p63 regulates cell proliferation and cell cycle progression-associated genes in stromal cells of giant cell tumor of the bone

Lau, Carol; Ng, Patrick Kwok Shing; Li, Man Shan; Tsui, Stephen Kwok‐Wing; Huang, Lin; Kumta, S. M.

doi:10.3892/ijo.2012.1727

Cited by 28 publications

(19 citation statements)

References 27 publications

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“…The role of p63 in GCTB oncogenesis is unknown. Recently Lau et al showed that p63 regulates tumour cell proliferation in GCTB by binding to CDC2 and CDC25C [24]. Further studies are required to unravel the function of p63-phenotypic, oncogenic or tumour suppressive-in GCTB.…”

Section: Resultsmentioning

confidence: 97%

A diagnosis of giant cell-rich tumour of bone is supported by p63 immunohistochemistry, when more than 50 % of cells is stained

Paula

Vasiljevic²,

Giorgi

et al. 2014

Virchows Arch

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Some primary malignant or benign tumours of bone contain numerous multinucleated cells. These "giant cell-rich tumours of bone" have overlapping features and clinical and radiological data are needed to reach an accurate pathological diagnosis. We studied the potential contribution of p63 immunohistochemistry to the reliability of the histological diagnosis. We performed a multicentric retrospective study of 291 giant cell-rich tumours of bone which included 119 giant cell tumours of bone (GCTB), 76 aneurysmal bone cysts (ABC), 49 chondroblastomas (CB), 15 nonossifying fibromas (NOF), 10 giant cell reparative granulomas (RG) of jaws, 1 giant cell lesion of small bones, 2 hyperparathyroidism-related brown tumours (BT), 17 bone sarcomas with numerous osteoclasts and 2 malignant giant cell tumours of bone. p63 is expressed in ABC, CB, NOF, RG, BT and GCTB, but its expression in more than 50 % of mononuclear cells is strongly suggestive of a diagnosis of GCTB. In contrast, malignant GCTB were mostly negative. Our results show that p63 is expressed in a broad range of benign giant cell-rich tumours of bone, consistent with data in the recent literature, while infrequent in malignant tumours. With a cut-off 50 %, the presence of p63 positive cells is useful in supporting a diagnosis of giant cell-rich tumour of bone. However, a final diagnosis cannot be made without due consideration of all clinical/radiological and pathological data.

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Section: Resultsmentioning

confidence: 97%

A diagnosis of giant cell-rich tumour of bone is supported by p63 immunohistochemistry, when more than 50 % of cells is stained

Paula

Vasiljevic²,

Giorgi

et al. 2014

Virchows Arch

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“…, Lau et al . , Shooshtarizadeh et al . ), as well as in neoplastic lymphocytes in patients with non‐Hodgkin's lymphoma (Hedvat et al .…”

Section: Discussionmentioning

confidence: 99%

Potential role of TP63 in apical periodontitis development

et al. 2019

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Aim To investigate the expression of TP63 in apical periodontitis (AP) tissues and the association of single nucleotide polymorphisms (SNPs) in the TP63 gene with AP using a case‐control dataset. Methodology Expression of TP63 in human AP lesions (apical abscess, radicular cyst, periapical granuloma) was evaluated using immunohistochemistry. A case‐control association study was performed to assess the association of TP63 polymorphisms in individuals having AP with or without associated pain. Cases were defined as subjects with deep caries and AP (n = 151) and subjects with symptomatic apical periodontitis or acute apical abscess (n = 124). Subjects without AP (n = 169) and asymptomatic (n = 196) were used as controls, respectively. Saliva samples were collected as source of genomic DNA. Twelve SNPs in the TP63 gene were selected for genotyping using Taqman chemistry in real‐time PCR. Data analysis was performed using PLINK software. The Bonferroni method was applied to correct for multiple testing; α ≤ 0.004 indicates significant differences between groups. Results TP63 expression was evident in apical abscesses and radicular cysts, while weaker expression was observed in periapical granulomas. Positive expression was observed in mononuclear cells in the granulation tissues of all AP lesions. Regarding the presence of AP, a trend for allelic association was observed for rs16864812 and rs9810322 (P = 0.04) and rs9810322 genotypes were also nominally associated with AP under a dominant model (P = 0.04). When considering the presence of periapical pain, a trend for allelic and genotypic association was observed for rs10155037 (P = 0.03). Haplotypes were also associated with AP and periapical pain (P ≤ 0.05). Conclusions Apical periodontitis is a complex multifactorial condition and it is likely that multiple genes and environmental effects may influence its susceptibility, progression or both. TP63 variants may play a role in AP pathogenesis and susceptibility, individually or interactively with other genes. Additional studies in other populations and functional studies are needed to improve understanding of the role of TP63 in AP.

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“…It has been suggested that mutations in p53 are correlated with the lung metastasis in GCTB [13]. In addition, the overexpression of p63 has been implicated in GCTB progression [14]. Thus, these proteins might play a regulatory role in the progression of GCTB.…”

Section: Introductionmentioning

confidence: 99%

Factors Affecting the Recurrence of Giant Cell Tumor of Bone After Surgery: A Clinicopathological Study of 80 Cases from a Single Center

Cheng

Zhang

et al. 2015

Cell Physiol Biochem

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Background/Aims: This aim of the present study was to identify specific markers determining the recurrence of the giant cell tumor of bone (GCTB). Methods: This study involved the clinicopathological analysis of 80 cases. All of the clinical features, pathological fracture, Campanacci grade, histological features and surgical methods were reviewed. Immunohistochemistry was used to detect the expression of Ki-67, CD147, mutant p53 and p63 in GCTB. Comparisons between different groups were performed using the Chi-square test. The risk factors affecting recurrence were analyzed using a binary logistic model. Kaplan-Meier analysis was employed for the survival analysis between the groups. Cell proliferation assays, migration and invasion assays were used to detect the function of CD147 on GCTB in vitro. Results: The univariate analysis showed that Ki-67 and CD147 expression, pathological fracture, Campanacci grade and surgical method were associated with recurrence. The multivariate analysis revealed that CD147 expression, Campanacci grade and surgical method were the factors affecting GCTB recurrence. In addition, the Kaplan-Meier analysis revealed that these factors affected tumor-free survival time. In vitro study revealed that the CD147 knockdown by small interfering RNA (siRNA) technique dramatically reduced the proliferation, migration and invasion of GCTB. Conclusion: Our results suggest that CD147 may serve as an adequate marker for GCTB recurrence. Campanacci grade is a risk factor for GCTB recurrence, which is also affected by the surgical method used.

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p63 regulates cell proliferation and cell cycle progression-associated genes in stromal cells of giant cell tumor of the bone

Cited by 28 publications

References 27 publications

A diagnosis of giant cell-rich tumour of bone is supported by p63 immunohistochemistry, when more than 50 % of cells is stained

A diagnosis of giant cell-rich tumour of bone is supported by p63 immunohistochemistry, when more than 50 % of cells is stained

Potential role of TP63 in apical periodontitis development

Factors Affecting the Recurrence of Giant Cell Tumor of Bone After Surgery: A Clinicopathological Study of 80 Cases from a Single Center

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