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Related Experiment Video

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Development of a Human Preclinical Model of Osteoclastogenesis from Peripheral Blood Monocytes Co-cultured with Breast Cancer Cell Lines

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Tumour-induced osteomalacia.

Salvatore Minisola¹, Munro Peacock², Seijii Fukumoto³

¹Department of Internal Medicine and Medical Disciplines, Sapienza University of Rome, Viale del Policlinico 155, 00161 Rome, Italy.

Nature Reviews. Disease Primers

|July 14, 2017

Summary

Tumour-induced osteomalacia (TIO) is a rare disorder caused by tumours secreting FGF23, leading to phosphate deficiency and bone issues. Identifying the small tumour and targeted therapies are key challenges.

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Area of Science:

Endocrinology
Oncology
Metabolic Bone Disease

Background:

Tumour-induced osteomalacia (TIO) is a rare paraneoplastic syndrome driven by fibroblast growth factor 23 (FGF23) secretion from tumours.
FGF23 dysregulation impacts renal phosphate handling and vitamin D metabolism, causing hypophosphatemia and osteomalacia.
Diagnosis relies on low serum phosphate with bone pain, fractures, and muscle weakness, often complicated by tumour localization difficulties.

Purpose of the Study:

To summarize the pathophysiology, diagnosis, and treatment of TIO.
To highlight emerging therapeutic strategies, including KRN23 and targeted therapies.
To discuss the significance of novel molecular drivers like FGFR1 fusions in TIO.

Main Methods:

Review of existing literature on TIO.
Analysis of the role of FGF23 in mineral metabolism.
Discussion of diagnostic criteria and imaging challenges.
Evaluation of current and novel treatment modalities.

Main Results:

TIO is characterized by hypophosphatemia and osteomalacia due to excess FGF23.
Surgical tumor resection is curative; medical management with phosphate and vitamin D is an alternative.
Anti-FGF23 antibody KRN23 shows promise for unresectable tumors.
FGFR1 fusions represent a key molecular driver in some TIO cases, offering therapeutic targets.

Conclusions:

Accurate diagnosis and localization of the causative tumor are critical for TIO management.
Targeted therapies, including KRN23 and potentially FGFR1-directed treatments, offer new hope.
Further research into the FGFR1 pathway may elucidate TIO pathogenesis and treatment strategies.