Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (797 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A bone tumor composed of cellular spindle-cell stroma containing scattered multinucleated giant cells resembling osteoclasts. The tumors range from benign to frankly malignant lesions. The tumor occurs most frequently in an end of a long tubular bone in young adults. (From Dorland, 27th ed; Stedman, 25th ed)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Where it fits in the MeSH classification
- Broader topics
- Giant Cell Tumors; Neoplasms, Bone Tissue
Research landscape
PubMed indexes 2,342 records tagged with the MeSH heading “Giant Cell Tumor of Bone” (counts retrieved 2026-10-29). 493 of them (21.1%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 840 records.
Reviews account for 323 records (13.8%) and meta-analyses for 20. Randomized controlled trials number 5 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 406 |
| 2000-2009 | 603 |
| 2010-2019 | 840 |
| 2020 onward | 493 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 323 | 13.8% |
| Meta-analyses | 20 | 0.9% |
| Randomized controlled trials | 5 | 0.2% |
Method: PubMed query "Giant Cell Tumor of Bone"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cancer and oncology
Cancer research spans very different kinds of evidence. Laboratory studies in cell lines and animal models reveal mechanisms but often do not translate to patients. Early-phase trials mainly test safety and dosing, while phase 3 randomized trials and their meta-analyses are the usual basis for treatment conclusions. Outcomes also differ in meaning: tumour shrinkage, progression-free survival and overall survival are not interchangeable, and screening studies can be distorted by lead-time and overdiagnosis. When reading a result, check the cancer type and stage studied, the comparison treatment, and which outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| H3F3A (Histone 3.3) G34W Immunohistochemistry: A Reliable Marker Defining Benign and Malignant Giant Cell Tumor of Bone | 2017 | Research article Design not recorded in structured metadata | 167 | cc by PMID 28505000 · DOI · PMC5510691 |
| Bisphosphonate treatment of aggressive primary, recurrent and metastatic Giant Cell Tumour of Bone | 2010 | Research article Design not recorded in structured metadata | 110 | cc by PMID 20799989 · DOI · PMC2940802 |
| Giant cell tumour of bone: new treatments in development | 2015 | Review article Design not recorded in structured metadata | 72 | cc by PMID 25617146 · DOI · PMC4448077 |
| Giant cell tumor of bone inhibits osteoblastogenesis via WNT5B | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 41872383 · DOI · PMC13469380 |
H3F3A (Histone 3.3) G34W Immunohistochemistry: A Reliable Marker Defining Benign and Malignant Giant Cell Tumor of Bone [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Giant cell tumor of bone (GCTB) is a locally aggressive subarticular tumor.
- Closing excerpt
- 3 mutations represent true malignant GCTB, even in the absence of a benign GCTB component.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (227 words)
Giant cell tumor of bone (GCTB) is a locally aggressive subarticular tumor. Having recently reported that H3.3 G34W mutations are characteristic of this tumor type, we have now investigated the sensitivity and specificity of the anti-histone H3.3 G34W rabbit monoclonal antibody in a wide variety of tumors including histologic mimics of GCTB to assess its value as a diagnostic marker. We also determined the incidence of H3.3 G34 mutations in primary malignant bone tumors as assessed by genotype and H3.3 G34W immunostaining. A total of 3163 tumors were tested. Totally, 213/235 GCTB (90.6%) showed nuclear H3.3 p.G34W immunoreactivity. This was not the case for the rare variants, p.G34L, M, and V, which occurred most commonly in the small bones of the hands, patella, and the axial skeleton. If these sites were excluded from the analysis, H3.3 G34W expression was found in 97.8% of GCTB. Malignant bone tumors initially classified as osteosarcomas were the only other lesions (n=11) that showed G34W expression. Notably an additional 2 previously reported osteosarcomas with a p.G34R mutation were not immunoreactive for the antibody. A total of 11/13 of these malignant H3.3-mutant tumors exhibited an osteoclast-rich component: when imaging was available all but one presented at a subarticular site. We propose that subarticular primary malignant bone sarcoma with H3.3 mutations represent true malignant GCTB, even in the absence of a benign GCTB component.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28505000 · DOI · PMC5510691
Bisphosphonate treatment of aggressive primary, recurrent and metastatic Giant Cell Tumour of Bone [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundGiant cell tumour of bone (GCTB) is an expansile osteolytic tumour which contains numerous osteoclast-like giant cells.
- Closing excerpt
- These studies highlight the need for the establishment of standardised protocols to assess the efficacy of bisphosphonate treatment of GCTB.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (198 words)
BackgroundGiant cell tumour of bone (GCTB) is an expansile osteolytic tumour which contains numerous osteoclast-like giant cells. GCTB frequently recurs and can produce metastatic lesions in the lungs. Bisphosphonates are anti-resorptive drugs which act mainly on osteoclasts.MethodIn this study, we have examined clinical and radiological outcomes of treatment with aminobisphosphonates on 25 cases of aggressive primary, recurrent and metastatic GCTB derived from four European centres. We also analysed in vitro the inhibitory effect of zoledronic acid on osteoclasts isolated from GCTBs.ResultsTreatment protocols differed with several different aminobisphosphonates being employed, but stabilisation of disease was achieved in most of these cases which were refractory to conventional treatment. Most inoperable sacral/pelvic tumours did not increase in size and no further recurrence was seen in GCTBs that had repeatedly recurred in bone and soft tissues. Lung metastases did not increase in size or number following treatment. Zoledronic acid markedly inhibited lacunar resorption by GCTB-derived osteoclasts in vitro.ConclusionOur findings suggest that bisphosphonates may be useful in controlling disease progression in GCTB and that these agents directly inhibit GCTB - derived osteoclast resorption. These studies highlight the need for the establishment of standardised protocols to assess the efficacy of bisphosphonate treatment of GCTB.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 20799989 · DOI · PMC2940802
Giant cell tumour of bone: new treatments in development [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Giant cell tumour of bone (GCTB) is a benign osteolytic tumour with three main cellular components: multinucleated osteoclast-like giant cells, mononuclear spindle-like stromal cells (the main neoplastic components) and mononuclear cells of the monocyte/macrophage lineage.
- Closing excerpt
- Recent advances in the understanding of GCTB pathogenesis are essential to develop new treatments for this locally destructive primary bone tumour.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (147 words)
Giant cell tumour of bone (GCTB) is a benign osteolytic tumour with three main cellular components: multinucleated osteoclast-like giant cells, mononuclear spindle-like stromal cells (the main neoplastic components) and mononuclear cells of the monocyte/macrophage lineage. The giant cells overexpress a key mediator in osteoclastogenesis: the RANK receptor, which is stimulated in turn by the cytokine RANKL, which is secreted by the stromal cells. The RANK/RANKL interaction is predominantly responsible for the extensive bone resorption by the tumour. Historically, standard treatment was substantial surgical resection, with or without adjuvant therapy, with recurrence rates of 20-56 %. Studies with denosumab, a monoclonal antibody that specifically binds to RANKL, resulted in dramatic treatment responses, which led to its approval by the United States Food and Drugs Administration (US FDA). Recent advances in the understanding of GCTB pathogenesis are essential to develop new treatments for this locally destructive primary bone tumour.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 25617146 · DOI · PMC4448077
Giant cell tumor of bone inhibits osteoblastogenesis via WNT5B [4]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionGiant cell tumor of bone (GCTB) induces overproduction of bone-resorbing osteoclasts through receptor activator of nuclear factor kappa B ligand (RANKL), leading to bone resorption and destruction.
- Closing excerpt
- ConclusionThese studies indicate that GCTB not only induces osteoclasts, but also possesses activity that inhibits bone formation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (225 words)
IntroductionGiant cell tumor of bone (GCTB) induces overproduction of bone-resorbing osteoclasts through receptor activator of nuclear factor kappa B ligand (RANKL), leading to bone resorption and destruction. Consequently, denosumab, a neutralizing antibody against RANKL (a cytokine essential for osteoclast induction), is used to treat patients with GCTB. However, the activity of bone formation in GCTB remains poorly understood. Here, we show that GCTB antagonizes bone formation by expressing WNT5B, which inhibits bone formation.Materials and methodsCo-culture of NCC-GCTB1-C1 (GCTB1s), a human GCTB cell line, with human adipose-derived stem cells (ADSCs) was performed with osteoblast induction medium. To identify the inhibitors of osteoblast differentiation, we reanalyzed the single-cell RNA sequencing data that was previously published. In addition, we performed spatial transcriptome analysis (Visium) against the section of paraffin block of GCTB. The targeted protein was knocked out using CRISPR/Cas9 and co-culture was performed.ResultsCo-culture of GCTB1s with ADSCs significantly inhibited mineralization of ADSCs. Reanalysis of single-cell RNA sequencing data indicated that GCTB tumors express WNT5B, and we observed that GCTB1s express WNT5B. We then knocked out WNT5B in GCTB1s using CRISPR/Cas9 and co-cultured them with ADSCs and observed significant rescue of mineralization in ADSCs relative to ADSCs cultured with GCTB1s expressing WNT5B. We also show that ADSC supernatants induce mineralization of GCTB1s.ConclusionThese studies indicate that GCTB not only induces osteoclasts, but also possesses activity that inhibits bone formation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41872383 · DOI · PMC13469380
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article From the archives of AFIP. Imaging of giant cell tumor and giant cell reparative granuloma of bone: radiologic-pathologic correlation [5]
- Research article Giant cell tumor of bone [6]
- Research article Recurrence of giant-cell tumors of the long bones after curettage and packing with cement [7]
- Research article Giant cell tumor of the extremity: A review of 349 cases from a single institution [8]
- Research article Giant cell tumor of bone: review, mimics, and new developments in treatment [9]
- Research article The clinical approach toward giant cell tumor of bone [10]
References
- Amary F, Berisha F, Ye H, Gupta M, Gutteridge A, Baumhoer D, et al.. H3F3A (Histone 3.3) G34W Immunohistochemistry: A Reliable Marker Defining Benign and Malignant Giant Cell Tumor of Bone. . 2017. PMID 28505000 · DOI · PMC5510691
- Balke M, Campanacci L, Gebert C, Picci P, Gibbons M, Taylor R, et al.. Bisphosphonate treatment of aggressive primary, recurrent and metastatic Giant Cell Tumour of Bone. . 2010. PMID 20799989 · DOI · PMC2940802
- López-Pousa A, Martín Broto J, Garrido T, Vázquez J. Giant cell tumour of bone: new treatments in development. . 2015. PMID 25617146 · DOI · PMC4448077
- Shimada M, Tsuyama T, Yoshimura N, Tateyama M, Matsunaga H, Homma F, et al.. Giant cell tumor of bone inhibits osteoblastogenesis via WNT5B. . 2026. PMID 41872383 · DOI · PMC13469380
- Murphey MD, Nomikos GC, Flemming DJ, Gannon FH, Temple HT, Kransdorf MJ. From the archives of AFIP. Imaging of giant cell tumor and giant cell reparative granuloma of bone: radiologic-pathologic correlation. Radiographics. 2001. PMID 11553835 · DOI
- Turcotte RE. Giant cell tumor of bone. Orthop Clin North Am. 2006. PMID 16311110 · DOI
- O'Donnell RJ, Springfield DS, Motwani HK, Ready JE, Gebhardt MC, Mankin HJ. Recurrence of giant-cell tumors of the long bones after curettage and packing with cement. J Bone Joint Surg Am. 1994. PMID 7989388 · DOI
- Errani C, Ruggieri P, Asenzio MA, Toscano A, Colangeli S, Rimondi E, et al.. Giant cell tumor of the extremity: A review of 349 cases from a single institution. Cancer Treat Rev. 2010. PMID 19879054 · DOI
- Chakarun CJ, Forrester DM, Gottsegen CJ, Patel DB, White EA, Matcuk GR. Giant cell tumor of bone: review, mimics, and new developments in treatment. Radiographics. 2013. PMID 23322837 · DOI
- van der Heijden L, Dijkstra PD, van de Sande MA, Kroep JR, Nout RA, van Rijswijk CS, et al.. The clinical approach toward giant cell tumor of bone. Oncologist. 2014. PMID 24718514 · DOI · PMC4012970
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.