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      Response of FGFR-2 Positive Adenoid Cystic Carcinoma to Futibatinib: A Case Report

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          Abstract

          Adenoid cystic carcinoma (ACC) is an uncommon and aggressive head and neck cancer mainly affecting minor salivary glands. It affects more women than men in their 60s and 70s. The tumor is typically locally aggressive and has a high rate of distant metastatic disease. This report unveils a potential avenue for targeted therapy for the management of metastatic disease: a patient with ACC who harbored a specific fibroblast growth factor receptor 2 (FGFR-2) mutation and responded significantly to a novel FGFR-2 inhibitor. This finding could pave the way for personalized treatment options for ACC patients with similar genetic alterations. Nevertheless, the use of futibatinib requires further investigation to optimize treatment protocols, including exploring combination therapies, identifying predictive biomarkers for treatment response, and developing strategies to overcome potential resistance.

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          Fibroblast growth factor receptors as treatment targets in clinical oncology

          Masaru Katoh (2018)
          FGFRs are receptor tyrosine kinases with a role in several biological processes, such as the regulation of development and tissue repair. However, alterations in FGFRs 1-4, such as amplifications, fusions and mutations, as well as aberrant epigenetic or transcriptional regulation and changes in tumour-stromal interactions in the tumour microenvironment, can lead to the development and/or progression of cancer. Similar to other kinase alterations, such alterations are targetable using small molecules or antibodies, and the benefits of FGFR inhibitors have been demonstrated in clinical trials involving subsets of patients with solid tumours harbouring FGFR alterations. However, the response rates in patients with FGFR alterations were relatively low, and responses in patients without detectable FGFR alterations were also observed. In this Review, the author describes the clinical experience with FGFR inhibitors to date, and highlights key aspects that might lead to improved response rates and/or the avoidance of acquired resistance, including the selection of patients who are most likely to benefit from treatment, and the use of FGFR inhibitors in combination regimens with other agents.
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            Futibatinib for FGFR2-Rearranged Intrahepatic Cholangiocarcinoma

            Lipika Goyal, Funda Meric-Bernstam, Antoine Hollebecque … (2023)
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              Truncated FGFR2 is a clinically actionable oncogene in multiple cancers

              Daniel Zingg, Jinhyuk Bhin, Julia Yemelyanenko … (2022)
              Somatic hotspot mutations and structural amplifications and fusions that affect fibroblast growth factor receptor 2 (encoded by FGFR2 ) occur in multiple types of cancer 1 . However, clinical responses to FGFR inhibitors have remained variable 1 – 9 , emphasizing the need to better understand which FGFR2 alterations are oncogenic and therapeutically targetable. Here we apply transposon-based screening 10 , 11 and tumour modelling in mice 12 , 13 , and find that the truncation of exon 18 (E18) of Fgfr2 is a potent driver mutation. Human oncogenomic datasets revealed a diverse set of FGFR2 alterations, including rearrangements, E1–E17 partial amplifications, and E18 nonsense and frameshift mutations, each causing the transcription of E18-truncated FGFR2 ( FGFR2 ΔE18 ). Functional in vitro and in vivo examination of a compendium of FGFR2 ΔE18 and full-length variants pinpointed FGFR2 -E18 truncation as single-driver alteration in cancer. By contrast, the oncogenic competence of FGFR2 full-length amplifications depended on a distinct landscape of cooperating driver genes. This suggests that genomic alterations that generate stable FGFR2 ΔE18 variants are actionable therapeutic targets, which we confirmed in preclinical mouse and human tumour models, and in a clinical trial. We propose that cancers containing any FGFR2 variant with a truncated E18 should be considered for FGFR-targeted therapies. Truncation of exon 18 of FGFR2 ( FGFR2 ΔE18 ) is a potent driver mutation in mice and humans, and FGFR-targeted therapy should be considered for patients with cancer expressing stable FGFR2 ΔE18 variants.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cureus
                Journal ID (iso-abbrev): Cureus
                Journal ID (issn): 2168-8184
                Title: Cureus
                Publisher: Cureus (Palo Alto (CA) )
                ISSN (Electronic): 2168-8184
                Publication date (Electronic, pub): 27 June 2024
                Publication date (Electronic, collection): June 2024
                Volume: 16
                Issue: 6
                Electronic Location Identifier: e63332
                Affiliations
                [1 ] Internal Medicine, Orange Park Medical Center, Orange Park, USA
                [2 ] Internal Medicine, HCA Florida Orange Park Hospital, Orange Park, USA
                [3 ] Hematology and Oncology, Florida Cancer Specialists and Research Institute, Fleming Island, USA
                Author notes
                Yoan E. Rodriguez ryoan66@ 123456yahoo.com
                Article
                DOI: 10.7759/cureus.63332
                PMC ID: 11283924
                PubMed ID: 39077220
                SO-VID: 15d233e3-6e2f-4262-99e2-8722dffcb7f4
                Copyright © Copyright © 2024, Rodriguez et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date accepted : 27 June 2024
                Categories
                Subject: Internal Medicine
                Subject: Oncology
                Subject: Therapeutics

                Keywords: salivary gland tumor,futibatinib,fibroblast growth factor inhibitor,fibroblast growth factor receptor (fgfr),adenoid cystic carcinoma (acc)
                Data availability:
                Keywords: salivary gland tumor, futibatinib, fibroblast growth factor inhibitor, fibroblast growth factor receptor (fgfr), adenoid cystic carcinoma (acc)

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