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    Comprehensive Immunohistochemical Analysis of Epithelial-Mesenchymal Transition Biomarkers in the Invasive Micropapillary Cancer of the Breast
    (Hindawi Ltd, 2024) Oz, Ozden; Tasli, Funda Alkan; Yuzuguldu, Resmiye Irmak; Zengel, Baha; Cavdar, Demet Kocatepe; Durak, Merih Guray; Durusoy, Raika
    Background: Invasive micropapillary carcinoma (IMPC) of the breast is commonly associated with a poor prognosis due to its high incidence of lymphovascular invasion and lymph node metastasis (LNM). Our study is aimed at investigating the prognostic significance of the expressions of E-cadherin (E-cad), N-cadherin (N-cad), CD44s, and beta-catenin (beta-cat). In addition, it is aimed at deciphering the consistency of these markers between the IMPC, the invasive breast carcinoma, no-special type (IBC-NST), and LNM components in the same IMPC cases. Methods: Sixty-two IMPC cases with LNM from 1996 to 2018 were analyzed. Immunohistochemical staining was performed separately on the three regions for each patient. Statistical analyses included Kaplan-Meier, Cox regression, and McNemar's statistical tests. Results: Loss of CD44 expression in IMPC, IBC-NST, and LNM areas was associated with poor prognosis in overall survival (OS) ( p = 0.010 , p < 0.0005 , p = 0.025 ). Loss of CD44 expression in the IBC-NST, gain of N-cad expression in the IMPC, and loss of beta-cat expression in the LNM areas were indicators of poor prognosis in disease-free survival (DFS) (p = 0.005 , p = 0.041 , p = 0.009). Conclusion: Our evaluation of this rare subtype, focusing on the expression of key epithelial-mesenchymal transition (EMT) molecules, revealed that it shares characteristics with the IBC-NST component within mixed tumors. Notably, contrary to expectations, a reduction in CD44 expression was found to adversely affect both OS and DFS. By conducting staining procedures simultaneously across three regions within the same patient, a novel approach has provided valuable insights into the mechanisms of EMT.
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    TAp73 beta Can Promote Hepatocellular Carcinoma Dedifferentiation
    (Mdpi, 2021) Iscan, Evin; Ekin, Umut; Yildiz, Gokhan; Oz, Ozden; Keles, Umur; Suner, Asli; Uzuner, Hamdiye
    Simple Summary Hepatocellular carcinoma (HCC) is a highly complex and heterogeneous type of cancer. Hepatocyte dedifferentiation is one of the important steps in the development of HCC. However, its molecular mechanisms are not well known. in this study, we report that transcriptionally active TAp73 isoforms are overexpressed in HCC. We also show that TAp73 beta suppresses the expression of the hepatocyte markers including CYP3A4, AFP, ALB, HNF4 alpha, while increasing the expression of several cholangiocyte markers in HCC cell lines. in conclusion, this report reveals a pro-oncogenic role for TAp73 beta in liver cancer. Hepatocyte dedifferentiation is a major source of hepatocellular carcinoma (HCC), but its mechanisms are unknown. We explored the p73 expression in HCC tumors and studied the effects of transcriptionally active p73 beta (TAp73 beta) in HCC cells. Expression profiles of p73 and patient clinical data were collected from the Genomic Data Commons (GDC) data portal and the TSVdb database, respectively. Global gene expression profiles were determined by pan-genomic 54K microarrays. The Gene Set Enrichment Analysis method was used to identify TAp73 beta-regulated gene sets. The effects of TAp73 isoforms were analyzed in monolayer cell culture, 3D-cell culture and xenograft models in zebrafish using western blot, flow cytometry, fluorescence imaging, real-time polymerase chain reaction (RT-PCR), immunohistochemistry and morphological examination. TAp73 isoforms were significantly upregulated in HCC, and high p73 expression correlated with poor patient survival. The induced expression of TAp73 beta caused landscape expression changes in genes involved in growth signaling, cell cycle, stress response, immunity, metabolism and development. Hep3B cells overexpressing TAp73 beta had lost hepatocyte lineage biomarkers including ALB, CYP3A4, AFP, HNF4 alpha. in contrast, TAp73 beta upregulated genes promoting cholangiocyte lineage such as YAP, JAG1 and ZO-1, accompanied with an increase in metastatic ability. Our findings suggest that TAp73 beta may promote malignant dedifferentiation of HCC cells.