Evidence map›Paper›PMID 26465941›Full record

ArticlePloS one2015

Fibroblast Growth Factor (FGF-2) and Its Receptors FGFR-2 and FGFR-3 May Be Putative Biomarkers of Malignant Transformation of Potentially Malignant Oral Lesions into Oral Squamous Cell Carcinoma.

Seema Nayak, Madhu Mati Goel, Annu Makker, Vikram Bhatia, Saumya Chandra, Sandeep Kumar, S P Agarwal

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 3 pooled it
2.6field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 3 syntheses or guidelines pooled it, 76 citations in OpenAlex.

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  5. Fibroblast growth factor receptor signaling in head and neck tumors: molecular pathogenesis and potential therapeutic targets.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

7 authors at 1 institution in 1 country.

Seema NayakDepartment of Pathology, King George's Medical University, Lucknow, U.P. - 226003, India.
Madhu Mati GoelDepartment of Pathology, King George's Medical University, Lucknow, U.P. - 226003, India.
Annu MakkerDepartment of Pathology, King George's Medical University, Lucknow, U.P. - 226003, India.
Vikram BhatiaDepartment of Pathology, King George's Medical University, Lucknow, U.P. - 226003, India.
Saumya ChandraDepartment of Pathology, King George's Medical University, Lucknow, U.P. - 226003, India.
Sandeep KumarAll India Institute of Medical Sciences Bhopal, M.P. - 462026, India.
S P AgarwalDepartment of Otorhinolaryngology, King George's Medical University Lucknow, U.P. - 226003, India.
King George's Medical University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There are several factors like angiogenesis, lymphangiogenesis, genetic alterations, mutational factors that are involved in malignant transformation of potentially malignant oral lesions (PMOLs) to oral squamous cell carcinoma (OSCC). Fibroblast growth factor-2 (FGF-2) is one of the prototypes of the large family of growth factors that bind heparin. FGF-2 induces angiogenesis and its receptors may play a role in synthesis of collagen. FGFs are involved in transmission of signals between the epithelium and connective tissue, and influence growth and differentiation of a wide variety of tissue including epithelia. The present study was undertaken to analyze expression of FGF-2 and its receptors FGFR-2 and FGFR-3 in 72 PMOLs, 108 OSCC and 52 healthy controls, and their role in risk assessment for malignant transformation of Leukoplakia (LKP) and Oral submucous fibrosis (OSMF) to OSCC. Immunohistochemistry was performed using antibodies against FGF-2, FGFR-2 and FGFR-3. IHC results were validated by Real Time PCR. Expression of FGF-2, FGFR-2 and FGFR-3 was upregulated from PMOLs to OSCC. While 90% (9/10) of PMOLs which showed malignant transformation (transformed) expressed FGF-2, only 24.19% cases (15/62) of PMOLs which were not transformed (untransformed) to OSCC expressed FGF-2. Similarly, FGFR-2 expression was seen in 16/62 (25.81%) of untransformed PMOLs and 8/10 (80%) cases of transformed PMOLs. FGFR-3 expression was observed in 23/62 (37.10%) cases of untransformed PMOLs and 6/10 (60%) cases of transformed PMOLs. A significant association of FGF-2 and FGFR-2 expression with malignant transformation from PMOLs to OSCC was observed both at phenotypic and molecular level. The results suggest that FGF-2 and FGFR-2 may be useful as biomarkers of malignant transformation in patients with OSMF and LKP.

Indexed as

AdultAgedAged, 80 and overBiomarkers, TumorCarcinoma, Squamous CellCase-Control StudiesCell Transformation, NeoplasticChildFemaleFibroblast Growth Factor 2Gene Expression Regulation, NeoplasticHumansLeukoplakia, OralMaleMiddle AgedMouth MucosaBiomarkers, TumorFGFR2 protein, humanFGFR3 protein, humanFibroblast Growth Factor 2Receptor, Fibroblast Growth Factor, Type 2Receptor, Fibroblast Growth Factor, Type 3

Identifiers

PMID26465941
PMCPMC4605495
OpenAlexW1829165872

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.