Immunohistochemical expression of p63, p53 and MIB-1 in urinary bladder carcinoma. A tissue microarray study of 158 cases

Compérat, Éva; Camparo, Philippe; Haus, R.; Chartier‐Kastler, Emmanuel; Bart, S.; Delcourt, A; Houlgatte, A.; François, Richard; Capron, Frédérique; Vieillefond, Annick

doi:10.1007/s00428-005-0092-2

Cited by 47 publications

(35 citation statements)

References 41 publications

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“…Urothelial transitional cell carcinoma expresses p53 protein and Ki-67 antigen [21][22][23]. The present study also showed p53 protein and Ki-67 antigen.…”

Section: Discussionsupporting

confidence: 67%

Sarcomatoid carcinoma of the urinary bladder: a case report with immunohistochemical and molecular genetic analysis

Terada

2009

Med Oncol

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The author reports a rare case of sarcomatoid carcinoma with an emphasis on immunohistochemical features. A 79-year-old man was admitted to our hospital because of hematuria. An endoscopy revealed a large polypoid tumor in the bladder, and urine cytology demonstrated malignant cells. A cystectomy was performed. The patient is now alive without metastasis 4 months after the operation. Grossly, a large polypoid tumor (5 x 6 x 5 cm) was present in the bladder. Microscopically, the tumor consisted of high-grade transitional cell carcinoma element (10% in area) and sarcomatoid element (90% in area). There was a gradual transition between the two. The tumor cells were invaded into peribladder tissue (pT3b). Immunohistochemically, the sarcomatoid element was positive for four types of pancytokeratins, high-molecular weight cytokeratin (CK), CK5/6, CK7, CK18, CK19, epithelial membrane antigen (EMA), vimentin, p53 protein, p63, Ki-67 (labeling = 92%), neuron-specific enolase (NSE), and platelet-derived growth factor receptor-alpha (PDGFRA). It was negative for CK14, CK20, melanosome, carcinoembryonic antigen (CEA), desmin, S100 protein, myoglobin, alpha-smooth muscle antigen (ASMA), CD34, chromogranin, synaptophysin, CD56, CD68, and KIT. The transitional cell carcinoma element showed similar immunoreactivity except for negative CK5/6, positive CK20, and negative vimentin. A molecular genetic analysis of KIT gene (exons 9, 11, 13, and 17) and PDGFRA (exons 12 and 18) gene with the use of PCR-direct sequencing showed no mutations. The present case is the first report of sarcomatoid carcinoma of the urinary bladder demonstrating extensive immunohistochemistry and mutational status of KIT and PDGFRA genes. The sarcomatoid carcinoma in the present case may be derived from sarcomatous differentiation of high-grade transitional cell carcinoma.

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“…Urothelial transitional cell carcinoma expresses p53 protein and Ki-67 antigen [21][22][23]. The present study also showed p53 protein and Ki-67 antigen.…”

Section: Discussionsupporting

confidence: 67%

Sarcomatoid carcinoma of the urinary bladder: a case report with immunohistochemical and molecular genetic analysis

Terada

2009

Med Oncol

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“…Consistent with the public data (Figure 1) and other reports [11], [12], real time PCR data revealed that superficial tumors expressed higher levels of epithelial markers E-cadherin and p63, whereas muscle-invasive tumors expressed higher levels of mesenchymal markers (vimentin, Zeb1, Zeb2, MMP2, MMP9)(Figure 3 A and B). As shown in Figure 3, superficial tumors as a group more consistently expressed E-cadherin and p63 [3], [4], [18]–[23] than did muscle-invasive tumors (p-value<0.0001, Figure S1A). Similarly to our cell line data, ΔN-p63 was the major isoform of p63 present in primary tumor tissue (Figure 3C).…”

Section: Resultsmentioning

confidence: 99%

p63 Expression Defines a Lethal Subset of Muscle-Invasive Bladder Cancers

et al. 2012

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Backgroundp63 is a member of the p53 family that has been implicated in maintenance of epithelial stem cell compartments. Previous studies demonstrated that p63 is downregulated in muscle-invasive bladder cancers, but the relationship between p63 expression and survival is not clear.Methodology/Principal FindingsWe used real-time PCR to characterize p63 expression and several genes implicated in epithelial-to-mesenchymal transition (EMT) in human bladder cancer cell lines (n = 15) and primary tumors (n = 101). We correlated tumor marker expression with stage, disease-specific (DSS), and overall survival (OS). Expression of E-cadherin and p63 correlated directly with one another and inversely with expression of the mesenchymal markers Zeb-1, Zeb-2, and vimentin. Non-muscle-invasive (Ta and T1) bladder cancers uniformly expressed high levels of E-cadherin and p63 and low levels of the mesenchymal markers. Interestingly, a subset of muscle-invasive (T2–T4) tumors maintained high levels of E-cadherin and p63 expression. As expected, there was a strongly significant correlation between EMT marker expression and muscle invasion (p<0.0001). However, OS was shorter in patients with muscle-invasive tumors that retained p63 (p = 0.007).Conclusions/SignificanceOur data confirm that molecular markers of EMT are elevated in muscle-invasive bladder cancers, but interestingly, retention of the “epithelial” marker p63 in muscle-invasive tumors is associated with a worse outcome.

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“…Immunostaining for p63 is typically present in more than 90% of the nuclei of the normal urothelia [2]. Many UCs retain a pattern of p63 expression, but p63 expression may be partially lost in high-grade UC [3,27]. Although p63 sensitivity for UC in our study (73.9%) was lower than that of previous studies (82.9%–91.7%) [3,6], its specificity was 100% for UC.…”

Section: Discussionmentioning

confidence: 99%

Differential Immunohistochemical Profiles for Distinguishing Prostate Carcinoma and Urothelial Carcinoma

Oh¹,

Chung²,

Kim

et al. 2016

J Pathol Transl Med

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BackgroundThe pathologic distinction between high-grade prostate adenocarcinoma (PAC) involving the urinary bladder and high-grade urothelial carcinoma (UC) infiltrating the prostate can be difficult. However, making this distinction is clinically important because of the different treatment modalities for these two entities. MethodsA total of 249 patient cases (PAC, 111 cases; UC, 138 cases) collected between June 1995 and July 2009 at Seoul St. Mary’s Hospital were studied. An immunohistochemical evaluation of prostatic markers (prostate-specific antigen [PSA], prostate-specific membrane antigen [PSMA], prostate acid phosphatase [PAP], P501s, NKX3.1, and α-methylacyl coenzyme A racemase [AMACR]) and urothelial markers (CK34βE12, p63, thrombomodulin, S100P, and GATA binding protein 3 [GATA3]) was performed using tissue microarrays from each tumor. ResultsThe sensitivities of prostatic markers in PAC were 100% for PSA, 83.8% for PSMA, 91.9% for PAP, 93.7% for P501s, 88.3% for NKX 3.1, and 66.7% for AMACR. However, the urothelial markers CK34βE12, p63, thrombomodulin, S100P, and GATA3 were also positive in 1.8%, 0%, 0%, 3.6%, and 0% of PAC, respectively. The sensitivities of urothelial markers in UC were 75.4% for CK34βE12, 73.9% for p63, 45.7% for thrombomodulin, 22.5% for S100P, and 84.8% for GATA3. Conversely, the prostatic markers PSA, PSMA, PAP, P501s, NKX3.1, and AMACR were also positive in 9.4%, 0.7%, 18.8%, 0.7%, 0%, and 8.7% of UCs, respectively.ConclusionsProstatic and urothelial markers, including PSA, NKX3.1, p63, thrombomodulin, and GATA3 are very useful for differentiating PAC from UC. The optimal combination of prostatic and urothelial markers could improve the ability to differentiate PAC from UC pathologically.

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Immunohistochemical expression of p63, p53 and MIB-1 in urinary bladder carcinoma. A tissue microarray study of 158 cases

Cited by 47 publications

References 41 publications

Sarcomatoid carcinoma of the urinary bladder: a case report with immunohistochemical and molecular genetic analysis

Sarcomatoid carcinoma of the urinary bladder: a case report with immunohistochemical and molecular genetic analysis

p63 Expression Defines a Lethal Subset of Muscle-Invasive Bladder Cancers

Differential Immunohistochemical Profiles for Distinguishing Prostate Carcinoma and Urothelial Carcinoma

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