Evidence map›Paper›PMID 29446010›Full record

ReviewJournal of endocrinological investigation2018

Phosphaturic mesenchymal tumors: what an endocrinologist should know.

J M Boland, P J Tebben, A L Folpe

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of endocrinological investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 3 pooled it
4.8field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 3 syntheses or guidelines pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  10. Emerging concepts on the FGF23 regulation and activity.Molecular and cellular biochemistry · 2025
    Review
  11. Review
  12. The Intricacies of Renal Phosphate Reabsorption-An Overview.International journal of molecular sciences · 2024
    Review
  13. Article
  14. Article
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  16. Article
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  18. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

J M BolandDivision of Anatomic Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 1st Street SW, Rochester, MN, 55905, USA.
P J TebbenDivision of Pediatric Endocrinology, Mayo Clinic, Rochester, MN, USA.
A L FolpeDivision of Anatomic Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 1st Street SW, Rochester, MN, 55905, USA. Folpe.Andrew@Mayo.edu.
Mayo Clinic · USMayo Clinic in Arizona · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-induced osteomalacia (TIO), also known as "oncogenic osteomalacia", is a rare cause of osteomalacia. TIO often has an insidious onset characterized clinically by progressive muscle weakness and bone pain with fractures. The hallmark biochemical finding is a persistent low serum phosphorus concentration due to renal phosphate wasting. The vast majority of cases of TIO result from production of the phosphaturic hormone fibroblast growth factor 23 (FGF23) by a histologically distinctive mesenchymal tumor, termed "phosphaturic mesenchymal tumor" (PMT). Circulating FGF23 induces internalization of renal sodium/phosphate co-transporters resulting in reduced proximal tubular phosphate reabsorption. FGF23 also inhibits production of 1α,25-dihydroxyvitamin D which is inappropriately low or normal in the context of hypophosphatemia. Diagnosis is often delayed owing to the rarity of the condition and an underappreciation for the role of phosphorus as a cause for the constellation of symptoms. Primary treatment for TIO is identification of the offending tumor and surgical removal. However, these tumors are notoriously difficult to find, precluding the opportunity for a curative surgery in many. In such cases, phosphate and calcitriol therapy is used to improve symptoms and heal the osteomalacia. Recently, molecular genetic studies have shown recurrent genetic events in PMT, including the novel fusions FN1-FGFR1 and less commonly FN1-FGF1. These fusion events are hypothesized to result in autocrine/paracrine signaling loops within the tumor, spurring tumorigenesis. This review will cover the clinical features, imaging characteristics, pathologic features, molecular genetic aspects, and therapy of PMT, with a brief discussion of other neoplasms that may cause TIO.

Indexed as

EndocrinologistsPhysician's RoleCalcitriolFibroblast Growth Factor-23Fibroblast Growth FactorsHumansNeoplasms, Connective TissueOsteomalaciaParaneoplastic SyndromesPhosphatesPhosphorusCalcitriolFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsPhosphatesPhosphorusHyperphosphaturiaHypophosphatemiaPhosphaturic mesenchymal tumorRicketsTumor-induced osteomalacia

Identifiers

PMID29446010
OpenAlexW2792883808

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.