Immunoexpression Of E-cadherin Research Articles

CLIC4 Function in the Epithelial-Mesenchymal Transition of Epithelial Odontogenic Lesions.

Odontogenic lesions constitute a heterogeneous group of lesions. CLIC4 protein regulates different cellular processes, including epithelial-mesenchymal transition and fibroblast-myofibroblast transdifferentiation. This study analyzed CLIC4, E-cadherin, Vimentin, and α-SMA immunoexpression in epithelial odontogenic lesions that exhibit different biological behavior. It analyzed the immunoexpression of CLIC4, E-cadherin, and Vimentin in the epithelial cells, as well as CLIC4 and α-SMA in the mesenchymal cells, of ameloblastoma (AM) (n = 16), odontogenic keratocyst (OKC) (n = 20), and adenomatoid odontogenic tumor (AOT) (n = 8). Immunoexpressions were categorized as score 0 (0% positive cells), 1 (< 25%), 2 (≥ 25% - < 50%), 3 (≥ 50% - < 75%), or 4 (≥ 75%). Cytoplasmic CLIC4 immunoexpression was higher in AM and AOT (p < 0.001) epithelial cells. Nuclear-cytoplasmic CLIC4 was higher in OKC's epithelial lining (p < 0.001). Membrane (p = 0.012) and membrane-cytoplasmic (p < 0.001) E-cadherin immunoexpression were higher in OKC, while cytoplasmic E-cadherin expression was higher in AM and AOT (p < 0.001). Vimentin immunoexpression was higher in AM and AOT (p < 0.001). Stromal CLIC4 was higher in AM and OKC (p = 0.008). Similarly, α-SMA immunoexpression was higher in AM and OKC (p = 0.037). Correlations in these proteins' immunoexpression were observed in AM and OKC (p < 0.05). CLIC4 seems to regulate the epithelial-mesenchymal transition, modifying E-cadherin and Vimentin expression. In mesenchymal cells, CLIC4 may play a role in fibroblast-myofibroblast transdifferentiation. CLIC4 may be associated with epithelial odontogenic lesions with aggressive biological behavior.

Immunoexpression of E-cadherin in oral potentially malignant disorders, oral squamous cell carcinoma and its correlation with clinicopathological parameters

The most common malignancy of the head and neck region is “oral squamous cell carcinoma” (OSCC) because of its low survival rate and the increasing incidence in some geographic areas. The process of invasion and metastasis, which is noted in most cancers, requires loss of cell-to-cell attachment. It is therefore important to identify a marker that would help in the identification of lesions that would acquire the ability to transform into OSCC. Cell-to-cell adhesion and cell motility are monitored by E-cadherin; its loss is associated with OSCC progression. Early detection, proper analysis, and correct handling of oral potentially malignant disorder (OPMD) are beneficial to preventing its malignant progression. Thus, the purpose of the present study is to identify the expression and determine the role of E-cadherin in OPMD and OSCC.

Immunoexpression of E-cadherin in oral potentially malignant disorders, oral squamous cell carcinoma and its correlation with clinicopathological parameters

The most common malignancy of the head and neck region is “oral squamous cell carcinoma” (OSCC) because of its low survival rate and the increasing incidence in some geographic areas. The process of invasion and metastasis, which is noted in most cancers, requires loss of cell-to-cell attachment. It is therefore important to identify a marker that would help in the identification of lesions that would acquire the ability to transform into OSCC. Cell-to-cell adhesion and cell motility are monitored by E-cadherin; its loss is associated with OSCC progression. Early detection, proper analysis, and correct handling of oral potentially malignant disorder (OPMD) are beneficial to preventing its malignant progression. Thus, the purpose of the present study is to identify the expression and determine the role of E-cadherin in OPMD and OSCC.

Immunohistochemical expression of E-cadherin and N-cadherin in endometrioid endometrial carcinoma and its precursor lesions

ObjectivesEndometrial carcinoma (EC), majority being endometroid endometrial carcinoma (EEC), is the most common invasive gynecological cancer world-wide. Epithelial mesenchymal transition (EMT) is the process that cells undergo to switch from a polarized epithelial phenotype to a motile mesenchymal phenotype. Loss of E-cadherin and expression of N-cadherin are a critical step for development and progression of malignant tumors. In present study we evaluated the immunohistochemical (IHC) expression of E-cadherin and N-cadherin with clinicopathological parameters of EEC and its precursors lesions. MethodsIt was a prospective nested case-control study involving women aged 35–70 years, whose endometrial biopsy were obtained for histological diagnosis. Signed informed consent was obtained before enrolling the women in the study, and the approval to conduct the study was obtained from the institutional ethics committee. The IHC was done to measure the E-cadherin and N-cadherin. ResultsReduced expression of E-cadherin was observed in 69% of cancer and 65% of precancer, however only 32% of normal proliferative endometrium showed reduced E-cadherin expression. N-cadherin expression was observed in 82% of EEC and 81% of precancer cases, while 11% of normal proliferative endometrium showed N-cadherin expression. Statistically significant downregulation of E-cadherin and upregulation of N-cadherin were observed in EEC and precancerous lesions as compared to normal control. ConclusionSince downregulation of E-cadherin was also associated with upregulation of N-cadherin, the integration of immuno-expression of both E-cadherin and N-cadherin might offer a potential therapeutic target for EEC.

Association between epithelial-mesenchymal transition markers, proliferative index, and oral epithelial dysplasia: an immunohistochemical study

This study aimed to correlate the immunoexpression of epithelial-mesenchymal transition markers, vimentin and E-cadherin (E-CAD), and putative markers, podoplanin (PDPN) and osteopontin (OTPN), with the expression of interleukin (IL-6), P53, and Ki-67, and with clinical and histologic parameters of oral epithelial dysplasia (ED). Immunohistochemical reactions were performed in 61 cases of leukoplakia with ED, graded as low-risk (LRED=38) and high-risk (HRED=23) for malignant transformation. Odds ratios (OR) and 95% CI were calculated using logistic regression analysis. High-risk epithelial dysplasia was more frequently observed in non-homogeneous leukoplakia (OR:7.66; CI:1.43-41.04), lesions on the tongue/floor of the mouth (OR:3.37; 95% CI:1.14-9.94), and intense PDPN expression (OR:9.17; CI:1.0-83.77). High-risk epithelial dysplasia exhibited higher Ki-67 expression than LRED (P=.013). Non-continuous PDPN was more likely to exhibit extensive loss of E-CAD than continuous PDPN expression (OR:5.81; CI:1.18-28.55). Intense OTPN was more likely to exhibit intense IL-6 than mild/moderate OTPN expression (OR: 8.06, 95% CI: 1.33-48.85). P53 expression was higher in the intense IL-6 group than in the mild/moderate expression group (P=.021). Our data support the potential of PDPN as a biomarker for malignant transformation owing to its association with HRED and loss of E-CAD expression. Additionally, we demonstrated a possible shared regulatory mechanism between IL-6 and OTPN expression.

Differential expression of Cadherins switch and Caveolin-2 during stages of oral carcinogenesis.

Oral squamous cell carcinoma (OSCC) accounts for 90% of oral malignancies, which may be preceded by oral potentially malignant disorders (OPMDs). Cancer progression involves the downregulation of epithelial markers (E-cadherin) and the upregulation of mesenchymal markers (N-cadherin), which together characterise the epithelial-mesenchymal transition (EMT). Furthermore, caveolin can act on cell adhesion and migration events that regulate the expression of the E-cadherin/α-β-catenin complex, thus favouring aggressive biological behaviour. This study aimed to analyse the immunoexpression of E-cadherin, N-cadherin and caveolin-2 at different stages of oral carcinogenesis to identify reliable biomarkers to predict malignant potential. Expressions of E-cadherin and N-cadherin in 14 normal oral mucosae (NOM), 14 OPMD and 33 OSCC specimens were evaluated using immunohistochemistry. Clinicopathological parameters were also assessed. E-cadherin immunoexpression was significantly reduced during the progression of oral carcinogenesis (P = 0.0018). N-cadherin immunoexpression did not show any statistical differences between these groups. However, a representative number of N-cadherin-positive OSCC cases did not express E-cadherin. The expression of caveolin-2 increased significantly with the progression of the disease, from NOM to OSCC (P value: 0.0028). These findings indicate that cadherin switch and caveolin-2 immunoexpression may be regulatory events in oral carcinogenesis.

Immunoexpression of E-cadherin, CD44 and Claudin 7 in gastric adenocarcinomas.

Gastric adenocarcinomas represent frequent malignant tumors in the digestive tract, with a high and constant mortality rate in last decades. The disturbance of the adhesion molecules expression, which normally is essential in maintaining epithelial homeostasis, has a critical role in the initiation and progression of tumors. In this study, we analyzed the immunoexpression of E-cadherin, cluster of differentiation 44 (CD44), and Claudin 7 in 58 cases of gastric adenocarcinomas, in relation to the histopathological parameters of the lesions' aggressiveness. Increased E-cadherin immunoexpression was observed in tubular adenocarcinomas, those of low grade and in stages I-III. CD44 presented high scores in discohesive, hepatoid, tubular, and tubulopapillary adenocarcinomas, those of high grade and in advanced stages. Claudin 7 associated increased scores for tubular, tubulopapillary and micropapillary tumors, those of low grade and mainly in stage I. The markers used in the study can be useful for assessing the aggressiveness of gastric adenocarcinomas, in the context of specific adapted therapy.

The role of cell adhesion molecules in the progression of bladder urothelial carcinomas.

Alteration of the intercellular adhesion system plays an essential role in the initiation and progression of bladder carcinomas. We followed the immunoexpression of adhesion molecules, E-cadherin, β-catenin and Claudin-1, in relation to the histopathological grade and the pT category in a number of 50 urothelial carcinomas of the bladder, based on a final staining score (FSS), calculated on the basis of reaction intensity and labeled cells number. E-cadherin immunoexpression was identified in the membrane of tumor cells, low FSS being associated with invasive high-grade carcinomas. β-catenin reactions were membranous in the case of low-grade noninvasive carcinomas and predominantly cytoplasmic and nuclear in the case of high-grade invasive ones, for which high FSS were associated. Claudin-1 was identified at the membrane level, the high FSS values being more frequent in the case of high-grade invasive carcinomas, although there were no significant statistical associations. Loss of E-cadherin expression and the associated positive linear relation of β-catenin and Claudin-1 indicate the usefulness of the analyzed markers in identifying the invasive aggressive phenotype of urothelial bladder carcinomas.

Potentiated action on the progression of OSMF by hypoxia mediated signaling pathway by the epithelial mesenchymal transition and angiogenic apparatus.

Epithelial-mesenchymal transition (EMT) is a complex process, in which epithelial cells acquire the characteristics of invasive mesenchymal cells. EMT has been implicated in cancer progression and metastasis as well as the formation of many tissues and organs during development. The aim of the study was to ascertain the role of hypoxia-mediated signaling pathways influencing EMT and angiogenesis in progression of oral submucous fibrosis (OSMF). Evaluation of the immunoexpression of alpha-smooth muscle actin (α-SMA), E-cadherin, vimentin, and factor VIII receptor antigen in OSMF and oral squamous cell carcinoma (OSCC) arising from OSMF was done. Differences between the different variables were analyzed using ANOVA test and Pearson's Chi-square test, and Mann-Whitney test was also calculated. The mean α-SMA positive myofibroblasts increased from Group 1 (OSMF) to Group 2 (OSCC), especially those in the deeper connective tissue stroma. The mean labeling index of vimentin and mean vessel density immunoexpression was more in Group 2 (OSCC) as compared to Group 1 (OSMF). Mean α-SMA correlated negatively with E-cadherin expression and positively with vimentin and factor VIII immunoexpression. E-cadherin expression correlated negatively with factor VIII and positively with Vimentin expression. The molecular mechanisms responsible for the development of OSCC in patients with OSMF require unification of multiple progressive pathogenetic mechanisms involved in the progression of the disease.

Gymnemic Acid Ameliorates Pancreatic β-Cell Dysfunction by Modulating Pdx1 Expression: A Possible Strategy for β-Cell Regeneration.

Endogenous pancreatic β-cell regeneration is a promising therapeutic approach for enhancing β-cell function and neogenesis in diabetes. Various findings have reported that regeneration might occur via stimulating β-cell proliferation, neogenesis, or conversion from other pancreatic cells to β-like cells. Although the current scenario illustrates numerous therapeutic strategies and approaches that concern endogenous β-cell regeneration, all of them have not been successful to a greater extent because of cost effectiveness, availability of suitable donors and rejection in case of transplantation, or lack of scientific evidence for many phytochemicals derived from plants that have been employed in traditional medicine. Therefore, the present study aims to investigate the effect of gymnemic acid (GA) on β-cell regeneration in streptozotocin-induced type 1 diabetic rats and high glucose exposed RIN5-F cells. The study involves histopathological and immunohistochemical analysis to examine the islet's architecture. Quantitative polymerase chain reaction (qPCR) and/or immunoblot were employed to quantify the β-cell regeneration markers and cell cycle proliferative markers. The immunoexpression of E-cadherin, β-catenin, and phosphoinositide 3-kinases/protein kinase B were significantly increased in GA-treated diabetic rats. On the other hand, treatment with GA upregulated the pancreatic regenerative transcription factor viz. pancreatic duodenal homeobox 1, Neurogenin 3, MafA, NeuroD1, and β-cells proliferative markers such as CDK4, and Cyclin D1, with a simultaneous downregulation of the forkhead box O, glycogen synthase kinase-3, and p21cip1 in diabetic treated rats. Adding to this, we noticed increased nuclear localization of Pdx1 in GA treated high glucose exposed RIN5-F cells. Our results suggested that GA acts as a potential therapeutic candidate for endogenous β-cell regeneration in treating type 1 diabetes.

Epithelial-mesenchymal transition modulates lower lip carcinogenesis and promotes cancer progression

ObjectiveTo investigate and compare the immunoexpression of E-cadherin, α-SMA, TGF-β and Snail proteins between cases of actinic cheilitis (AC) and squamous cell carcinoma of the lower lip (LLSCC). Study designE-cadherin, α-SMA, TGF-β and Snail antibody immunostaining was analyzed semiquantitatively in 54 AC cases and in 49 LLSCCs. The cases were classified as low and high expression for analysis of the association with clinicopathological variables and overall survival (OS) and disease-free survival (DFS) rates. ResultsHigh expression of E-cadherin (cytoplasmic) (p = 0.001) and α-SMA (p < 0.001) was identified in LLSCCs, as well as low expression of TGF-β in LLSCCs (p < 0.001) and high expression of Snail in AC cases (p = 0.006). Survival analysis revealed that high expression of α-SMA at the tumor invasion front, a network immunostaining pattern of this protein, and high expression of TGF-β in tumor buds were significantly associated with poor OS (p < 0.05). There was a higher risk of death among LLSCC cases with high expression of α-SMA (HR = 5.90, p = 0.03). High expression of TGF-β in tumor buds was significantly associated with poor DFS (p = 0.007) and with a higher risk of negative outcomes for DFS (HR = 4.44, p = 0.014). ConclusionsThe present results suggest the potential involvement of dysregulation of proteins associated with epithelial-mesenchymal transition in the modulation of lip carcinogenesis and greater aggressiveness of LLSCC.

Demographic study of 366 cases of oral leukoplakia and immunohistochemical analysis - An institutional study.

Background:It has been reported that oral squamous cell carcinoma (OSCC) is associated with the presence of potentially malignant disorders (PMDs) in 15%–48% of cases. Among PMDs, oral leukoplakia (OL) is the most common, with 16%–62% of cases associated with OSCC. Hence, in the present study, we have analyzed demographic data and re-evaluated immunohistochemical (IHC) data of OL cases and aimed to correlate the clinical, histopathological and IHC aspects of OL.Materials and Methods:The data of histopathologically diagnosed cases of OL were retrieved from the archives. These data were further evaluated for age, gender, duration, site, size, side, habits, clinical staging and histopathological grading. IHC re-evaluation of OL tissues was done using epithelial cadherin (E-cadherin), n = 20; human MutL homolog 1 (hMLH1), n = 30; CD1a (n = 30); vimentin (n = 30); Ki-67 (n = 30); heat shock protein-70 (HSP-70), n = 30; p16INK4, n = 20; and mucin-1 (MUC1), n = 30. All the results and observations were subjected to descriptive statistical analysis.Results:The male: female ratio was 7.5:1; right side and buccal mucosa were more commonly affected. The duration of the lesion ranged from 1 to 30 years. One hundred and twelve patients were habituated to tobacco chewing, while 171 patients came with a combined habit of smoke and smokeless tobacco usage. Clinically, most of the lesions were of stage 2 while histopathologically they were of mild dysplasia. There was a decrease in the immunoexpression of E-cadherin, hMLH1 and CD1a, while there was an increase in the immunoexpression of vimentin, Ki-67, HSP-70, MUC1 and p16INK4.Conclusion:The study of different biomarkers such as cytoplasmic, membranous and nuclear in OL will help in better understanding and application of a reliable marker for diagnostic and prognostic purpose.

Insights into molecular pathways of endometriosis and endometriosis-related ovarian carcinoma.

Background: Endometriosis is a benign estrogen-dependent gynecological disease involving components of the female genital tract (uterus, Fallopian tubes, ovaries, large, round, and utero-sacral ligaments) and intra- and extraperitoneal regions. Since the moment of its etiopathogeny has been identified, the intrinsic capacity of endometriosis malignant transformation has been hypothesized. Patients, Materials and Methods: Our study included a total number of 50 patients diagnosed with endometriosis (31 cases) and endometriosis-related ovarian carcinoma (EOC) (19 cases). A clinicopathological and immunohistochemical study directed towards the detection of atypical transition lesions and the similitudes in epithelial–mesenchymal transition (EMT) phenomenon [E-cadherin/β-catenin/cytokeratin 18 (CK18)], apoptosis [B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X (Bax)], and hormonal dynamics mirrored by the immunoexpression of estrogen receptor (ER) and progesterone receptor (PR) in endometriosis and EOC glands and stroma has been performed. Results: Our study showed a higher immunoexpression of CK18 and E-cadherin in endometriosis than in neoplastic counterparts, while β-catenin had a stronger immunoexpression in tumors compared with endometriotic areas, with statistically significant differences between the studied groups. Bcl-2/Bax higher rate in endometriosis had a statistically significant association to a more aggressive tumor behavior (p=0.020). ER immunoexpression was stronger in endometriosis, with less negative scores compared to EOC, while PR immunoexpression was stronger in endometriosis, with a lower percent of negative scores compared to EOC. PR immunostaining was correlated to ovarian location of endometriosis (p=0.004) and tumor grade of EOC (p=0.027). Stromal ER and PR immunoexpression has been significantly lower in endometriosis in comparison to tumor stroma (p=0.001) and PR stromal immunoexpression had been higher in more differentiated tumors compared to less differentiated types (p=0.005). Conclusions: Our study supports that endometriosis is a precursor of EOC by the identification and the coexistence of both lesions in the investigated cases, the identification of intermediate lesions, as well as the expression of EMT immunomarkers, along with apoptosis and steroid receptors immunoexpression.

Association of CDH1 -160 C → A and -347 G→ GA polymorphisms and expression of E-cadherin and gastric cancer: A case-control study.

The loss of function of the E-cadherin (CDH1) gene with -160 C→A and -347 G→GA polymorphisms is regarded as a critical step for gastric cancer. It was aimed to investigate possible association of these polymorphisms and immunoexpression of E-cadherin with gastric cancer. Gastric adenocarcinoma patients and individuals with benign gastric pathologies were included in this case-control study. Demographic data and pathological findings were recorded. Immunohistochemical staining of E-cadherin expression and analysis of -160 C→A and -347 G→GA polymorphisms were done. Differences between allele frequencies of -160 C→A and -347 G→GA polymorphisms and expression of E-cadherin were the primary outcomes. There were 78 gastric cancer patients (Group A) and 113 individuals with benign gastric pathologies (Group B). The number of male patients and mean age were higher in Group A (p <0.001). -160 C→A and 347 G→GA polymorphisms and their allelic distributions showed no difference between the groups (p> 0.05 for all). There was a significant association between -160 C→A polymorphism and grade of E-cadherin expression (p= 0.013). There were no significant differences between survival rates with -160 C→A, 347 G→GA and intensity of E-cadherin expression (p> 0.05 for all). There was no significant association between -160 C→A and -347 G→GA polymorphisms and gastric cancer. There was no impact of E-cadherin expression on tumoral features and survival in gastric cancer. -160 C→A polymorphism may influence the expression of E-cadherin in gastric cancer.

Possible Role of TGF-β1, MMP-2, E-CAD, β-Catenin and Antioxidants in Pathogenesis of Placenta Accreta

Objectives Placenta accreta (PA) can be life-threatening due to postpartum hemorrhage and may lead to cesarean hysterectomy. We investigated the expression of Matrix metalloproteinase-2 (MMP-2), β-catenin, E-cadherin (E-CAD), transforming growth factor β1 (TGF-β1), glutathione peroxidase 1 (GPx-1), reduced glutathione (GSH) and superoxide dismutase (SOD) in PA compared to controls to determine if alterations may contribute to PA. Materials and methods: Twenty six PA and 31 controls were evaluated immunohistochemically for expression of MMP-2, β-catenin and E-CAD on villous and extravillous trophoblasts. TGF-β1 and GPx-1 mRNA levels were evaluated by rt-PCR. We measured biochemical levels of GSH and SOD. Results: Significant increases of MMP-2 immunoexpression, GPx-1 mRNA, SOD and GSH levels, decreases in immunoexpression of E-CAD and β-catenin and TGF-β1 mRNA were found in PA. Conclusion: These findings suggest that loss of cell-cell adhesion and increased antioxidants level may have a role in PA.

Prediction of metastasis in oral squamous cell carcinoma through phenotypic evaluation and gene expression of E-cadherin, β-catenin, matrix metalloproteinase-2, and matrix metalloproteinase-9 biomarkers with clinical correlation.

CONTEXT:Controversies prevail regarding the true predictive role of epithelial–mesenchymal transition (EMT) biomarkers in metastasis of oral squamous cell carcinoma (OSCC). There is also limited research carried on till date wherein the protein and gene expression of EMT biomarkers have been investigated simultaneously in the Indian population.AIM:The aim of this study was to assess the gene expression and quantitative protein expression of EMT biomarkers using conventional method and MATLAB software and to determine if there is any difference in the expression between metastatic and nonmetastatic OSCCs with clinicopathologic correlation.SETTINGS AND DESIGN:Twenty metastatic and nonmetastatic OSCC tissue sections each were obtained from department archives. Gene expression and quantified protein expression of EMT markers were done and correlated with clinical parameters.SUBJECTS AND METHODS:Sections immunostained for EMT biomarkers were evaluated using semi-quantitative and quantitative (MATLAB) methods. Gene expression using semi-quantitative reverse transcriptase–polymerase chain reaction was done. These findings were correlated with clinical parameters.STATISTICAL ANALYSIS USED:Pearson's Chi-square test, Student's t-test, and univariate logistic regression analysis were performed using SPSS software.RESULTS:The low immunoexpression of E-cadherin and β-catenin and the high expression of matrix metalloproteinase (MMP)-2 and MMP-9 correlate with Stages III and IV showing high metastatic risk. Furthermore, the upregulated MMP-2 and MMP-9 gene expressions in advanced clinical stages of OSCC have high metastatic potential.CONCLUSIONS:This study is the first of its kind to employ texture and color segmentation in MATLAB to objectively assess the protein expression of EMT biomarkers. This research is instrumental in studying the protein and gene expressions of EMT markers with clinical correlation.

TWIST AND E-CADHERIN IMMUNOEXPRESSION IN ACTINIC CHEILITES

Objective To investigate the immunohistochemical expression of TWIST and E-cadherin in actinic cheilitis (AC). Study Design The immunohistochemical expression of TWIST and E-cadherin was analyzed in 86 cases of AC with varying degrees of epithelial dysplasia. The epithelial immunostaining was semi-quantitatively evaluated according to the scores: (1) 75% positive cells. Median comparisons of E-cadherin and TWIST expression scores according to histologic grade were performed using the nonparametric Mann-Whitney test. Results Analysis of TWIST and E-cadherin expression in the AC epithelium revealed membrane and cytoplasmic immunoreactivity for E-cadherin in all epithelial layers except in the keratin layer. For TWIST, nuclear and cytoplasmic immunoreactivity were observed in all epithelial layers except in the keratin layer. No statistically significant differences were observed in the medians of the E-cadherin and TWIST scores in relation to the histologic grade of the AC (P > .05). Conclusions The results of this study suggest that the high immunoexpression of TWIST and E-cadherin has been observed in cases of AC; however, these proteins do not appear to be associated with the varying degrees of epithelial dysplasia in the analyzed cases.

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

ABSTRACT 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.

OVEREXPRESSION OF TWIST AND REDUCED E-CADHERIN EXPRESSION ARE ASSOCIATED WITH POOR BIOLOGICAL BEHAVIOR IN LOWER LIP SQUAMOUS CELL CARCINOMA: AN IMMUNOHISTOCHEMICAL STUDY

Objectives This study aimed to evaluate the immunoexpression of Twist and E-Cadherin in 59 lower lip squamous cell carcinomas (LLSCC) and to verify their relationship with clinical and histopathological parameters (tumor size, regional lymph node metastasis, clinical stage, outcome, recurrence and tumor histological grade. Possible correlations between these two proteins were also evaluated. Findings Higher expression of E-Cadherin was observed in LLSCCs classified in early clinical stages (stage I) (p Conclusion The results of this study suggest the potential involvement of Twist and E-Cadherin proteins in the modulation of events related to tumor progression and the poor prognosis of LLSCC.

Gestational trophoblastic neoplasms (GTNs) do not display epithelial-to-mesenchymal transition (EMT) features.

Although epithelial-to-mesenchymal transition (EMT) has been described in the development of complete hydatidiform moles and the invasion of the maternal decidua by trophoblasts during normal human placentation, its implication in gestational trophoblastic neoplasm (GTN) without villi is totally unknown. We studied the immunoexpression of EMT transcription factors (TWIST1, ZEB1, ZEB2), E-cadherin, and vimentin in 18 trophoblastic tumors and pseudo-tumors. Weak nuclear TWIST1 immunostaining was seen in 5% to 10% of all trophoblastic cells, without ZEB1 and ZEB2 nuclear staining. Trophoblastic cells did not express vimentin, and the expression of E-cadherin was maintained in all cases, indicating the absence of EMT features in GTN.