Adamantinoma of Long Bones: Disease-Characteristics Research Report

Scope and evidence note

This report concerns adamantinoma of long bones, not ameloblastoma of the jaw, adamantinomatous craniopharyngioma, or adamantinoma-like Ewing sarcoma (ALES). Those are biologically distinct entities whose similar names commonly produce database-search false positives. Evidence for adamantinoma is limited by extreme rarity; much of the quantitative literature consists of retrospective referral-center series, pathology cohorts, case reports, and narrative reviews rather than prospective trials.

The most useful recent sources retrieved were Węgrzyniak et al., published 30 August 2023 (DOI: 10.12775/JEHS.2023.47.01.003), and Monteiro et al., accepted 9 February 2024. The major primary clinical benchmark remains Keeney et al.’s 85-case series, published 1 August 1989 (DOI: 10.1002/1097-0142(19890801)64:3%3C730::AID-CNCR2820640327%3E3.0.CO;2-P).

Table: This compact table summarizes the most evidence-supported knowledge-base fields for adamantinoma of long bones, emphasizing distinctions among classic, OFD-like, and adamantinoma-like Ewing entities. It is useful for rapid curation because it combines clinical facts, molecular caveats, and suggested ontology mappings in one place.

1. Disease information

Definition and classification

Adamantinoma is an exceedingly rare, primary, usually low-grade malignant bone neoplasm characterized by epithelial tumor cells embedded in an osteofibrous or fibroblastic stroma. Its canonical location is the anterior cortex and diaphysis of the tibia. The 2020 WHO classification uses the name “adamantinoma of long bones”, places it among “other mesenchymal tumours of bone,” and recognizes classic, osteofibrous-dysplasia-like (OFD-like), and dedifferentiated forms. OFD-like adamantinoma is classified as intermediate/locally aggressive, whereas classic and dedifferentiated forms are malignant. The 2008 review’s abstract states directly: “Adamantinoma is a primary low-grade, malignant bone tumor that is predominantly located in the mid-portion of the tibia.” (jain2008adamantinomaaclinicopathological pages 1-2, wegrzyniak2023currentclinicopathologicalcharacterisation pages 1-5, wegrzyniak2023currentclinicopathologicalcharacterisation pages 5-9)

Identifiers and synonyms

• MONDO: MONDO:0002422, adamantinoma. Open Targets returned this disease record but no established associated therapeutic target. (OpenTargets Search: adamantinoma)
• Common names: adamantinoma; adamantinoma of long bones; long-bone adamantinoma; tibial adamantinoma.
• Subtype synonyms: differentiated adamantinoma, juvenile adamantinoma, intracortical adamantinoma, regressive adamantinoma, and OFD-like adamantinoma have historically overlapped, although current WHO terminology favors OFD-like adamantinoma.
• MeSH: Adamantinoma is an indexed disease concept; curators should verify the current identifier in the target terminology release.
• ICD: There is no sufficiently specific ICD-10-CM code for adamantinoma. Coding generally uses the malignant bone-neoplasm code selected by anatomical site; ICD-O morphology coding should be checked against the applicable registry edition.
• OMIM/Orphanet: No hereditary Mendelian disease entry or causal-gene record was established in the retrieved evidence. A specific Orphanet identifier should not be asserted without direct registry verification.

The evidence summarized here is aggregated disease-level literature, not individual EHR-derived data. The 2024 report is an individual clinical case and is identified as such. (monteiro2024adamantinomadetíbia pages 1-4, monteiro2024adamantinomadetíbia pages 4-6)

2. Etiology and risk factors

The cause remains unknown. Epithelial differentiation is strongly supported by broad cytokeratin staining and ultrastructural features including basal lamina and desmosomes. Historical hypotheses—embryonic displacement of basal epidermal cells, traumatic implantation, synovial, vascular, or mesenchymal origin—have not yielded a proven initiating cause. The embryonic-displacement hypothesis was motivated by the tumor’s anterior tibial predilection, where skin lies close to developing bone. (jain2008adamantinomaaclinicopathological pages 1-2)

Risk, protective, and gene–environment factors

• Germline risk: No validated causal germline variant, susceptibility locus, familial syndrome, founder mutation, carrier state, or Mendelian inheritance pattern is established.
• Age/sex: Typical presentation is in the second through fifth decades, especially ages 20–40. A slight male excess is repeatedly reported. These are demographic associations, not demonstrated causal factors. (keeney1989adamantinomaoflong pages 1-2, jain2008adamantinomaaclinicopathological pages 1-2, wegrzyniak2023currentclinicopathologicalcharacterisation pages 5-9)
• Trauma: Trauma has often been reported, but evidence is inconsistent. In the 85-case series, only 12 patients had a trauma history and the authors could not infer causality; an older literature review reported trauma in approximately 60%. Trauma may simply draw attention to a pre-existing lesion. (keeney1989adamantinomaoflong pages 1-2, keeney1989adamantinomaoflong pages 2-3, keeney1989adamantinomaoflong pages 6-7, jain2008adamantinomaaclinicopathological pages 1-2)
• Environmental/lifestyle/occupational exposures: No reproducible association with smoking, alcohol, diet, radiation, toxins, pollution, occupation, or physical inactivity is established.
• Infection: No bacterial, viral, fungal, or parasitic cause is known.
• Protective factors and gene–environment interactions: None validated.

3. Phenotypes

Presentation is typically insidious, chronic, and progressive. In the 85-case series, among 65 patients with known symptoms, 34 had pain plus swelling, 14 painless swelling, 14 pain alone, and three pathological fracture. Symptom duration ranged from two weeks to 50 years; 41/64 patients had symptoms for less than five years and 23 for at least five years. (keeney1989adamantinomaoflong pages 1-2)

There are no robust disease-specific EQ-5D, SF-36, PROMIS, or utility estimates. Quality of life may be impaired by pain, reduced weight-bearing, deformity, fracture, major resection, graft or prosthetic complications, limb-length discrepancy, repeated reconstruction, or amputation. The 2024 pediatric case explicitly reported limitation of daily activities. (monteiro2024adamantinomadetíbia pages 4-6)

4. Genetic and molecular information

Tumor genetics

Adamantinoma is not presently a hereditary single-gene disorder. Reported abnormalities are tumor-level/somatic research findings, not clinically validated constitutional pathogenic variants.

• Aneuploidy and recurrent extra copies of chromosomes 7, 8, 12, 19, and 21 have been reported. (jain2008adamantinomaaclinicopathological pages 6-8, wegrzyniak2023currentclinicopathologicalcharacterisation pages 5-9)
• A 2019 molecular study summarized by the 2023 review proposed KMT2D mutation and increased DLK1 expression as potential markers. These are candidate findings—not sufficient to define a causal gene, ACMG pathogenic germline variant, or approved treatment target. (wegrzyniak2023currentclinicopathologicalcharacterisation pages 5-9)
• Open Targets listed zero established target associations for MONDO:0002422. This is important negative evidence against importing BRAF/SMO findings from ameloblastoma or CTNNB1 findings from adamantinomatous craniopharyngioma. (OpenTargets Search: adamantinoma)
• No validated modifier gene, allele frequency, penetrance estimate, pharmacogenomic marker, or standard ClinVar-classified disease variant is established.

Protein and immunophenotypic findings

The epithelial tumor cells express broad cytokeratins, particularly KRT5, KRT14, and KRT19, and commonly p63; EMA is often reported but may be variable. Older studies found p53 immunoreactivity in epithelial cells. The osteofibrous stroma is vimentin-positive. Keratin expression and epithelial ultrastructure support true epithelial differentiation. (amr2026managementoftibial pages 4-6, jain2008adamantinomaaclinicopathological pages 1-2, wegrzyniak2023currentclinicopathologicalcharacterisation pages 5-9)

A 2024 classic-tumor case was AE1/AE3-positive in the epithelial component and p63-positive, but EMA, CK19, CD34, and the reported CK99 stain were negative, illustrating that a panel plus morphology is more reliable than any single marker. (monteiro2024adamantinomadetíbia pages 4-6)

Epigenetics and structural abnormalities

No reproducible disease-defining methylation class, histone-mark signature, enhancer alteration, or chromosomal translocation is established for true adamantinoma. This differs critically from ALES, which usually has a FET–ETS fusion such as EWSR1::FLI1. Molecular testing is particularly appropriate in a small-round-cell, head-and-neck, or otherwise atypical “adamantinoma-like” lesion. (rekhi2025osteofibrousdysplasia(ofd) pages 8-10)

5. Environmental information

No causal toxin, radiation exposure, pollutant, occupational exposure, lifestyle behavior, or infectious agent has been demonstrated. Trauma is best treated as an uncertain historical association rather than an environmental cause. Consequently, there are no evidence-based dietary, exercise, exposure-avoidance, antimicrobial, or vaccination recommendations specific to disease prevention.

6. Mechanism and pathophysiology

Current causal model

1. An unidentified initiating event produces an epithelial neoplastic clone in cortical bone.
2. Tumor epithelial cells proliferate as nests, cords, tubules, basaloid islands, squamous areas, or spindle-shaped cells.
3. Epithelial–stromal signaling promotes a prominent fibro-osseous response, yielding the characteristic biphasic lesion.
4. Slow longitudinal growth causes cortical osteolysis, sclerosis, expansion, medullary extension, deformity, pain, and sometimes fracture.
5. Cortical breakthrough permits soft-tissue extension; lymphovascular dissemination produces regional-node and pulmonary metastases.
6. In rare cases, dedifferentiation generates a high-grade pleomorphic sarcomatous component and more aggressive behavior. (jain2008adamantinomaaclinicopathological pages 2-4, wegrzyniak2023currentclinicopathologicalcharacterisation pages 5-9, wegrzyniak2023currentclinicopathologicalcharacterisation pages 9-13)

The epithelial component has greater Ki-67 and growth-factor/receptor expression than the stroma in older studies, supporting the interpretation that epithelial cells are the neoplastic driver and that osteofibrous tissue is at least partly reactive. Nevertheless, whether OFD, OFD-like adamantinoma, and classic adamantinoma form a universal biological continuum remains disputed. Documented progression supports a continuum in some patients, but older clinicopathologic work did not establish that ordinary OFD is invariably a precursor. (jain2008adamantinomaaclinicopathological pages 4-5, wegrzyniak2023currentclinicopathologicalcharacterisation pages 5-9)

Suggested annotations include GO epithelial cell proliferation, GO extracellular matrix organization, GO cell population proliferation, and GO epithelial cell differentiation; cell types include CL epithelial cell and CL fibroblast. There is no established disease-specific metabolic, autophagic, immune-checkpoint, inflammatory, mitochondrial, or ion-channel mechanism.

Molecular profiling and advanced technologies

Small genomic/cytogenetic studies exist, but no validated transcriptomic classifier, clinical proteomic or metabolomic signature, lipidomic profile, single-cell atlas, spatial-transcriptomic map, integrated multi-omics cohort, or CRISPR/RNAi dependency screen was identified. These are major research gaps.

7. Anatomical structures affected

• Primary organ/system: skeleton, especially long bones of the lower limb.
• Canonical site: anterior cortex of the tibial diaphysis; suggested terms: UBERON tibia, UBERON cortical bone, UBERON diaphysis.
• Secondary local structures: medullary cavity/bone marrow, periosteum, adjacent fibula, subcutaneous tissue, and other soft tissues.
• Frequency: Reviews estimate 97% occur in long bones and 80–85% in the tibia. In the primary 85-case series, 70/85 involved the tibia; 11 of those also involved the fibula. Six arose in femur, three ulna, two humerus, two fibula, one radius, and one pretibial soft tissue. Approximately 90% were diaphyseal. (keeney1989adamantinomaoflong pages 1-2, keeney1989adamantinomaoflong pages 2-3, jain2008adamantinomaaclinicopathological pages 1-2)
• Distant sites: lung and regional lymph nodes predominate; bone, vertebral column, brain, and other sites are rare.
• Lateralization: no meaningful biological laterality is established; the 85-case series had 34 right and 32 left lesions among cases with known side. (keeney1989adamantinomaoflong pages 2-3)
• Subcellular compartments: diagnostic keratins are cytoplasmic/cytoskeletal; p63/p53 are nuclear. No organelle-specific pathogenic defect is known.

8. Temporal development

Classic adamantinoma most often presents from adolescence through middle adulthood, with a median/typical age around 25–35 years; OFD-like disease is enriched in children and adolescents, generally under 20. The 85-case series had an age range of 3–72 years and mean age 25.9 years. (keeney1989adamantinomaoflong pages 1-2, jain2008adamantinomaaclinicopathological pages 1-2, jain2008adamantinomaaclinicopathological pages 2-4)

The course is chronic and slowly progressive rather than episodic. Local recurrence in the 85-case series occurred after a mean 4.7 years, range 3 months–19.4 years; lymph-node metastasis occurred after a mean 5.8 years, and lung metastasis after a mean 8.2 years, range 1.1–17.9 years. Events several decades after treatment have also been reported, supporting prolonged—often lifelong—surveillance. Spontaneous remission is not expected for classic adamantinoma; apparent regression is discussed principally in OFD/OFD-like lesions. (amr2026managementoftibial pages 6-7, keeney1989adamantinomaoflong pages 3-6)

9. Inheritance and population

Adamantinoma is sporadic, with no established autosomal dominant, autosomal recessive, X-linked, mitochondrial, polygenic, or anticipation pattern. Penetrance, carrier frequency, germline mosaicism, founder effects, consanguinity, and prenatal risk are therefore not applicable.

It accounts for approximately 0.1–0.5% of primary bone tumors, but reliable population incidence and point-prevalence estimates per 100,000 are not well established. No consistent ethnic, geographic, or endemic pattern is known. The 85-case cohort included 45 males, 39 females, and one patient of unknown sex; reviews summarize the sex ratio as approximately 5:4 male:female. (keeney1989adamantinomaoflong pages 1-2, jain2008adamantinomaaclinicopathological pages 1-2, wegrzyniak2023currentclinicopathologicalcharacterisation pages 5-9)

10. Diagnostics

Recommended work-up

1. Plain radiography: typically central or eccentric, longitudinal, multilocular osteolysis with septation, peripheral sclerosis, cortical expansion/thinning, and a “soap-bubble” appearance.
2. MRI of the entire involved bone: best for skip/satellite foci, medullary extent, cortical breakthrough, soft-tissue involvement, and surgical margins. Typical signal is low/intermediate on T1 and high on T2/STIR, with enhancement. Two patterns are described: a solitary lobulated focus or multiple small nodules in one or more foci.
3. CT: clarifies cortical destruction and mineralization; chest CT is important for pulmonary staging.
4. Biopsy planned with the definitive sarcoma surgeon: central and extensive sampling is crucial because peripheral OFD-like areas may lack obvious epithelial nests.
5. Histology and IHC: establish biphasic architecture and epithelial differentiation.
6. Molecular testing where morphology is atypical: fusion testing helps exclude ALES and synovial sarcoma. (monteiro2024adamantinomadetíbia pages 4-6, jain2008adamantinomaaclinicopathological pages 2-4, jain2008adamantinomaaclinicopathological pages 9-10, wegrzyniak2023currentclinicopathologicalcharacterisation pages 9-13)

Pathology

Classic tumors contain bland epithelial nests within fibrous stroma. Patterns include tubular, basaloid, squamous, spindle-cell, and OFD-like forms. Mitoses are usually sparse—historically 0–2 per 10 high-power fields—and marked atypia is unusual outside dedifferentiated disease. OFD-like tumors are predominantly fibro-osseous and may contain only tiny keratin-positive epithelial clusters. (keeney1989adamantinomaoflong pages 2-3, jain2008adamantinomaaclinicopathological pages 2-4, wegrzyniak2023currentclinicopathologicalcharacterisation pages 9-13)

Differential diagnosis

The principal differentials are OFD, fibrous dysplasia, OFD-like adamantinoma, osteosarcoma, Ewing/ALES, intraosseous synovial sarcoma, metastatic carcinoma, epithelioid vascular tumors, nonossifying fibroma, and osteomyelitis. OFD is generally benign and strictly intracortical; true adamantinoma more often extends toward marrow and contains demonstrable epithelial tumor cells. ALES commonly arises in head/neck soft tissue or bone, expresses CD99/NKX2.2 and keratins, and is defined by a FET–ETS fusion. (rekhi2025osteofibrousdysplasia(ofd) pages 8-10, jain2008adamantinomaaclinicopathological pages 2-4, jain2008adamantinomaaclinicopathological pages 8-9)

No diagnostic blood/urine test, circulating biomarker, liquid biopsy, validated WES/WGS panel, CMA, mitochondrial assay, or repeat-expansion test is recommended routinely. There is no population screening or cascade testing.

11. Outcome and prognosis

In the 85-case primary series, 26/85 (31%) developed local recurrence, 13/85 (15%) lung metastases, 6/85 (7%) lymph-node metastases, and 11 died from disease. Nine of 13 patients with lung metastasis had preceding local recurrence, and recurrence significantly increased pulmonary-metastasis risk. (keeney1989adamantinomaoflong pages 1-2, keeney1989adamantinomaoflong pages 3-6, keeney1989adamantinomaoflong pages 6-7)

Broader reviews report local recurrence around 18–32%, metastasis approximately 12–30%, and mortality around 13–18%, but these estimates mix eras and treatments. A modern synthesis cited 5- and 10-year recurrence estimates of 8.6% and 18.6%, 10-year disease-specific survival of 92%, and recurrence-free survival of 72%; interpretation requires caution because source populations and subtype composition differ. (jain2008adamantinomaaclinicopathological pages 6-8, amr2026managementoftibial pages 6-7, amr2026managementoftibial pages 8-9, kumar2021anunusualcase pages 6-7)

Adverse factors reported across retrospective studies include inadequate/intralesional surgery or positive margins, male sex, pain, symptom duration under five years, local recurrence, pathological fracture, skip lesions/periosteal involvement, younger age, and absence of squamous differentiation. Margin status is the most actionable and consistent factor. These associations should not be treated as validated individual-risk calculators. (jain2008adamantinomaaclinicopathological pages 6-8, amr2026managementoftibial pages 8-9, keeney1989adamantinomaoflong pages 1-2, keeney1989adamantinomaoflong pages 6-7)

12. Treatment

Standard treatment

Wide en-bloc resection with histologically negative margins is the treatment of choice. Limb salvage is preferred when adequate margins and useful function are achievable. Reconstruction may use intercalary allograft, vascularized fibular autograft, bone transport/distraction osteogenesis, endoprosthetic reconstruction, or combinations selected by tumor length, joint involvement, age, and remaining growth. Suggested NCIT terms include Surgical Resection, Wide Excision, Limb Salvage Procedure, Bone Grafting, Reconstructive Surgical Procedure, and Amputation. (jain2008adamantinomaaclinicopathological pages 6-8, amr2026managementoftibial pages 8-9, kumar2021anunusualcase pages 6-7, wegrzyniak2023currentclinicopathologicalcharacterisation pages 5-9)

Amputation is reserved for unresectable or repeatedly recurrent disease, inability to obtain margins, major neurovascular involvement, infection, or failed reconstruction; it has not shown an inherent survival advantage over adequate wide resection. Curettage and other intralesional procedures are inappropriate for classic adamantinoma because of high recurrence risk. (amr2026managementoftibial pages 6-7, wegrzyniak2023currentclinicopathologicalcharacterisation pages 5-9)

Systemic and radiation treatment

Conventional chemotherapy and radiotherapy have no established routine efficacy. Anecdotal use of tyrosine-kinase inhibitors such as pazopanib or sunitinib has been discussed for unresectable/metastatic disease, but there is no validated response rate, approved adamantinoma-specific target, or standard regimen. Genotype-guided therapy, checkpoint inhibition, CAR-T therapy, gene therapy, ASOs/siRNA, and mRNA therapy are investigational or unsupported. (jain2008adamantinomaaclinicopathological pages 6-8, amr2026managementoftibial pages 8-9, kumar2021anunusualcase pages 6-7)

A ClinicalTrials.gov search did not identify a relevant adamantinoma interventional study; retrieved hits concerned similarly named ameloblastoma or craniopharyngioma and must not be assigned to this disease.

Supportive care

Management includes analgesia, fracture precautions, physical and occupational therapy, gait training, orthotics/prosthetics when appropriate, surveillance of graft union and hardware, and psychosocial support. Reconstruction can require repeated revision because of nonunion, graft fracture, infection, limb-length discrepancy, or prosthetic failure. No adamantinoma-specific pharmacogenomic guidance exists.

13. Prevention

There is no known primary prevention because no modifiable cause is established. There is no population, newborn, carrier, prenatal, or germline screening program and no vaccine or prophylactic drug.

Secondary prevention consists of prompt specialist assessment of persistent tibial pain, swelling, deformity, or a characteristic cortical lesion and avoiding unplanned curettage. Tertiary prevention includes complete initial resection, fracture prevention, rehabilitation, and very long-term local and chest surveillance. Genetic counseling is not routinely indicated for familial risk, although counseling about the absence of demonstrated heritability may be useful.

14. Other species and natural disease

No well-validated naturally occurring veterinary counterpart, breed predisposition, orthologous causal gene, cross-species susceptibility, or comparative spontaneous-disease cohort was identified. Adamantinoma is not infectious and has no zoonotic or cross-species transmission potential. Reports using “adamantinoma” in veterinary or older pathology sources require careful review because the term has historically been applied to odontogenic tumors.

15. Model organisms and experimental systems

No standardized mouse, rat, zebrafish, invertebrate, genetically engineered, humanized, patient-derived xenograft, organoid, iPSC, or validated cell-line model was identified. Consequently, no model has been shown to reproduce the human tibial cortical localization, biphasic epithelial–osteofibrous architecture, prolonged latency, or late metastatic behavior. Development of authenticated patient-derived cultures, organoids, xenografts, and spatial/single-cell datasets is a major unmet research need.

Recent developments and expert interpretation

The 2023 review emphasizes three practical developments: adoption of the 2020 WHO three-part classification, increasing use of combined immunohistochemical and genetic assessment, and MRI-based definition of full tumor extent before wide-margin surgery. Its abstract concludes that “confirmation of the immunohistochemical profile, as well as the genetic profile…is essential for diagnosis” and that the best treatment remains resection with large margins. (wegrzyniak2023currentclinicopathologicalcharacterisation pages 1-5)

The 2024 tibial case illustrates current real-world implementation: serial radiography, CT and MRI; centrally sampled biopsy; morphology plus p63/AE1-AE3 IHC; and limb-preserving resection/reconstruction. It also demonstrates the risk of misleading early imaging labels and postoperative functional complications in young patients. (monteiro2024adamantinomadetíbia pages 1-4, monteiro2024adamantinomadetíbia pages 4-6)

The central expert conclusion is that adamantinoma remains a surgically curable but deceptively persistent malignancy. Accurate subtype assignment, exclusion of molecular mimics, complete initial resection, and decades-long surveillance are more clinically consequential than presently available molecular-targeting strategies.

References

1. (wegrzyniak2023currentclinicopathologicalcharacterisation pages 1-5): A Węgrzyniak, W Wokurka, and D Drobek. Current clinicopathological characterisation of adamantinoma-a review of the literature. Unknown journal, 2023.

2. (wegrzyniak2023currentclinicopathologicalcharacterisation pages 5-9): A Węgrzyniak, W Wokurka, and D Drobek. Current clinicopathological characterisation of adamantinoma-a review of the literature. Unknown journal, 2023.

3. (jain2008adamantinomaaclinicopathological pages 1-2): Deepali Jain, Vijay K Jain, Rakesh K Vasishta, Prabhat Ranjan, and Yashwant Kumar. Adamantinoma: a clinicopathological review and update. Diagnostic Pathology, 3:8-8, Feb 2008. URL: https://doi.org/10.1186/1746-1596-3-8, doi:10.1186/1746-1596-3-8. This article has 130 citations and is from a peer-reviewed journal.

4. (rekhi2025osteofibrousdysplasia(ofd) pages 8-10): B Rekhi, R Jayan, R Jayan, and B Rekhi. Osteofibrous dysplasia (ofd) and adamantinoma: a comprehensive review and updates. Histology and histopathology, pages 18950, Jun 2025. URL: https://doi.org/10.14670/hh-18-950, doi:10.14670/hh-18-950. This article has 3 citations and is from a peer-reviewed journal.

5. (keeney1989adamantinomaoflong pages 1-2): Gary L. Keeney, K. Krishnan Unni, John W. Beabout, and Douglas J. Pritchard. Adamantinoma of long bones. a clinicopathologic study of 85 cases. Cancer, 64:730-737, Aug 1989. URL: https://doi.org/10.1002/1097-0142(19890801)64:3<730::aid-cncr2820640327>3.0.co;2-p, doi:10.1002/1097-0142(19890801)64:3<730::aid-cncr2820640327>3.0.co;2-p. This article has 218 citations and is from a domain leading peer-reviewed journal.

6. (jain2008adamantinomaaclinicopathological pages 2-4): Deepali Jain, Vijay K Jain, Rakesh K Vasishta, Prabhat Ranjan, and Yashwant Kumar. Adamantinoma: a clinicopathological review and update. Diagnostic Pathology, 3:8-8, Feb 2008. URL: https://doi.org/10.1186/1746-1596-3-8, doi:10.1186/1746-1596-3-8. This article has 130 citations and is from a peer-reviewed journal.

7. (keeney1989adamantinomaoflong pages 2-3): Gary L. Keeney, K. Krishnan Unni, John W. Beabout, and Douglas J. Pritchard. Adamantinoma of long bones. a clinicopathologic study of 85 cases. Cancer, 64:730-737, Aug 1989. URL: https://doi.org/10.1002/1097-0142(19890801)64:3<730::aid-cncr2820640327>3.0.co;2-p, doi:10.1002/1097-0142(19890801)64:3<730::aid-cncr2820640327>3.0.co;2-p. This article has 218 citations and is from a domain leading peer-reviewed journal.

8. (kumar2021anunusualcase pages 6-7): Arvind Kumar, Ruchi Sharma, Anil Kumar Verma, Abhijeet Tiwari, and Jyoti Mishra. An unusual case of adamantinoma of long bone. Autopsy & Case Reports, 11:e2021276, May 2021. URL: https://doi.org/10.4322/acr.2021.276, doi:10.4322/acr.2021.276. This article has 7 citations.

9. (wegrzyniak2023currentclinicopathologicalcharacterisation pages 9-13): A Węgrzyniak, W Wokurka, and D Drobek. Current clinicopathological characterisation of adamantinoma-a review of the literature. Unknown journal, 2023.

10. (jain2008adamantinomaaclinicopathological pages 6-8): Deepali Jain, Vijay K Jain, Rakesh K Vasishta, Prabhat Ranjan, and Yashwant Kumar. Adamantinoma: a clinicopathological review and update. Diagnostic Pathology, 3:8-8, Feb 2008. URL: https://doi.org/10.1186/1746-1596-3-8, doi:10.1186/1746-1596-3-8. This article has 130 citations and is from a peer-reviewed journal.

11. (amr2026managementoftibial pages 4-6): Yasser Amr, Aye Htun, and Simerjit Singh. Management of tibial adamantinoma: balancing oncologic cure and reconstructive longevity. Cureus, Aug 2026. URL: https://doi.org/10.7759/cureus.113794, doi:10.7759/cureus.113794. This article has 0 citations.

12. (jain2008adamantinomaaclinicopathological pages 4-5): Deepali Jain, Vijay K Jain, Rakesh K Vasishta, Prabhat Ranjan, and Yashwant Kumar. Adamantinoma: a clinicopathological review and update. Diagnostic Pathology, 3:8-8, Feb 2008. URL: https://doi.org/10.1186/1746-1596-3-8, doi:10.1186/1746-1596-3-8. This article has 130 citations and is from a peer-reviewed journal.

13. (monteiro2024adamantinomadetíbia pages 4-6): LS de Sousa Monteiro and LF Vitule. Adamantinoma de tíbia: adamantinoma of the tibia. Unknown journal, 2024.

14. (jain2008adamantinomaaclinicopathological pages 9-10): Deepali Jain, Vijay K Jain, Rakesh K Vasishta, Prabhat Ranjan, and Yashwant Kumar. Adamantinoma: a clinicopathological review and update. Diagnostic Pathology, 3:8-8, Feb 2008. URL: https://doi.org/10.1186/1746-1596-3-8, doi:10.1186/1746-1596-3-8. This article has 130 citations and is from a peer-reviewed journal.

15. (jain2008adamantinomaaclinicopathological pages 8-9): Deepali Jain, Vijay K Jain, Rakesh K Vasishta, Prabhat Ranjan, and Yashwant Kumar. Adamantinoma: a clinicopathological review and update. Diagnostic Pathology, 3:8-8, Feb 2008. URL: https://doi.org/10.1186/1746-1596-3-8, doi:10.1186/1746-1596-3-8. This article has 130 citations and is from a peer-reviewed journal.

16. (keeney1989adamantinomaoflong pages 6-7): Gary L. Keeney, K. Krishnan Unni, John W. Beabout, and Douglas J. Pritchard. Adamantinoma of long bones. a clinicopathologic study of 85 cases. Cancer, 64:730-737, Aug 1989. URL: https://doi.org/10.1002/1097-0142(19890801)64:3<730::aid-cncr2820640327>3.0.co;2-p, doi:10.1002/1097-0142(19890801)64:3<730::aid-cncr2820640327>3.0.co;2-p. This article has 218 citations and is from a domain leading peer-reviewed journal.

17. (amr2026managementoftibial pages 6-7): Yasser Amr, Aye Htun, and Simerjit Singh. Management of tibial adamantinoma: balancing oncologic cure and reconstructive longevity. Cureus, Aug 2026. URL: https://doi.org/10.7759/cureus.113794, doi:10.7759/cureus.113794. This article has 0 citations.

18. (amr2026managementoftibial pages 8-9): Yasser Amr, Aye Htun, and Simerjit Singh. Management of tibial adamantinoma: balancing oncologic cure and reconstructive longevity. Cureus, Aug 2026. URL: https://doi.org/10.7759/cureus.113794, doi:10.7759/cureus.113794. This article has 0 citations.

19. (OpenTargets Search: adamantinoma): Open Targets Query (adamantinoma, 6 results). Buniello, A. et al. (2025). Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery. Nucleic Acids Research.

20. (monteiro2024adamantinomadetíbia pages 1-4): LS de Sousa Monteiro and LF Vitule. Adamantinoma de tíbia: adamantinoma of the tibia. Unknown journal, 2024.

21. (keeney1989adamantinomaoflong pages 3-6): Gary L. Keeney, K. Krishnan Unni, John W. Beabout, and Douglas J. Pritchard. Adamantinoma of long bones. a clinicopathologic study of 85 cases. Cancer, 64:730-737, Aug 1989. URL: https://doi.org/10.1002/1097-0142(19890801)64:3<730::aid-cncr2820640327>3.0.co;2-p, doi:10.1002/1097-0142(19890801)64:3<730::aid-cncr2820640327>3.0.co;2-p. This article has 218 citations and is from a domain leading peer-reviewed journal.

Artifacts

• Edison artifact artifact-00

Reference Validation

Checked with linkml-reference-validator 0.2.1.

Unresolved references

These identifiers did not resolve to a record and may be fabricated. A lookup that failed for transport reasons is indistinguishable from one that failed because the record does not exist, so spot-check before acting on them:

• DOI:10.14670/hh-18-950 (3 mentions) - Identifier did not resolve to a record