Treatment outcome with a selective RET tyrosine kinase inhibitor selpercatinib in children with multiple endocrine neoplasia type 2 and advanced medullary thyroid carcinoma.

Children Medullary thyroid carcinoma Multiple endocrine neoplasia type 2 Paediatric RET proto-oncogene Selpercatinib Tyrosine kinase inhibitor

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:
11 Oct 2021
Historique:
received: 04 07 2021
revised: 03 09 2021
accepted: 11 09 2021
pubmed: 15 10 2021
medline: 15 10 2021
entrez: 14 10 2021
Statut: aheadofprint

Résumé

Medullary thyroid carcinoma (MTC) in the context of multiple endocrine neoplasia type 2 (MEN2) is caused by mutations in the RET proto-oncogene. Therefore, in children with MEN2 and advanced MTC, the RET tyrosine kinase (TK) pathway is a target for treatment with selpercatinib, a selective RET TK inhibitor. A retrospective review of the clinical, genetic, biochemical (calcitonin and carcinoembryonic antigen [CEA]) and imaging data of six medically untreated children with MEN2 and recurrent and or progressive MTC. The main parameters were safety and objective treatment response to selpercatinib. Six children (three males and three females, aged 3-12 years), four with MEN2B and two MEN2A, are reported. All had initial total thyroidectomy and extensive neck dissections but subsequently developed recurrent and progressive disease. All experienced an improvement in clinical symptoms with a concomitant biochemical response evidenced by significant fall in serum calcitonin and CEA concentrations. The fall in serum calcitonin was evident within 2 weeks of the start of selpercatinib, and responses were ongoing at a median follow-up of 13 months (range, 11-22 months). Four children with measurable radiological disease had good volume reduction. The most common adverse effects were transient but reversible grade 1 or 2 increase in alanine aminotransferase, serum bilirubin and constipation. No child required a dose modification or had to discontinue selpercatinib because of a drug-related adverse event. Selpercatinib has shown excellent therapeutic efficacy with minimal toxicity in children with MEN2 and progressive metastatic RET-mutated MTC.

Sections du résumé

BACKGROUND BACKGROUND
Medullary thyroid carcinoma (MTC) in the context of multiple endocrine neoplasia type 2 (MEN2) is caused by mutations in the RET proto-oncogene. Therefore, in children with MEN2 and advanced MTC, the RET tyrosine kinase (TK) pathway is a target for treatment with selpercatinib, a selective RET TK inhibitor.
PATIENTS AND METHODS METHODS
A retrospective review of the clinical, genetic, biochemical (calcitonin and carcinoembryonic antigen [CEA]) and imaging data of six medically untreated children with MEN2 and recurrent and or progressive MTC. The main parameters were safety and objective treatment response to selpercatinib.
RESULTS RESULTS
Six children (three males and three females, aged 3-12 years), four with MEN2B and two MEN2A, are reported. All had initial total thyroidectomy and extensive neck dissections but subsequently developed recurrent and progressive disease. All experienced an improvement in clinical symptoms with a concomitant biochemical response evidenced by significant fall in serum calcitonin and CEA concentrations. The fall in serum calcitonin was evident within 2 weeks of the start of selpercatinib, and responses were ongoing at a median follow-up of 13 months (range, 11-22 months). Four children with measurable radiological disease had good volume reduction. The most common adverse effects were transient but reversible grade 1 or 2 increase in alanine aminotransferase, serum bilirubin and constipation. No child required a dose modification or had to discontinue selpercatinib because of a drug-related adverse event.
CONCLUSION CONCLUSIONS
Selpercatinib has shown excellent therapeutic efficacy with minimal toxicity in children with MEN2 and progressive metastatic RET-mutated MTC.

Identifiants

pubmed: 34649088
pii: S0959-8049(21)00607-9
doi: 10.1016/j.ejca.2021.09.012
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

38-46

Informations de copyright

Copyright © 2021 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest statement The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Ananth Shankar (A)

Children and Young People's Cancer Services, University College London Hospitals NHS Foundation Trust, London, UK. Electronic address: ananth.shankar@nhs.net.

Tom Kurzawinski (T)

Department of Endocrine Surgery, University College London Hospitals NHS Foundation Trust, London, UK.

Emma Ross (E)

Department of Paediatric Oncology, University Hospitals of Leicester NHS Trust, Leicester, UK.

Sara Stoneham (S)

Children and Young People's Cancer Services, University College London Hospitals NHS Foundation Trust, London, UK.

Tim Beale (T)

Department of Head and Neck Radiology, University College London Hospitals NHS Foundation Trust, London, UK.

Ian Proctor (I)

Department of Cellular Pathology, University College London Hospitals NHS Foundation Trust, London, UK.

Tony Hulse (T)

Department of Paediatric Endocrinology, Guy's and St Thomas' NHS Foundation Trust, London, UK.

Kate Simpson (K)

Department of Pharmacy, University College London Hospitals NHS Foundation Trust, London, UK.

Mark N Gaze (MN)

Department of Oncology, University College London Hospitals NHS Foundation Trust, National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK.

Elene Cattaneo (E)

Children's and Adolescent Services, East Suffolk and North Essex NHS Foundation Trust, Colchester, UK.

Evelien Gevers (E)

Centre for Endocrinology, William Harvey Research Institute, Queen Mary University of London and Department of Paediatric Endocrinology, Barts Health NHS Trust, London, UK.

Lynley Marshall (L)

Department of Paediatric and Adolescent Oncology, The Royal Marsden NHS Foundation Trust, Sutton and The Institute of Cancer Research, London, UK.

Johnathan G Hubbard (JG)

Department of Surgery, Guys & St Thomas' NHS Foundation Trust, London, UK.

Caroline Brain (C)

Department of Paediatric Endocrinology, Great Ormond Street Hospital for Children NHS Foundation Trust, London, UK.

Classifications MeSH