Role of podoplanin expression in deciding the invasive potential of ameloblastoma – A retrospective IHC study

Ganvir, Sindhu M; Khobragade, Pratima G; Bamane, Swati A.; Kumavat, Ramnivas; Dalmia, Amit

doi:10.1016/j.jobcr.2016.07.001

Cited by 5 publications

(3 citation statements)

References 21 publications

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“…The MDM2 positive nuclei were found predominantly in peripheral ameloblast-like cells and it was also seen in central stellate reticulum-like cells suggesting that the peripheral cells have an anti-apoptotic and proliferative phenotype than the central cells. This also, in accordance with other study stated that the proliferative activity of ameloblastomas is nearly limited to the outer layer of the epithelial islands (44) .…”

Section: Discussionsupporting

confidence: 93%

Immunohistochemical Expression of Cortactin, E-Cadherin, and MDM2 Proteins in Solid Ameloblastoma versus Odontogenic Keratocyst (An immunohistochemical study)

et al. 2019

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Purpose:The extent of invasion can be analyzed by the expression and production of various genes and proteins by lesional cells. However, current clinical parameters lack the potential to predict the neoplastic behavior in solid ameloblastoma (SAB) and odontogenic keratocyst (OKC). Cortactin, an F-actin binding protein, overexpression has been correlated with advanced clinic pathological stage and poor prognosis in several tumors. E-cadherin belongs to the classical cadherins which. Low E-cadherin expression correlated to aggressive, poorly differentiated, high-grade carcinomas and low patient survival. Human-murine double minute 2 (MDM2), contributes to the promotion of cell growth, survival, invasion, and therapeutic resistance, overexpression of MDM2 has been observed in various human cancers and can contribute to genomic instability, thus, further promoting tumorigenesis. The purpose of this work was to investigate the role of Cortactin, E-Cadherin, MDM2 proteins expression in SAB and OKC and correlate the expression of these markers with the aggressive behavior of these tumors. Material and method: 10 case of solid ameloblastoma with its different histologic variants and 10 cases of the keratocystic odontogenic tumor were collected as paraffin embedded blocks. An immunohistochemical investigation using, Cortactin, E-Cadherin, and MDM2 antibodieswere done for all specimens. Results: The mean area percent of immunoexpression of Cortactin was greatest in SAB while, the mean area percent of immunoexpression of E-Cadherin, MDM2 were greatest in OKC. Conculsion:According to the current study, the absence of any significant differences between AB and OKC indicate the neoplastic and aggressive nature of OKC similar to AB.

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Section: Discussionsupporting

confidence: 93%

Immunohistochemical Expression of Cortactin, E-Cadherin, and MDM2 Proteins in Solid Ameloblastoma versus Odontogenic Keratocyst (An immunohistochemical study)

et al. 2019

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“…In this study, there was no difference in the expression of CD34 and VEGFR3 in follicular and plexiform of ameloblastoma, but in the study of Ganvir et al 24 the expression of podoplanin associated with the cell type and its arrangement was reported in ameloblastoma.…”

Section: Discussioncontrasting

confidence: 62%

Expression of CD34, VEGFR3 and eosinophil density in selected odontogenic tumors- a pilot study

ArabSheibani

Seifi

Salehinejad

et al. 2020

Journal of Oral Biology and Craniofacial Research

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Background: Limited statistically and clinically significant studies have been down on connective tissue factors in the odontogenic tumors. Therefore, the aim of this study was to determine the biological behavior of two selected epithelial odontogenic tumors (Ameloblastoma and Adenomatoid odontogenic tumor) by detecting CD34, VEGFR3 and eosinophil densities. Methods: In this cross-sectional study, paraffin blocks including 20 cases of ameloblastoma and 20 (AOT), were selected. Totally, 4 sections were prepared for hematoxylin-eosin, Congo red staining, immunohistochemistry with CD34 and VEGFR3. Expression of VEGFR3, CD34 and lymphatic, blood vessels and eosinophil densities was examined. Results: The mean of blood, lymphatic vessels and eosinophils densities in ameloblastoma were 14.9 ± 6.4, 4.4 ± 2 and 3.2 ± 2.7, respectively; and in AOT, they were 8.9 ± 3.4, 3.6 ± 1.3 and 1.2 ± 07, respectively. There was a significant difference in eosinophils and blood vessels densities between the two lesions (p = 0.005; p = 0.003). By increasing the density of eosinophils, the density of the blood vessels increased in both lesions (r = 0.539, P = 0.001) There was no positive relationship between eosinophils and lymphatic vessels densities in the two above mentioned odontogenic lesions (p = 0.288, R = 0.191) Conclusion: It can be suggested that tumor angiogenesis and eosinophil densities may play a more effective role than lymphangiogenesis in local invasive behavior of ameloblastoma rather than AOT.

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“…In addition, location and distribution of expressed protein are emerged in various parts of tissue. For instance, it was reported significant expression of podoplanin in invasive odontogenic tumors by immunohistochemistry technique that emphasized the diagnostic role of this marker on neoplastic behavior [ 9 ]. Also, overexpression of MDM2 and p53 was demonstrated in solid multicystic ameloblastoma (SMA) and keratocystic odontogenic tumor (KOT) as IHC markers [ 10 ].…”

Section: Diagnostic Markers In Odontogenic Tumorsmentioning

confidence: 99%

New diagnostic molecular markers and biomarkers in odontogenic tumors

et al. 2021

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Odontogenic tumors comprised of complex heterogeneous lesions that diverse from harmatomas to malignant tumors with different behavior and histology. The etiology of odontogenic tumors is not exactly determined and pathologists deal with challenges in diagnosis of odontogenic tumors because they are rare and obtained experiences are difficult to evaluate. In this study, we describe immunohistochemical and molecular markers in diagnosis of odontogenic tumors besides advanced diagnostic technique. Immunohistochemical features of odontogenic tumors beside the clinical features and radiological finding can help us to determine the correct diagnosis. Although these markers are neither specific nor sensitive enough, but analysis of gene expression provides definitive confirmation of diagnosis. In addition, “-omics” technology detected specific molecular alternation associated with etiology such as genomics, epigenomics, transcriptomics, proteomics and metabolomics. The post transcriptional events such as DNA methylation and chromatin remodeling by histone modification affect the changes in epigenome. Furthermore, non-coding RNAs like micro-RNAs, long noncoding RNA (lncRNA) and small non-coding RNA (snoRNA) play regulatory role and impact odontogenesis. Molecular marker propose their potential role in etiopathogenesis of odontogenic tumors and suitable candidate in diagnostic, prognostic and therapeutic approaches in addition to patient management. For future evaluations, organoid represents in vitro tumor model-study for tumor behavior, metastasis and invasion, drug screening, immunotherapy, clinical trial, hallmarks association with prognosis and evolution of personalized anti-cancer therapy. Moreover, organoid biobank help us to check genetic profile. We think more investigation and studies are needed to gain these knowledges that can shift therapeutic approaches to target therapy.

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Role of podoplanin expression in deciding the invasive potential of ameloblastoma – A retrospective IHC study

Cited by 5 publications

References 21 publications

Immunohistochemical Expression of Cortactin, E-Cadherin, and MDM2 Proteins in Solid Ameloblastoma versus Odontogenic Keratocyst (An immunohistochemical study)

Immunohistochemical Expression of Cortactin, E-Cadherin, and MDM2 Proteins in Solid Ameloblastoma versus Odontogenic Keratocyst (An immunohistochemical study)

Expression of CD34, VEGFR3 and eosinophil density in selected odontogenic tumors- a pilot study

New diagnostic molecular markers and biomarkers in odontogenic tumors

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