High Expressions of Lgr5 and ALDH1 in Primary Epithelial Ovarian Cancer Correlate with Advanced Tumor Stage and Grade as well as Poor Prognosis of the Patients

2015 ◽  
Vol 81 (2) ◽  
pp. 162-168 ◽  
Author(s):  
Yanan Sun ◽  
Xiaopeng Jia ◽  
Xiaohua Wu
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Poor Prognosis ◽  
Tumor Stage ◽  
Advanced Tumor Stage ◽  
Advanced Tumor ◽  
Primary Epithelial Ovarian Cancer

scholarly journals E-Cadherin expression in human tumors: a tissue microarray study on 10,851 tumors

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Eike Burandt ◽  
Felix Lübbersmeyer ◽  
Natalia Gorbokon ◽  
Franziska Büscheck ◽  
Andreas M. Luebke ◽  
...  
Keyword(s):  
Tissue Microarray ◽  
Poor Prognosis ◽  
Triple Negative ◽  
Lobular Carcinoma ◽  
Tumor Stage ◽  
Advanced Tumor Stage ◽  
Carcinoma Of The Breast ◽  
Advanced Tumor ◽  
Tumor Entities ◽  
E Cadherin

Abstract Background The E-Cadherin gene (CDH1, Cadherin 1), located at 16q22.1 encodes for a calcium-dependent membranous glycoprotein with an important role in cellular adhesion and polarity maintenance. Methods To systematically determine E-Cadherin protein expression in normal and cancerous tissues, 14,637 tumor samples from 112 different tumor types and subtypes as well as 608 samples of 76 different normal tissue types were analyzed by immunohistochemistry in a tissue microarray format. Results E-Cadherin was strongly expressed in normal epithelial cells of most organs. From 77 tumor entities derived from cell types normally positive for E-Cadherin, 35 (45.5%) retained at least a weak E-Cadherin immunostaining in ≥99% of cases and 61 (79.2%) in ≥90% of cases. Tumors with the highest rates of E-Cadherin loss included Merkel cell carcinoma, anaplastic thyroid carcinoma, lobular carcinoma of the breast, and sarcomatoid and small cell neuroendocrine carcinomas of the urinary bladder. Reduced E-Cadherin expression was linked to higher grade (p = 0.0009), triple negative receptor status (p = 0.0336), and poor prognosis (p = 0.0466) in invasive breast carcinoma of no special type, triple negative receptor status in lobular carcinoma of the breast (p = 0.0454), advanced pT stage (p = 0.0047) and lymph node metastasis in colorectal cancer (p < 0.0001), and was more common in recurrent than in primary prostate cancer (p < 0.0001). Of 29 tumor entities derived from E-Cadherin negative normal tissues, a weak to strong E-Cadherin staining could be detected in at least 10% of cases in 15 different tumor entities (51.7%). Tumors with the highest frequency of E-Cadherin upregulation included various subtypes of testicular germ cell tumors and renal cell carcinomas (RCC). E-Cadherin upregulation was more commonly seen in malignant than in benign soft tissue tumors (p = 0.0104) and was associated with advanced tumor stage (p = 0.0276) and higher grade (p = 0.0035) in clear cell RCC, and linked to advanced tumor stage (p = 0.0424) and poor prognosis in papillary RCC (p ≤ 0.05). Conclusion E-Cadherin is consistently expressed in various epithelial cancers. Down-regulation or loss of E-Cadherin expression in cancers arising from E-Cadherin positive tissues as well as E-Cadherin neo-expression in cancers arising from E-Cadherin negative tissues is linked to cancer progression and may reflect tumor dedifferentiation.

Upregulation of microRNA-203 is associated with advanced tumor progression and poor prognosis in epithelial ovarian cancer

2013 ◽  
Vol 30 (3) ◽  
Author(s):  
Shaosheng Wang ◽  
Xiaohong Zhao ◽  
Jie Wang ◽  
Yingmei Wen ◽  
LinJing Zhang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Tumor Progression ◽  
Poor Prognosis ◽  
Advanced Tumor

scholarly journals HSD17B6 downregulation predicts poor prognosis and drives tumor progression via activating Akt signaling pathway in lung adenocarcinoma

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Tian Tian ◽  
Fu Hong ◽  
Zhiwen Wang ◽  
Jiaru Hu ◽  
Ni Chen ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Grade ◽  
Tumor Stage ◽  
Advanced Tumor Stage ◽  
Large Tumor ◽  
Mesenchymal Transition ◽  
Advanced Tumor

AbstractLung adenocarcinoma is one of the most frequent tumor subtypes, involving changes in a variety of oncogenes and tumor suppressor genes. Hydroxysteroid 17-Beta Dehydrogenase 6 (HSD17B6) could synthetize dihydrotestosterone, abnormal levels of which are associated with progression of multiple tumors. Previously, we showed that HSD17B6 inhibits malignant progression of hepatocellular carcinoma. However, the mechanisms underlying inhibiting tumor development by HSD17B6 are not clear. Moreover, its role in lung adenocarcinoma (LUAD) is yet unknown. Here, we investigated its expression profile and biological functions in LUAD. Analysis of data from the LUAD datasets of TCGA, CPTAC, Oncomine, and GEO revealed that HSD17B6 mRNA and protein expression was frequently lower in LUAD than in non-neoplastic lung tissues, and its low expression correlated significantly with advanced tumor stage, large tumor size, poor tumor differentiation, high tumor grade, smoking, and poor prognosis in LUAD. In addition, its expression was negatively regulated by miR-31-5p in LUAD. HSD17B6 suppressed LUAD cell proliferation, migration, invasion, epithelial–mesenchymal transition (EMT), and radioresistance. Furthermore, HSD17B6 overexpression in LUAD cell lines enhanced PTEN expression and inhibited AKT phosphorylation, inactivating downstream oncogenes like GSK3β, β-catenin, and Cyclin-D independent of dihydrotestosterone, revealing an underlying antitumor mechanism of HSD17B6 in LUAD. Our findings indicate that HSD17B6 may function as a tumor suppressor in LUAD and could be a promising prognostic indicator for LUAD patients, especially for those receiving radiotherapy.

ΔTAp73 Upregulation Correlates With Poor Prognosis in Human Tumors: Putative In Vivo Network Involving p73 Isoforms, p53, and E2F-1

2006 ◽  
Vol 24 (5) ◽  
pp. 805-815 ◽  
Author(s):  
Gemma Domínguez ◽  
José M. García ◽  
Cristina Peña ◽  
Javier Silva ◽  
Vanesa García ◽  
...  
Keyword(s):  
Poor Prognosis ◽  
Cell Transformation ◽  
Tumor Stage ◽  
Advanced Tumor Stage ◽  
Breast Cancer Patients ◽  
Oncogenic Ras ◽  
Advanced Tumor ◽  
Tumor Tissues ◽  
Ras Status

Purpose Although full-length TAp73 variants largely mimic p53 suppressor activities, the transactivation-deficient transcripts ΔTAp73 exert an oncogenic effect by inactivating p53 and TAp73 suppressor properties. Additionally, ΔTAp73 may cooperate with oncogenic RAS to induce cell transformation, confer drug resistance, and induce the phosphorylation of phosphorylated Rb. Here, we study the expression of TAp73 and ΔTAp73 variants and assess possible associations with E2F-1, p53 and K-ras status. We address the possible clinical relevance of alterations in these genes. Patients and Methods We determine in 113 colon and 60 breast cancer patients (a) the expression levels of TAp73, ΔTAp73 (ΔEx2p73, ΔEx2/3p73, and ΔNp73), and E2F-1 transcripts by quantitative real-time reverse transcriptase polymerase chain reaction (PCR); (b) mutations in the first exon of K-ras by PCR–single-stranded confirmational polymorphism; and (c) p53 status by immunohistochemistry. Tumor characteristics were examined in each patient. Results Both suppressor and oncogenic isoforms of TP73 were significantly coupregulated in tumor tissues. Associations were observed between (a) p53 wild type status and upregulation of some TP73 variants; (b) overexpression of E2F-1 and some TP73 forms; and (c) upregulation of ΔTAp73 variants and advanced pathologic stage, lymph node metastasis, vascular invasion, presence of polyps, and tumor localization. Conclusion Overexpression of TP73 variants in tumor tissues indicates that they may be involved in colon and breast carcinogenesis. The association between upregulation of ΔTAp73 isoforms and poor prognosis features, specifically advanced tumor stage, suggests that they may be of practical clinical prognostic value. Interestingly, the in vivo associations identified here may indicate a functional network involving p73 variants, p53, and E2F-1.

scholarly journals MAGEA3 Expression in Cutaneous Squamous Cell Carcinoma Is Associated with Advanced Tumor Stage and Poor Prognosis

2017 ◽  
Vol 137 (3) ◽  
pp. 775-778 ◽  
Author(s):  
Melody Abikhair ◽  
Nazanin Roudiani ◽  
Hiroshi Mitsui ◽  
James G. Krueger ◽  
Anna Pavlick ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Poor Prognosis ◽  
Tumor Stage ◽  
Cutaneous Squamous Cell Carcinoma ◽  
Advanced Tumor Stage ◽  
Advanced Tumor

scholarly journals High Expression of PC4 is Associate With Lymphatic Metastasis and Predicts Poor Prognosis in Lung Adenocarcinoma Probably via CCR7/VEGF-C/VEGFR-3 Cascade

2021 ◽  
Author(s):  
ShaoLin Tao ◽  
XueMei Wang ◽  
LiCheng Wu ◽  
Cheng Shen ◽  
QunYou Tan
Keyword(s):  
Lung Adenocarcinoma ◽  
Lymphatic Metastasis ◽  
Poor Prognosis ◽  
A549 Cells ◽  
Tumor Stage ◽  
High Expression ◽  
Normal Lung ◽  
Advanced Tumor Stage ◽  
Advanced Tumor ◽  
Protein Expressions

Abstract Purpose: PC4 is a novel marker for diagnosis and treatment of advanced human cancers metastasis. This study aimed to verify that high expression of PC4 is associated with lymphatic metastasis and predicts poor prognosis in lung adenocarcinoma probably via CCR7/VEGF-C/VEGFR-3 cascade.Methods: PC4 protein expressions in 96 lung adenocarcinoma cases, CCR7/VEGF-C/VEGFR-3 protein expressions in 23 lung adenocarcinoma cases, and PC4 clinical outcome in 83 lung adenocarcinoma cases and TCGA as validation were evaluated, respectively. Small interfering RNA was used to explore the relationship of PC4 and the VEGF-C/VEGF-D/VEGFR-3 axis in A549 cells. The correlations between PC4 and CCR7, CCR7 and VEGF-C/VEGFR-3 were analyzed in A549 cells and adenocarcinoma tissues, respectively.Results: The results shown PC4 protein highly expressed in tumor tissue compared with normal lung tissue. High expressions of PC4 were remarkably associated with advanced tumor stage (P=0.032), lymphatic metastasis (P=0.004) and poor clinical outcomes (the cohort: HR: 2.135, 95% CI: 1.279-3.562; TCGA: HR: 2.983, 95% CI: 1.249-7.127) in lung adenocarcinoma. CCR7 expressions were remarkably decreased after PC4 RNAi in A549 cells, and significantly correlated with the expressions of VEGF-C and VEGFR-3 in adenocarcinoma tissues.Conclusion: CCR7/VEGF-C/VEGFR-3 expressions in lung adenocarcinoma were closely associated with lymphatic metastasis. Overexpression of PC4 is a predictor of lymphatic metastasis and poor prognosis in lung adenocarcinoma. PC4 plays important oncogenic roles probably via activation of CCR7/VEGF-C/VEGFR-3, which warrants further study.

Association of the AA genotype of the BCL2 (–938C>A) promoter polymorphism with better survival in ovarian cancer

2009 ◽  
Vol 24 (4) ◽  
pp. 223-229 ◽  
Author(s):  
Martin Heubner ◽  
Pauline Wimberger ◽  
Friedrich Otterbach ◽  
Sabine Kasimir-Bauer ◽  
Winfried Siffert ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Histological Grade ◽  
Tumor Stage ◽  
Promoter Polymorphism ◽  
Genotype Distribution ◽  
Single Nucleotide ◽  
Kaplan Meier ◽  
Potential Association ◽  
Primary Epithelial Ovarian Cancer

Background Bcl-2 plays a key role in the regulation of apoptosis. Recently, a novel regulatory single nucleotide polymorphism (–938C>A) in the inhibitory P2 BCL2 promoter was described. In this study we investigated its potential association with survival in epithelial ovarian cancer. Experimental design Patients (n=110) with primary epithelial ovarian cancer were retrospectively genotyped by pyrosequencing. Results Genotype distribution was not significantly different between 110 ovarian cancer patients and 120 healthy controls, suggesting that genotypes of this polymorphism do not increase the susceptibility to ovarian cancer. Kaplan-Meier curves showed a significant association of the AA genotype with increased survival (p=0.002). Multivariate analysis revealed that the BCL2–938AC/CC genotype (hazard ratio 4.5; p=0.003) was an independent prognostic factor compared to other prognostic factors such as age, histological grade or tumor stage. Conclusion The results suggest a role for the BCL2-938C>A polymorphism as a marker for survival in patients with epithelial ovarian cancer.

Association of nuclear accumulation of p53 with ERG fusion and poor prognosis in prostate cancer.

2012 ◽  
Vol 30 (5_suppl) ◽  
pp. 124-124
Author(s):  
Sarah Minner ◽  
Antje Krohn ◽  
Hueseyin Sirma ◽  
Ronald Simon ◽  
Markus Graefen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Poor Prognosis ◽  
Statistical Power ◽  
Tumor Stage ◽  
Nuclear Accumulation ◽  
Cancer Tissue ◽  
Positive Staining ◽  
Advanced Tumor Stage ◽  
Advanced Tumor ◽  
Psa Recurrence

124 Background: We have previously shown that nuclear accumulation of p53 is rare in prostate cancer but strongly linked to early biochemical recurrence (Schlomm et al., Modern Pathology, 2008). The current study was designed to study the association between ERG fusion and p53 in a large series of prostate cancers. Methods: A prostate cancer tissue microarray (TMA) was constructed from 4,699 radical prostatectomie specimens with histological, pathological, and clinical follow-up data. Immunohistochemistry was applied to detect nuclear p53 accumulation as a marker for defective p53 and to detect ERG expression as a surrogate for ERG gene fusion. Results: Nuclear accumulation of p53 was detected in 62/3,667 (1.7%) analyzable tissue spots. Positive staining was significantly linked to advanced tumor stage (p<0.0001), high Gleason score (p<0.0001), presence of lymph node metastases (p=0.0005), and early PSA recurrence (p<0.0001) in all cancers. ERG expression was found in 1,990/4,266 (46.6%) analyzable cancers, but was unrelated to tumor phenotype or patient prognosis. Results of both p53 and ERG were available from 3,392 tumors. Presence of nuclear p53 staining was linked to ERG fusion positive cancers: 40 (2.7%) of 1,491 ERG-positive cancers, but only 20 (1.1%) of 1,901 ERG-negative tumors showed nuclear p53 staining (p=0.0004). A Kaplan-Meier survival analysis of p53 in the subsets of 1,699 ERG positive and 1,280 ERG negative cancers revealed that nuclear p53 accumulation was strongly linked to early PSA recurrence in both subsets (p<0.0001 each). Conclusions: These data demonstrate that the poor prognosis of prostate cancer patients with nuclear p53 accumulation is independently from the ERG fusion status, but suggest a distinct biological role of p53 inactivation in ERG fusion positive cancers. The very high number of prostate cancer samples included in the TMA used in this study allows for analysis of rare events such as p53 alterations with high statistical power.

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