Histology and histopathology Vol.34,nº11 (2019)
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- PublicationOpen AccessPrognostic value of mutant p53, Ki-67, and TTF-1 and their correlation with EGFR mutation in patients with non-small cell lung cancer.(Celular e Histiologia Universidad de Murcia, Departamento de Biologia, 2019) Zhu, Wang-Yu; Hu, Xiao-Fei; Fang, Ke-Xin; Kong, Qiong-Qiong; Cui, Ri; Feng, Hai; He, Jian-Ying; Zhang, Yong-kui; Le, Han-BoIntroduction. The clinical characteristics of non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutation have been well studied. However, the correlation of EGFR mutation with mutant p53, Ki-67, and thyroid transcription factor 1 (TTF-1) and their prognostic value remain indistinct. Material and methods. Clinical and pathological characteristics and overall survival were analysed retrospectively in 523 surgically resected NSCLC patients. The expression levels of p53, Ki-67, and TTF-1 protein were detected by immunohistochemistry, and an amplification refractory mutation system was used to access the status of EGFR mutations. Results. Of 523 patients with surgically resected NSCLC, 210 patients (38.4%) harboured EGFR mutations. Compared to the EGFR wild-type lung cancer, mutated EGFR harboured significantly increased mutant p53-positive or TTF-1-positive tumors (P<0.001 and <0.001, respectively). Former or current smokers, pathological stage and mutant p53-or TTF-1-positive status were independent predictors of EGFR mutation (P=0.001, 0.014, 0.014 and <0.001, respectively). Patients with p53 under expression had significantly better overall survival in the whole cohort and wild-type EGFR cohort (P=0.0010 and 0.0020, respectively) as well as in Ki-67-negative and TTF-1-positive patients (P<0.0001 and 0.0009, and P<0.0001 and 0.0004, respectively). Interestingly, in patients harbouring EGFR mutations, p53-under expression and Ki-67-negative cases still had better survival than positive cases, whereas there was no obvious difference between TTF- 1-negative and TTF-1-positive cases (P=0.0198, 0.0068 and 0.3684, respectively). Finally, in NSCLC patients with wild-type EGFR, positive Ki-67 expression was the independent predictor for the worst survival (P=0.022). Conclusion. The expression levels of mutant p53, Ki-67, and TTF-1 were correlated with EGFR mutation. High expression of mutant p53 and Ki-67 correlated with poor survival in the entire cohort, EGFR mutation or wild-type cohort. In addition, Ki-67 might have an impact on the prognosis for patients with NSCLC with wild-type EGFR.
- PublicationOpen AccessHigh expression of DEK is associated with poor prognosis in hepatocellular carcinoma.(Celular e Histiologia Universidad de Murcia, Departamento de Biologia, 2019) Lee, Soo Yeon; Jung, Wonkyung; Lee, Jinhwan; Kim, Aeree; Kim, Han Kyeom; Kim, Baek-HuiDEK is an oncogene that has been identified as part of the DEK-CAN fusion gene. DEK plays a role in carcinogenesis through WNT signaling and induces cell proliferation through cyclin-dependent kinase signaling. DEK overexpression has been reported in HCC, but the clinical significance is unclear. This study enrolled 221 cases of HCC. The expression of DEK protein was evaluated by immunohistochemical staining. Cdk4, cyclin D1, Wnt10b, E-cadherin, and β-catenin were also immunohistochemically stained and analyzed for correlation. The association of clinicopathologic factors with DEK expression was analyzed. DEK expression was observed in 44.8% (99/221) of cases. DEK expression showed a statistical association with clinicopathologic factors, including Edmondson-Steiner grade, presence of vascular emboli, and multiplicity (p<0.05). Among the other IHC markers, the expression of cdk4 was correlated with DEK expression (p<0.05). Patients with high DEK expression showed a significantly lower overall survival rate (p=0.006). However, the disease-free survival rate did not differ significantly. In addition, in a Cox regression model analysis, DEK expression was an independent prognostic factor. In summary, high expression of DEK was observed in HCC and was associated with poor prognostic marker expression and poor prognosis.
- PublicationOpen AccessUnique expression profiles of mucin proteins in interstitial pneumonia-associated lung adenocarcinomas(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Tateishi, Yoko; Kataoka, Toshiaki; Okudela, Koji; Nakashima, Yu; Mitsui, Hideaki; Matsumura, Mai; Umeda, Shigeaki; Arai, Hiromasa; Baba, Tomohisa; Suzuki, Takehisa; Koike, Chihiro; Tajiri, Michihiko; Takemura, Tamiko; Ogura, Takashi; Masuda, Munetaka; Ohashi, KenichiIn order to clarify idiopathic interstitial pneumonia (IIP)-associated lung adenocarcinoma (LADC), we herein focused on the expression profiles of mucin proteins, the most common cellular differentiation markers. The expression of the mucin (MUC) 1, MUC2, MUC3B, MUC4, MUC5AC, MUC5B, MUC6, MUC7, MUC9, and MUC21 proteins was examined immunohistochemically and their levels were semi- quantified in 80 IIP-associated LADCs and 106 non-IIP LADCs. LADCs were divided into low and high expressers based on thresholds obtained from the receiver operating characteristic (ROC) curves of each mucin protein. Low expressers of MUC1, MUC7, and MUC21 and high expressers of MUC4, MUC5AC, MUC5B, and MUC9 were dominant in the IIP group. Multivariate analyses confirmed that the correlations between mucin expression profiles and IIP-associated LADCs were independent of putative confounding factors, such as smoking, gender, histological types, and cytological types. Thus, the expression profiles of these mucin proteins significantly differed between the IIP and non-IIP groups. IIP-associated LADCs appear to have unique cellular differentiation features and they may develop through a distinct histogenetic pathway. This is the first study to demonstrate that IIP-associated LADCs have unique mucin expression profiles.
- PublicationOpen AccessResearch progress on SIRT1 and sepsis.(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Li, Lincheng; Liu, Mingchuan; Cao, Mengyuan; Bai, XiaozhiSIRT1, a member of the sirtuin family, belongs to the NAD + -dependent class III histone deacetylase. SIRT1 can regulate gene expression by catalyzing non-histone and histone lysine residues deacetylation. SIRT1 also plays important roles in glucose and lipid metabolism, cell aging, tumorigenesis and inflammation. Recent studies indicate that SIRT1 can inhibit the inflammatory responses via regulating several inflammatory signaling pathways. It is closely related to the occurrence and development of sepsis and other inflammatory diseases. Research has been done on relevant signaling pathways of SIRT1 as well as its target genes during inflammation. SIRT1 is a hot spot in uncontrolled inflammatory response research. This article focuses on the role of SIRT1 in inflammation, especially its targets and involved signaling pathways in sepsis, and tries to provide more convincing evidence for the clinical treatment of sepsis and other inflammatory diseases.
- PublicationOpen AccessSmall molecule GSK-3 antagonists play a pivotal role in reducing the local inflammatory response, in promoting resident stem cell activation and in improving tissue repairing in regenerative dentistry(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Tatullo, Marco; Makeeva, Irina; Rengo, Sandro; Rengo, Carlo; Spagnuolo, Gianrico; Codispoti, BrunaRegenerative dentistry is attracting growing interest in the scientific community, mainly because of its translational and promising therapeutic approach. The latest research carried out by the scientific community are aimed at triggering the local cellular response, in order to induce a physiological self- repairing of damaged oral tissues. Such physiological processes mainly involve the activation of local stem cell populations: mesenchymal stem cells, in fact, retain the ability to proliferate and to differentiate towards functional mature elements, thus leading towards healing of damaged tissues. Glycogen Synthase Kinase-3 (GSK-3) is a key- regulator of the Wnt/β-catenin pathway; it phosphorylates β-catenin, that then is degraded in the cytosol. The activation of such signalling, mediated by Wnt ligand/receptor association, inhibits GSK-3, leading to translocation of β-catenin to the nucleus and to gene transcription. Selective inhibitors of GSK-3 have been linked to the activity of Wnt signalling and to the regeneration of injured tissues, including complex dental and oral structures. Small Molecule GSK-3 Antagonists are the most interesting class of molecules acting with a "Bystander effect": reducing local inflammation and local bone resorption and triggering the activity and differentiation of resident "sleeping" MSCs. The aim of this narrative topical review is to describe the current knowledge on the role of small molecule GSK-3 antagonists in regenerative dentistry, with strategic insights towards the translational applications in nanomaterials in dentistry and in dental repairing.