patients with TRK fusion sarcomas had initiated larotrectinib therapy: two (6%) patients had bone sarcomas, four (11%) had gastrointestinal stromal tumors, and 30 (83%) had soft tissue sarcomas. All patients were evaluable for response and demonstrated an objective response rate of 58% (95% confidence interval, 41-74). Patients responded well to larotrectinib regardless of number of prior lines of therapy. Adverse events (AEs) were mostly grade 1/2. Grade 3 treatment-emergent AEs (TEAEs) occurred in 15 (42%) patients. There were no grade 4 TEAEs. Two grade 5 TEAEs were reported, neither of which were considered related to larotrectinib. Four (11%) patients permanently discontinued treatment due to TEAEs.
CONCLUSIONS
Larotrectinib demonstrated robust and durable responses, extended survival benefit, and a favorable safety profile in adult patients with TRK fusion sarcomas with longer follow-up. These results continue to demonstrate that testing for NTRK gene fusions should be incorporated into the clinical management of adult patients with various types of sarcomas.
PLAIN LANGUAGE SUMMARY
Tropomyosin receptor kinase (TRK) fusion proteins result from translocations involving the NTRK gene and cause cancer in a range of tumor types. Larotrectinib is an agent that specifically targets TRK fusion proteins and is approved for the treatment of patients with TRK fusion cancer. This study looked at how well larotrectinib worked in adult patients with sarcomas caused by TRK fusion proteins. Over half of patients had a durable response to larotrectinib, with no unexpected side effects. These results show that larotrectinib is safe and effective in adult patients with TRK fusion sarcomas.

Identifiants

pubmed: 37769113
doi: 10.1002/cncr.35036
doi:

Substances chimiques

larotrectinib PF9462I9HX
Tropomyosin 0
Pyrazoles 0
Protein Kinase Inhibitors 0
Oncogene Proteins, Fusion 0
Receptor, trkA EC 2.7.10.1

Banques de données

ClinicalTrials.gov
['NCT02122913', 'NCT02637687', 'NCT02576431']

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

3772-3782

Subventions

Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2023 The Authors. Cancer published by Wiley Periodicals LLC on behalf of American Cancer Society.

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Auteurs

Shivaani Kummar (S)

Stanford Cancer Center, Stanford University, Palo Alto, California, USA.

Lin Shen (L)

Department of Gastrointestinal Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital and Institute, Beijing, China.

David S Hong (DS)

The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Ray McDermott (R)

St. Vincent's University Hospital and Cancer Trials Ireland, Dublin, Ireland.

Vicki L Keedy (VL)

Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Michela Casanova (M)

Paediatric Oncology Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.

George D Demetri (GD)

Dana-Farber Cancer Institute and Ludwig Center at Harvard Medical School, Boston, Massachusetts, USA.

Afshin Dowlati (A)

University Hospitals Ahuja Medical Center, Beachwood, Ohio, USA.

Soledad Gallego Melcón (SG)

Pediatric Oncology and Hematology, Vall d'Hebron Children's Hospital, Barcelona, Spain.

Ulrik N Lassen (UN)

Department of Oncology, Rigshospitalet, Copenhagen, Denmark.

Serge Leyvraz (S)

Charité-Universitätsmedizin Berlin, Berlin, Germany.

Tianshu Liu (T)

Zhongshan Hospital-Fudan University, Shanghai, China.

Victor Moreno (V)

START MADRID-FJD, Hospital Fundación Jiménez Díaz, Madrid, Spain.

Jyoti Patel (J)

Northwestern University, Chicago, Illinois, USA.

Tejas Patil (T)

Department of Medicine, Division of Medical Oncology, University of Colorado, Aurora, Colorado, USA.

Atrayee Basu Mallick (AB)

Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.

Nuno Sousa (N)

Instituto Portugues de Oncologia do Porto Francisco Gentil, Porto, Portugal.

Makoto Tahara (M)

National Cancer Center Hospital East, Kashiwa, Japan.

David S Ziegler (DS)

Sydney Children's Hospital, Randwick, New South Wales, Australia.
Australia and School of Women's and Children's Health, University of New South Wales Sydney, Sydney, New South Wales, Australia.

Ricarda Norenberg (R)

Chrestos Concept GmbH & Co. KG, Essen, Germany.

Pierre Arvis (P)

Bayer Pharmaceuticals, Loos, France.

Nicoletta Brega (N)

Bayer Pharmaceuticals, Milan, Italy.

Alexander Drilon (A)

Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Weill Cornell Medical College, New York, New York, USA.

Daniel S W Tan (DSW)

Division of Medical Oncology, National Cancer Centre Singapore, Duke-NUS Medical School, Singapore, Singapore.

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