Clinical complexity of utilizing FGFR inhibitors in cancer therapeutics

Chandana, Sreenivasa R; Babiker, Hani M.; Mahadevan, Daruka

doi:10.1080/13543784.2020.1838484

Cited by 10 publications

(11 citation statements)

References 103 publications

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“…A number of pan-FGFR (eg, erdafitinib) and selective FGFR1-3 (eg, infigratinib) or FGFR4 (eg, fisogatinib) agents have been tested in clinical trials for cholangiocarcinoma, bladder cancer, and other solid tumors, with several others currently in the pipeline. 154 The dermatologic toxicities for pan-and selective FGFR inhibitors have been recently reviewed, 155 and are listed in Table 1. [156][157][158] Altered calcium-phosphate homeostasis resulting in hyperphosphatemia is a frequent adverse event from FGFR inhibitors and hyperphosphatemia occurs in 45% to 100% of patients treated with pan-FGFR and FGFR1-3 inhibitors.…”

Section: Fgfr Inhibitorsmentioning

confidence: 99%

Diverse landscape of dermatologic toxicities from small‐molecule inhibitor cancer therapy

et al. 2021

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Background: Advances in molecular biology and genetics have contributed to breakthrough treatments directed at specific pathways associated with the development of cancer. Small-molecule inhibitors (Nibs) aimed at a variety of cellular pathways have been efficacious; however, they are associated with significant dermatologic toxicities. Methods: We conducted a comprehensive review of dermatologic toxicities associated with Nibs categorized into the following five groups: (a) mitogen-activated protein kinase; (b) growth factor/multi-tyrosine kinase; (c) cell division/DNA repair; (d) signaling associated with myeloproliferative neoplasms; and (e) other signaling pathways. Prospective phase I, II, or III clinical trials, retrospective literature reviews, systematic reviews/meta-analyses, and case reviews/reports were included for analysis.Results: Dermatologic toxicities reviewed were associated with every class of Nibs and ranged from mild to severe or life-threatening adverse skin reactions.Inflammatory reactions manifesting as maculopapular, papulopustular/acneiform, and eczematous lesions were frequent types of dermatologic toxicities seen with Nibs.Squamous cell carcinoma with keratoacanthoma-like features was associated with a subset of Nibs. Substantial overlap in dermatologic toxicities was found between Nibs.Conclusions: Dermatologic toxicities from Nibs are diverse and may overlap between classes of Nibs. Recognition of the various types of toxicities from Nibs is critical for patient care in the era of "oncodermatology/dermatopathology."

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Section: Fgfr Inhibitorsmentioning

confidence: 99%

Diverse landscape of dermatologic toxicities from small‐molecule inhibitor cancer therapy

et al. 2021

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“…In addition, there are several drugs that have been or are being developed to suppress FGFR/FGF signaling, 36 and some FGFR small molecule inhibitors, such as erdafitinib and pemigatinib, have been approved by the Food and Drug Administration for the treatment of malignant tumors such as urothelial carcinoma and cholangiocarcinoma. 42 At present, FGFR inhibitors for NSCLC are still in clinical trials, but it is already starting to pay off. 43 With regard to the FGFR gene, only when we explore its molecular mechanism and biological effects, can we really develop targeted drugs with high specificity and sensitivity.…”

Section: Discussionmentioning

confidence: 99%

FGFR2-ERC1: A Subtype of FGFR2 Oncogenic Fusion Variant in Lung Adenocarcinoma and the Response to Anlotinib

Hong¹,

Weng²,

Zhou³

et al. 2022

OTT

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Background Fibroblast growth factor receptor (FGFR) fusions in non-small cell lung cancer (NSCLC) are small genomic events. At present, there is no standard treatment strategy for patients with NSCLC carrying an FGFR fusion. Case Presentation We report the case of a 45-year-old female patient who was diagnosed with lung adenocarcinoma and underwent right upper lobectomy and postoperative adjuvant chemotherapy. After 13 months, the patient’s lung lesions progressed. Next-generation sequencing of venous blood and lung tissues confirmed an FGFR2-ERC1 fusion, and she received chemotherapy and immunotherapy. Two months later, the patient’s lung lesions progressed again. Based on the target effect of anlotinib on FGFR, the patient was subsequently treated with anlotinib, and the progression-free survival interval exceeded 8.0 months. Conclusion These findings showed that patients with lung adenocarcinoma carrying an FGFR2-ERC1 fusion gene may benefit from anlotinib. This case provided evidence to support the use of anlotinib in the treatment of NSCLC patients with FGFR fusion gene subtypes.

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“…The FGF/FGFR axis is also a promising therapeutic target in melanoma [ 151 ]. Several small-molecule inhibitors of FGFR receptors and other RTK (such as dovitinib) are available in clinics [ 138 ].…”

Section: Targeting Phenotypic Plasticity: Identifying New Vulnerabili...mentioning

confidence: 99%

Understanding Molecular Mechanisms of Phenotype Switching and Crosstalk with TME to Reveal New Vulnerabilities of Melanoma

Najem

Soumoy

Sabbah

et al. 2022

Cells

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Melanoma cells are notorious for their high plasticity and ability to switch back and forth between various melanoma cell states, enabling the adaptation to sub-optimal conditions and therapeutics. This phenotypic plasticity, which has gained more attention in cancer research, is proposed as a new paradigm for melanoma progression. In this review, we provide a detailed and deep comprehensive recapitulation of the complex spectrum of phenotype switching in melanoma, the key regulator factors, the various and new melanoma states, and corresponding signatures. We also present an extensive description of the role of epigenetic modifications (chromatin remodeling, methylation, and activities of long non-coding RNAs/miRNAs) and metabolic rewiring in the dynamic switch. Furthermore, we elucidate the main role of the crosstalk between the tumor microenvironment (TME) and oxidative stress in the regulation of the phenotype switching. Finally, we discuss in detail several rational therapeutic approaches, such as exploiting phenotype-specific and metabolic vulnerabilities and targeting components and signals of the TME, to improve the response of melanoma patients to treatments.

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Clinical complexity of utilizing FGFR inhibitors in cancer therapeutics

Cited by 10 publications

References 103 publications

Diverse landscape of dermatologic toxicities from small‐molecule inhibitor cancer therapy

Diverse landscape of dermatologic toxicities from small‐molecule inhibitor cancer therapy

FGFR2-ERC1: A Subtype of FGFR2 Oncogenic Fusion Variant in Lung Adenocarcinoma and the Response to Anlotinib

Understanding Molecular Mechanisms of Phenotype Switching and Crosstalk with TME to Reveal New Vulnerabilities of Melanoma

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