Abnormal distribution of E-cadherin and β-catenin in different histologic types of cancer of the uterine cervix

Rodríguez-Sastre, María Alexandra; González‐Maya, Leticia; Delgado, Ricardo; Lizano, Marcela; Tsubaki, Gerardo; Mohar, Alejandro; García‐Carrancá, Alejandro

doi:10.1016/j.ygyno.2004.12.062

Cited by 63 publications

(87 citation statements)

References 34 publications

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“…These results are similar to those of Rodriguez-Sastre et al 33 , who found that membrane E-cadherin exhibited a tendency to disappear in 40% of SILs.…”

Section: Discussionsupporting

confidence: 92%

Progressive loss of E-cadherin immunoexpression during cervical carcinogenesis

Cavalcante

Sampaio²,

Filho³

et al. 2014

Acta Cir. Bras.

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Brazil. Conception, design, intellectual and scientific content of the study; critical analysis; final approval of the manuscript. ABSTRACT PURPOSE:To investigate E-cadherin immunoexpression during cervical carcinogenesis. METHODS:We assessed the immunohistochemical expression of E-cadherin in squamous intraepithelial lesions (SIL -52 cases), squamous cell carcinoma (SCC) of the uterine cervix (23 cases) and also in eight cases of cervicitis. RESULTS:The results show very different E-cadherin membrane expression levels when cervicitis (88%), SILs (73%) and SCC (17%) were compared. In SILs, higher E-cadherin loss was seen in less differentiated cells in the basal third of the epithelium. This study suggests that the absence of E-cadherin expression in the membrane is a molecular event that is observed more often in SCC of the uterine cervix than in SILs or cervicitis.CONCLUSIONS: E-cadherin is an essential molecule during the process of cervical carcinogenesis and in this context exhibits a different expression pattern according to the epithelial thickness layer.

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“…These results are similar to those of Rodriguez-Sastre et al 33 , who found that membrane E-cadherin exhibited a tendency to disappear in 40% of SILs.…”

Section: Discussionsupporting

confidence: 92%

Progressive loss of E-cadherin immunoexpression during cervical carcinogenesis

Cavalcante

Sampaio²,

Filho³

et al. 2014

Acta Cir. Bras.

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“…6,7,24 Interestingly, ECAD nuclear distribution correlates with lymph node and liver metastases in human pancreatic endocrine tumors. 6 Nuclear labeling was not observed in any of the canine round cell tumors in this study.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical Expression of E-cadherin Does Not Distinguish Canine Cutaneous Histiocytoma From Other Canine Round Cell Tumors

Ramos‐Vara

Miller

2011

Vet Pathol

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Immunohistochemistry for E-cadherin (ECAD) has been used to distinguish canine cutaneous histiocytoma from other leukocytic neoplasms (''round cell tumors''). To determine the specificity of this test, 5 types of canine cutaneous round cell tumors were evaluated for immunohistochemical expression of ECAD. Tumors of all 5 types had variable cytoplasmic, plasma membrane, and/ or paranuclear ECAD expression: All 13 cutaneous histiocytomas were ECADþ; all but 1 of 14 mast cell tumors expressed ECAD; 10 of 12 epitheliotropic lymphomas reacted with E-cadherin antibody; of 72 plasmacytomas, 54 were ECADþ; and 5 of 5 histiocytic sarcomas were positive. Conclusions based on these results include the following: First, immunoreactivity for ECAD is not limited to leukocytes of cutaneous histiocytoma; second, antibody to ECAD also labels neoplastic cells in most mast cell tumors, plasmacytomas, cutaneous histiocytic sarcomas, and epitheliotropic lymphomas; third, although most histiocytomas have membranous ECAD expression, the immunoreactivity varies among round cell tumors and is frequently concurrent in different cellular compartments; fourth, the distinctively paranuclear ECAD expression pattern in epitheliotropic lymphomas might distinguish them from other round cell tumors; and, fifth, ECAD should be used with other markers (eg, MUM1 for plasmacytomas, KIT for mast cell tumors, CD3 and CD79a for lymphomas) to distinguish among canine round cell tumors.

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“…Nevertheless, Uren et al (54) observed that Wnt was required for transformation of cultured keratinocytes expressing HPV. Analysis of cervical tumors commonly showed heightened levels of WIF1 silencing in cervical cancer b-catenin, clearly suggestive of dysregulation of Wnt/b-catenin signaling (55,56). High b-catenin immunoreactivity in cervical adenocarcinoma is associated with reduced disease-free survival (57), and altered b-catenin expression has been documented in cervical SCC as well (55).…”

Section: Discussionmentioning

confidence: 99%

“…Analysis of cervical tumors commonly showed heightened levels of WIF1 silencing in cervical cancer b-catenin, clearly suggestive of dysregulation of Wnt/b-catenin signaling (55,56). High b-catenin immunoreactivity in cervical adenocarcinoma is associated with reduced disease-free survival (57), and altered b-catenin expression has been documented in cervical SCC as well (55). Considering the role of WIF1 as an antagonist of Wnt/ b-catenin signaling, epigenetic silencing of its gene would result, at least in part, in dysregulation of this oncogenic mechanism.…”

Section: Discussionmentioning

confidence: 99%

WIF1 is a frequent target for epigenetic silencing in squamous cell carcinoma of the cervix

et al. 2011

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Aberrant activation of the Wnt/b-catenin signaling axis is a prominent oncogenic mechanism in numerous cancers including cervical cancer. Wnt inhibitory factor-1 (WIF1) is a secreted protein that binds Wnt and antagonizes Wnt activity. While the WIF1 gene is characterized as a target for epigenetic silencing in some tumor types, WIF1 expression has not been examined in human cervical tissue and cervical cancer. Here, we show that WIF1 is unmethylated and its gene product is expressed in normal cervical epithelium and some cultured cervical tumor lines. In contrast, several cervical cancer lines contained dense CpG methylation within the WIF1 gene, and expression of both WIF1 transcript and protein was restored by culturing cells in the presence of the global DNA demethylating agent 5-aza-2#-deoxycytidine. Using single-molecule MAPit methylation footprinting, we observed differences in chromatin structure within the WIF1 promoter region between cell lines that express and those that do not express WIF1, consistent with transcriptional activity and repression, respectively. The WIF1 promoter was aberrantly methylated in $60% (10 of 17) high-grade highly undifferentiated squamous cell cervical tumors examined, whereas paired normal tissue showed significantly lower levels of CpG methylation. WIF1 protein was not detectable by immunohistochemistry in tumors with quantitatively high levels of WIF1 methylation. Of note, WIF1 protein was not detectable in two of the seven unmethylated cervical tumors examined, suggesting other mechanisms may contribute WIF1 repression. Our findings establish the WIF1 gene as a frequent target for epigenetic silencing in squamous cell carcinoma of the cervix. Background

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Abnormal distribution of E-cadherin and β-catenin in different histologic types of cancer of the uterine cervix

Cited by 63 publications

References 34 publications

Progressive loss of E-cadherin immunoexpression during cervical carcinogenesis

Progressive loss of E-cadherin immunoexpression during cervical carcinogenesis

Immunohistochemical Expression of E-cadherin Does Not Distinguish Canine Cutaneous Histiocytoma From Other Canine Round Cell Tumors

WIF1 is a frequent target for epigenetic silencing in squamous cell carcinoma of the cervix

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