Cell proliferative activity and expression of cell‐cell adhesion factors (E‐cadherin, α‐, β‐, and γ‐catenin, and p120) in sarcomatoid renal cell carcinoma

Kuroiwa, Kentaro; Konomoto, Tatsuo; Kumazawa, Joichi; Naito, Seiji; Tsuneyoshi, Masazumi

doi:10.1002/jso.1082

Cited by 20 publications

(14 citation statements)

References 25 publications

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“…Interestingly, we noted a significant difference in staining between type 1 and type 2 papillary renal cell carcinomas, indicating that E-cadherin can be used as an additional marker for the separation of these two biologically distinct tumor entities. The lack of Ecadherin immunoreactivity in the sarcomatoid tumor components of 13 otherwise conventional tumors in our series confirms the report by Kuroiwa et al, 53 who showed a decrease in E-cadherin immunoreactivity in the sarcomatoid compared to the better differentiated components in their study of 11 cases of sarcomatoid renal cancers.…”

Section: Discussionsupporting

confidence: 92%

Expression of MUC1 (EMA) and E-cadherin in renal cell carcinoma: a systematic immunohistochemical analysis of 188 cases

et al. 2004

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MUC1 (epithelial membrane antigen) is a membrane-associated mucin known to interfere with both cell-cell and cell-matrix adhesions. Overexpression has been associated with poor prognosis in a variety of cancers. We investigated the expression of MUC1 (using two different antibodies, MA695 and E29) and E-cadherin in renal cell carcinomas (137 conventional, 23 chromophobe, 20 papillary, and eight unclassified tumors) with respect to diagnostic and prognostic significance using a tissue microarray technique. Immunoreactivity was correlated with histological subtype, pT-stage, and grade using the v 2 test or the Fisher's exact test, respectively. Impact on disease-free survival was analyzed using the Kaplan-Meier method and the log-rank test. Immunoreactivity of more than 10% of cancer cells with MA695, E 29, and E-cadherin antibodies was found in 112/133 (84%), 86/133 (65%), and 7/131 (5%) conventional, 20/22 (91%), 19/22 (86%), and 21/22 (95%) chromophobe, 13/20 (65%), 8/20 (40%), and 3/20 (15%) papillary as well as 5/8 (63%), 5/8 (63%), and 4/8 (50%) unclassified carcinomas, respectively. The two different MUC1 antibodies yielded comparable staining results. A diffuse cytoplasmic staining pattern for MUC1 was found exclusively in chromophobe carcinomas, whereas conventional and papillary subtypes showed predominantly membranous staining (Po0.0001). Regarding papillary carcinomas, MUC1 was predominantly associated with type 1 (P ¼ 0.0001), and E-cadherin with type 2 (P ¼ 0.049) tumors. The cellular staining pattern of MUC1 in conventional tumors was related to pT-stage (P ¼ 0.002) and tumor grade (P ¼ 0.001): Low-stage (pT1/pT2) and grade (G1/G2) tumors showed a predominantly apical membranous staining, high-stage (pT3a/pT3b) and grade (G3/G4) tumors a predominantly circumferential membranous staining (with or without additional diffuse cytoplasmic immunoreactivity), which, in the conventional subtype, was associated with poor prognosis (Po0.0001). In conclusion, MUC1 and E-cadherin are diagnostically and prognostically useful markers in renal tumor pathology, especially when cellular staining patterns are considered. Keywords: kidney; cancer; MUC1; EMA; E-cadherin; differential diagnosis; prognosisMucins are high-molecular-weight (4200 kDa) glycoproteins with oligosaccharides attached to an apomucin protein backbone (core peptide) by Oglycosidic linkage.

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Section: Discussionsupporting

confidence: 92%

Expression of MUC1 (EMA) and E-cadherin in renal cell carcinoma: a systematic immunohistochemical analysis of 188 cases

et al. 2004

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“…In mouse model of β-cell tumors of the pancreas, e-cadherin loss is a causal prerequisite for progression from adenoma to invasive carcinomas (32). In addition to many reports about e-cadherin expression in cancer by others, we have reported e-cadherin expression in prostate cancer (21) and renal cancer (33,34) and the methylation of e-cadherin promoter in bladder cancer (35). then, the relationship between entpD6 and e-cadherin Figure 4.…”

Section: Discussionmentioning

confidence: 73%

Ectonucleoside triphosphate diphosphohydrolase 6 expression in testis and testicular cancer and its implication in cisplatin resistance

Tada

Yokomizo

Shiota³

et al. 2011

Oncol Rep

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Abstract. the development of resistance to cisplatin during treatment of testicular cancer constitutes a major obstacle to the cure of testicular cancer. to resolve its mechanism will provide useful information for making clinical decisions. We found 4 and 15 gene expressions were, respectively, up-regulated and down-regulated in cisplatin-resistant testicular cancer nec-8/DDp cells compared with their parental nec-8 cells (about 2.5-fold) using cDnA microarray analysis. After screening, we selected the entpD6 among these 19 genes. entpD6 was less expressed in cancerous region compared with that in non-cancerous lesion. In addition, entpD6 expression in seminoma was higher than that in other testicular tumors. entpD6 expression was involved in cellular sensitivity to cisplatin through an interaction with e-cadherin. entpD6 is a promising molecular biomarker of cisplatin resistance in testicular cancer, and also a novel therapeutical target modulating cisplatin resistance in testicular cancer.

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“…Sarcomatoid RCC has been proposed as an example of epithelial-to-mesenchymal (EMT), as evidenced by increased expression of N-Cadherin and Snail among other markers (24-26). We were able to show in our samples that the expression of N-cadherin was higher in sarcomatoid tissue compared to surrounding clear cell tissue (P=0.05, Figure 5).…”

Section: Resultsmentioning

confidence: 99%

RNA-seq Reveals Aurora Kinase–Driven mTOR Pathway Activation in Patients with Sarcomatoid Metastatic Renal Cell Carcinoma

Pal

Tong

et al. 2015

Molecular Cancer Research

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Sarcomatoid metastatic renal cell carcinoma (mRCC) is associated with a poor prognosis and the biology of the disease has been inadequately characterized. RNA sequencing (RNA-seq) was performed on adjacent benign, clear cell, and sarcomatoid components from clinical specimens with sarcomatoid mRCC. M phase and cell cycle pathways were enriched in sarcomatoid versus adjacent clear cell components, suggesting greater cell proliferation. The expression of aurora kinase A (AURKA) was increased as part of these pathways, and its increased expression was validated by quantitative PCR (qPCR). Immunohistochemical (IHC) analysis revealed that AURKA levels were increased in sarcomatoid tissue compared to their benign or clear cell parts. The increase in AURKA correlated with increased mTOR pathway activity, as evidenced by increased expression of phosphorylated mTOR (S2448) and ribosomal protein S6K (T389). When AURKA was stably expressed in a RCC cell line (Renca), it resulted in increased expression and activity of mTOR, suggesting that over-expression of AURKA can activate the mTOR pathway. These results warrant the analysis of a larger clinical cohort and suggest that targeting AURKA and/or mTOR in patients with sarcomatoid mRCC should be explored. Implications Comparative RNA-seq of adjacent sarcomatoid and clear cell histology renal cell carcinoma indicates a proliferative phenotype and increased AURKA-dependent activation of mTOR signaling in sarcomatoid RCC, which could be targeted by available agents.

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Cell proliferative activity and expression of cell‐cell adhesion factors (E‐cadherin, α‐, β‐, and γ‐catenin, and p120) in sarcomatoid renal cell carcinoma

Cited by 20 publications

References 25 publications

Expression of MUC1 (EMA) and E-cadherin in renal cell carcinoma: a systematic immunohistochemical analysis of 188 cases

Expression of MUC1 (EMA) and E-cadherin in renal cell carcinoma: a systematic immunohistochemical analysis of 188 cases

Ectonucleoside triphosphate diphosphohydrolase 6 expression in testis and testicular cancer and its implication in cisplatin resistance

RNA-seq Reveals Aurora Kinase–Driven mTOR Pathway Activation in Patients with Sarcomatoid Metastatic Renal Cell Carcinoma

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