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1.
Zu-cheng Xie Tian-tian Li Bin-liang Gan Xiang Gao Li Gao Gang Chen Xiao-hua Hu 《Pathology, research and practice》2018,214(5):644-654
Background
Lung squamous cell cancer (LUSC) is a common but challenging malignancy. It is important to illuminate the molecular mechanism of LUSC. Thus, we aim to explore the molecular mechanism of miR-136-5p in relation to LUSC.Methods
We used the Cancer Genome Atlas (TCGA) database to investigate the expression of miR-136-5p in relation to LUSC. Then, we identified the possible miR-136-5p target genes through intersection of the predicted miR-136-5p target genes and LUSC upregulated genes from TCGA. Bioinformatics analysis was performed to determine the key miR-136-5p targets and pathways associated with LUSC. Finally, the expression of hub genes, correlation between miR-136-5p and hub genes, and expected significance of hub genes were evaluated via the TCGA and Genotype-Tissue Expression (GTEx) project.Results
MiR-136-5p was significantly downregulated in LUSC patients. Glucuronidation, glucuronosyltransferase, and the retinoic acid metabolic process were the most enriched metabolic interactions in LUSC patients. Ascorbate and aldarate metabolism, pentose and glucuronate interconversions, and retinol metabolism were identified as crucial pathways. Seven hub genes (UGT1A1, UGT1A3, UGT1A6, UGT1A7, UGT1A10, SRD5A1, and ADH7) were found to be upregulated, and UGT1A1, UGT1A3, UGT1A6, UGT1A7, and ADH7 were negatively correlated with miR-136-5p. UGT1A7 and ADH7 were the most significantly involved miR-136-5p target genes, and high expression of these genes was correlated with better overall survival and disease-free survival of LUSC patients.Conclusions
Downregulated miR-136-5p may target UGT1A7 and ADH7 and participate in ascorbate and aldarate metabolism, pentose and glucuronate interconversions, and retinol metabolism. High expression of UGT1A7 and ADH7 may indicate better prognosis of LUSC patients. 相似文献2.
Dongyi Zhu Li Gu Zhanxia Li Wenjing Jin Qingchun Lu Tao Ren 《Pathology, research and practice》2019,215(5):861-872
Background
MiR-138-5p is regarded as a tumour suppressor in many cancers. Transforming growth factor beta (TGF-β) often acts as a tumor promotor at the late stages of human cancers. However, the function of miR-138-5p on lung adenocarcinoma cells induced by TGF-β remains to be further confirmed.Methods
RT-qPCR was used to detect the expression of human lung adenocarcinoma tissues, adjacent normal tissues, and relative cell lines. When the lung adenocarcinoma cells A549 and H1299 were transfected with negative control (NC), miR-138-5p mimics and miR-138-5p inhibitor by lipofectamine3000 and treated with or without TGF-β1, the lung adenocarcinoma cell function was detected by Immunofluorescence, Western blotting (WB), cell counting Kit-8 (CCK8), colony formation, EdU, Wound-healing and Transwell assays. The relation between miR-138-5p and zinc finger E-box-binding homeobox 2 (ZEB2) was detected by RT-qPCR, WB, and Luciferase reporter assays. When ZEB2 was knocked down, the lung adenocarcinoma cell function was detected by WB, CCK8 and Transwell assays.Results
The expression of miR-138-5p was decreased in lung adenocarcinoma tissues and cell lines. When treated with or without TGF-β1, overexpression of miR-138-5p suppressed EMT, proliferation and metastasis of A549 and H1299. ZEB2 was verified as the direct target of miR-138-5p. Downregulation of ZEB2 suppressed EMT, proliferation and metastasis of lung adenocarcinoma cell, which could be reversed by miR-138-5p inhibitor.Conclusions
MiR-138-5p inhibits epithelial-mesenchymal transition, growth and metastasis of lung adenocarcinoma cells through targeting ZEB2. 相似文献3.
Yongpan Sun Hong Mei Chuan Xu Hongjun Tang Wei Wei 《Pathology, research and practice》2018,214(1):119-125
Background
Many studies have shown that differentially expressed miRs in body fluids can serve as biomarkers in non-invasive detection of the cancers. However, the clinical significance of plasma miRs in the diagnosis of lung adenocarcinoma (LA) is still not clear. Therefore, we examined the LA-specific miRs in plasma, which could be utilized to diagnosis and monitor LA in routine clinical practice.Methods
Twenty-eight LA cases and twenty-eight healthy controls were recruited to our study. MiRs differential expression in plasma was measured by miRNA Microarray assay and revalidated by using qRT-PCR based absolute quantification methods The diagnostic power of circulating miRs in LA was evaluated using the receiver operating characteristics (ROC) curves and the area under the ROC curves (AUC).Results
Tumor tissues and plasma levels of miR-339-5p were significantly down-regulated in LA patients compared with those in the control group, whereas the levels of miR-21 in LA patients were significantly higher than control group. ROC analysis showed that miR-339-5p and miR-21 could distinguish LA patients from healthy controls with high AUC (0.900 and 0.880, respectively), sensitivity (0.821 and 0.821, respectively) and specificity (0.929 and 0.964, respectively). Importantly, the combination of miR-339-5p and miR-21 markedly improved AUC (0.963), sensitivity (0.929) and specificity (0.929).Conclusion
Plasma miR-339-5p or miR-21 could serve as a potential biomarker for diagnosis of LA, however, the combination of miR-339-5p and miR-21 was more efficient for LA detection. 相似文献4.
Zhao-jia Gao Wei-dong Yuan Jun-qiang Yuan Kai Yuan Yong Wang 《Pathology, research and practice》2018,214(5):700-705
Purpose
Lung cancer, the leading cause of cancer-related death worldwide, shows a poor 5-year overall survival rate. In our previous study, we demonstrated that miR-486-5p can be a potential blood-based biomarker for early diagnosis and recurrence prediction of non-small cell lung cancer (NSCLC). The aim of the present study was to investigate the possible roles and related target genes of miR-486-5p in NSCLC progression.Methods
pcDNA3.1(+)/Pri-miR486 recombinant plasmid and miR-486-5p inhibitor were transfected into NSCLC cells and theirs effects were evaluated by qRT-PCR. Then, MTT assay and Colony formation assay were performed to determine the potential roles of miR-486-5p played on NSCLC cellular proliferation and cloning in vitro. We also initially investigated the target genes of miR-486-5p by using bioinformatic methods, qRT-PCR and western blot.Results
pcDNA3.1(+)/Pri-miR486 recombinant plasmid significantly upregulated the expression of miR-486-5p, while miR-486-5p inhibitor significantly downregulated its expression. Upregulation of miR-486-5p promoted the cellular proliferation and cloning, while miR-486-5p silencing restrained the cellular proliferation and cloning. Furthermore, four potential target genes (PIK3R1, PTEN, MAP3K7 and FOXO1) of miR-486-5p were screened out. Finally, we found that upregulation of miR-486-5p in NSCLC cells significantly reduced PTEN and increased AKT expression levels, whereas miR-486-5p silencing increased PTEN and reduced AKT expression. Therefore, we believe that miR-486-5p can regulate PTEN-PI3 K/AKT signaling.Conclusions
miR-486-5p acts as an oncogene in the progression of NSCLC by influencing PTEN-PI3 K/AKT signaling. miR-486-5p may provide potential therapeutic targets for NSCLC. 相似文献5.
6.
Limin Xu Xuting Xu Huilian Huang Zhihong Ma Shuangmei Zhang Pingping Niu Yingrong Chen Jinliang Ping Ping Lu Caihua Yu Lishan Min Jing Chen Licheng Dai Shunli Dong 《Pathology, research and practice》2018,214(5):776-783
Objective
Non-small cell lung cancer (NSCLC) accounts for 80–85% of lung cancer cases which cause most of cancer-related deaths globally. As our previous study discovered miR-1260b can be regarded as a specific signature for metastasis in NSCLC patients. However, the molecular mechanisms of miR-1260b underlying NSCLC progression and metastasis remain dismal.Methods
The expression of miR-1260b in NSCLC tissues and cell lines were examined by real-time PCR, the effects of miR-1260b on cell migration, invasion and proliferation were evaluated in vitro. Furthermore, luciferase reporter assay was performed to identify the targets of miR-1260b, and the association between miR-1260b and its target gene was determined by real-time PCR and western blot assay.Results
The results showed that miR-1260b was significantly upregulated in NSCLC cell lines. The inhibition of miR-1260b expression decreased the migratory and invasive rates in A549 cells while miR-1260b overexpression had the opposite effect. Furthermore, PTPRK was identified as a direct target of miR-1260b, and PTPRK expression was inversely correlated with miR-1260b in NSCLC cell lines and clinical tissues.Conclusions
These results suggested that miR-1260b may play an important role in NSCLC metastasis progression and could serve as a putative target for diagnosis and treatment of NSCLC. 相似文献7.
Wei-ning Cen Jin-shu Pang Jia-cheng Huang Jia-yin Hou Wen-guang Bao Rong-quan He Jie Ma Zhi-gang Peng Xiao-hua Hu Fu-chao Ma 《Pathology, research and practice》2018,214(11):1835-1847
Background
The specific expression level and clinical significance of miR-375-3p in HNSCC had not been fully stated, as well as the overall biological function and molecular mechanisms. Therefore, we purpose to carry out a comprehensive meta-analysis to further explore the clinical significance and potential function mechanism of miR-375-3p in HNSCC.Methods
HNSCC-related data was gained from Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA), and peer-reviewed journals. A meta-analysis was carried out to comprehensively explore the relationship between miR-375-3p expression level and clinicopathological features of HNSCC. And summary receiver operating characteristic (SROC) curve analysis was applied for evaluating disease diagnosis value of miR-375-3p. In addition, a biological pathway analysis was also performed to assess the possible molecular mechanism of miR-375-3p in HNSCC.Results
A total of 24 available records and references were added into analysis. The overall pooled meta-analysis outcome revealed a relatively lower expression level of miR-375-3p in HNSCC specimens than that in non-cancerous controls (P?<?0.001). And SROC curve analysis showed that the pooled area under the SROC curve (AUC) was 0.90 (95%CI: 0.88–0.93). In addition, biological pathway analysis indicated that LAMC1, EDIL3, FN1, VEGFA, IGF2BP2, and IGF2BP3 maybe the latent target genes of miR-375-3p, which were greatly enriched in the pathways of beta3 integrin cell surface interactions and the binding of RNA via the insulin-like growth factor-2 mRNA-binding protein (IGF2BPs/IMPs/VICKZs).Conclusion
MiR-375-3p expression clearly decreased in HNSCC samples compared with non-cancerous controls. Meanwhile, miR-375-3p may serve as a tumor suppressor via regulating tumor-related genes LAMC1, EDIL3, FN1, VEGFA, IGF2BP2, and IGF2BP3 in HNSCC. 相似文献8.
Chui-Ming Jia Yu-Yang Tian Li-Na Quan Li Jiang Ai-Chun Liu 《Pathology, research and practice》2018,214(9):1388-1394
Background
Though the levels of diagnosis and treatment of multiple myeloma (MM) have been largely improved recent years, the prognosis of these patients remain unacceptable. It is urgent for us to discover the exact mechanism and determine some new indicators for MM. MiRNAs play a critical role in the occurrence and progression of cancers, including MM. MiR-26b-5p has been reported to be closely related to cells proliferation in human pulmonary cancer, hepatocellular carcinoma and so on.Material and methods
Here, we measured the expression of miR-26b-5p in MM samples and cell lines by real-time PCR. Then, Kaplan-Meier Curves were applied to assess the effect of miR-26b-5p expression on MM patients prognosis. Functionally, MTT assay and Flow cytometry were conducted to explore the functions of miR-26b-5p in cells proliferation and apoptosis. Furthermore, bioinformatics tools, Pearson's correlation coefficient analysis, gain-and loss of-function experiments and rescue experiment were used to determine the relationship between JAG1 and miR-26b-5p in MM cells. In addition, we also confirmed the role of JAG1 in MM cells proliferation and apoptosis by gain-and loss of-function experiments.Results
Here, we reported for the first time that miR-26b-5p was under-expressed in MM by real-time PCR. Clinically, Kaplan-Meier Curves showed that MM patients with lower miR-26b-5p expression had worse prognosis. Functionally, MTT assay revealed that miR-26b-5p inhibited cells proliferation. Flow cytometry indicated that miR-26b-5p accelerated tumor cells apoptosis. Furthermore, bioinformatics tools, Pearson's correlation coefficient analysis gain-and loss of-function experiments showed that JAG1 was the target of miR-26b-5p in MM cells. And, gain-and loss of-function experiments for JAG1 confirmed that JAG1 was an oncogene in MM cells. What’s more, rescue experiment showed that JAG1 mediated the function of miR-26b-5p in MM cells.Conclusion
MiR-26b-5p acts as a tumor suppressor through suppressing cells proliferation and inducing cells apoptosis via directly targeting JAG1 in MM. MiR-26b-5p could be a potential and ponderable tumor target for MM in future. 相似文献9.
Yue Zhu Ying Han Tian Tian Peihong Su Guan Jin Juan Chen Yungui Cao 《Pathology, research and practice》2018,214(3):374-379
Objective
This study aimed to demonstrate the predictive value of miR-21-5p, miR-34a, and human telomerase RNA component (hTERC) in cervical cancer (CC) development and evaluated their potential possibility for future clinical applications.Methods
Specimens were collected from the normal cervix, cervical intraepithelial neoplasia (CIN) I, CIN II/III, cervical squamous cell carcinoma. Cytological evaluations and histopathologic examinations were conducted in all subjects, along with the assessment of human papillomavirus (HPV) DNA. The expression levels of the miR-21-5p and miR-34a were detected by RT-PCR. hTERC amplification was detected by dual-color interphase fluorescence in situ hybridization (FISH). Then miRNA, hTERC expressions were compared with the cytological and histologic examination.Results
Compared to that in the benign samples, the expression of miR-21-5p and miR-34a in abnormal samples was significantly upregulated and downregulated, gradually corresponding to the severity of cervical lesions (P?<?0.05). There was a trend toward an increasing amplification of hTERC with the increasing severity of cervical lesions. miR-21-5p and miR-34a expression, and hTERC amplification were more specific than HPV positivity in differentiating low-grade cervical disorders from high-grade ones (P?<?0.05).Conclusions
MiR-21-5p upregulation, miR-34a downregulation, and hTERC amplification were associated with the aggressive progression of CC, which suggests that miR-21-5p, miR-34a and hTERC might serve as surrogate markers for CC progression and potential molecular targets for blockage of the development of CC. 相似文献10.
Bi Tang Ling Xuan Mingming Tang Hongju Wang Jing zhou Jinjun Liu Shili Wu Miaonan Li Xiaojing Wang Heng Zhang 《Pathology, research and practice》2018,214(10):1686-1693
Background
miR-93 is recently recognized to perform anti-inflammatory action in the pathological process of cardiomyocytes dysfunction. However, it remains unclear whether miR-93-3p involves in lipopolysaccharide (LPS)-induced inflammation and apoptosis in H9c2 cells. The present study aimed to investigate the functions of miR-93-3p and its target, toll-like receptor 4 (TLR4), in LPS-stimulated cardiomyocytes.Material and methods
Cell viability was analyzed by CCK-8 assay. AnnexinV-FITC/PI staining and lactate dehydrogenase (LDH) assay were used to evaluate the cell death. The mRNA and protein levels were assayed by RT-qPCR and western blotting, respectively. The targeted gene was predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay.Results
LDH stimulation resulted in the suppression of cell viability and the increase in apoptosis rate, inflammatory cytokines and LDH levels, while inhibition of TLR4 with TAK-242 or overexpression of miR-93-3p dramatically blocked LPS-induced inflammation and apoptosis in cardiomyocytes. Intriguingly, bioinformatics analysis and experimental data suggested that TLR4 was a direct target of miR-93-3p, which could inhibit TLR4 expression by transfected with miR-93-3p mimics or elevate the expression of TLR4 by transfected with miR-93-3p inhibitors. Overexpression of TLR4 carried out an opposite effect to miR-93-3p and positively regulated LPS-induced inflammation and apoptosis in cardiomyocytes.Conclusion
miR-93-3p showed the protective effects against LPS-induced inflammation and apoptosis in cardiomyocytes by inhibiting TLR4 expression. 相似文献11.
Li Gao Li-jie Zhang Sheng-hua Li Li-li Wei Bin Luo Rong-quan He Shuang Xia 《Pathology, research and practice》2018,214(5):732-749
Background
MiR-452-5p has been reported to be down-regulated in prostate cancer, affecting the development of this type of cancer. However, the molecular mechanism of miR-452-5p in prostate cancer remains unclear. Therefore, we investigated the network of target genes of miR-452-5p in prostate cancer using bioinformatics analyses.Materials and methods
We first analyzed the expression profiles and prognostic value of miR-452-5p in prostate cancer tissues from a public database. Gene Ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG), PANTHER pathway analyses, and a disease ontology (DG) analysis were performed to find the molecular functions of the target genes from GSE datasets and miRWalk. Finally, we validated hub genes from the protein–protein interaction (PPI) networks of the target genes in the Human Protein Atlas (HPA) database and Gene Expression Profiling Interactive Analysis (GEPIA). Narrowing down the optimal target genes was conducted by seeking the common parts of up-regulated genes from GEPIA, down-regulated genes from GSE datasets, and predicted genes in miRWalk.Results
Based on mining of GEO and ArrayExpress microarray chips and miRNA-Seq data in the TCGA database, which includes 1007 prostate cancer samples and 387 non-cancer samples, miR-452-5p is shown to be down-regulated in prostate cancer. GO, KEGG, and PANTHER pathway analyses suggested that the target genes might participate in important biological processes, such as transforming growth factor beta signaling and the positive regulation of brown fat cell differentiation and mesenchymal cell differentiation, as well as the Ras signaling pathway and pathways regulating the pluripotency of stem cells and arrhythmogenic right ventricular cardiomyopathy (ARVC). Nine genes—GABBR, PNISR, NTSR1, DOCK1, EREG, SFRP1, PTGS2, LEF1, and BMP2—were defined as hub genes in the PPI network. Three genes—FAM174B, SLC30A4, and SLIT1—were jointly shared by GEPIA, the GSE datasets, and miRWalk.Conclusions
Down-regulated miR-452-5p might play an essential role in the tumorigenesis of prostate cancer. 相似文献12.
Xinyue Song Chaoran Zhao Longyang Jiang Shu Lin Jia Bi Qian Wei Lifeng Yu Lin Zhao Minjie Wei 《Pathology, research and practice》2018,214(12):2046-2053
Background
Pituitary homeobox 1 (PITX1) is a member of the PITX gene family which is vital to proper development of early embryo. However, the relationship of PITX1 expression and overall survival (OS) in non-small cell lung cancer (NSCLC) is not clear.Methods
In our study, bioinformatic analysis was performed using UCSC Xena Browser. We used data based on the Cancer Genome Atlas-lung cancer (TCGA-LUNG). Kaplan Meier curves of overall survival were used to investigate the association between PITX1 gene expression and OS in NSCLC patients by the UCSC Xena browser.Results
Compared with normal lung tissue, PITX gene family was upregulated in NSCLC. Furthermore, higher PITX1 expression was significantly associated with worse OSin 2 yrs., 5 yrs. and 10 yrs. OS (p?=? 0.004754, 0.01469, 0.02935 respectively) in lung adenocarcinoma (LUAD) patients, but not in lung squamous cell carcinoma (LUSC) patients. PITX1 expression increased in male patients, advanced TNM stage, advanced T stage and advanced regional lymph node status of LUAD patients. PITX1 expressed lowest in bronchioid subtype, meanwhile PITX1 expression was highest in squamoid and magnoid subtype. The high DNA methylation of PITX1 indicated the poor OS in LUAD patients. GSEA revealed that inflammatory response, TNFα signaling via NFκB, TGFβ signaling, IL6 JAK STAT3 signaling and interferon Gamma response were significantly enriched in high PITX1 expression.Conclusion
These findings suggested that PITX1 might serve as a potential biomarker for early detection and prognosis prediction of LUAD patients. 相似文献13.
Zhi Ding Haitao Lan Rui Xu Xiang Zhou Yong Pan 《Pathology, research and practice》2018,214(12):1993-1999
Background
Long noncoding RNAs (lncRNAs) have been considered as significant regulators in many cancer progression, such as proliferation, invasion and other path of evolution. Nevertheless, we have not had a grasp of the role of lncRNA TP73-AS1 in gastric cancer (GC).Methods
qRT-PCR analysis was first conducted to examine the TP73-AS1 level in both GC tissues and cell lines. Then gain or loss-of-function assays were carried out to detect the effect of TP73-AS1 on GC development. In mechanism, bioinformatics analysis and luciferase reporter assays were used to search and confirm the target gene of TP73-AS1. Finally, rescue assays were performed to confirm the influence of TP73-AS1-miR-194-5p-SDAD1 axis on GC development.Results
TP73-AS1 was upregulated in GC tissues and cell lines. Furthermore, TP73-AS1 exerted oncogenic role in GC through promoting cell growth and metastasis. In addition, TP73-AS1 was certified as a ceRNA by regulating miR-194-5p/SDAD1 axis.Conclusions
TP73-AS1 accelerates tumor progression in gastric cancer through regulating miR-194-5p/SDAD1 axis. 相似文献14.
You Zhou Xiao Zheng Lu-jun Chen Bin Xu Jing-ting Jiang 《Pathology, research and practice》2019,215(2):335-342
Background
The aim of the study was to measure the expression of microRNA (miR)-181b in patients with lung cancer, investigate its biological function and elucidate the underlying mechanisms associated with the development of lung cancer.Methods
miR-181b expression in tissues was measured via RT-qPCR. After A549 cells were transfected with miR-181b mimic or si-Sox6, the proliferation, migration and cell cycle distribution of A549 were evaluated using cell counting kit-8 assay, transwell assay and flow cytometry. The levels of cell cycle-related proteins and Sox6 were analyzed by western blotting. Gene targets of miR-181b were predicted via bioinformatics analysis and verified using a dual-luciferase reporter gene assay.Results
Expression of miR-181b was significantly downregulated in lung cancer tissues (P?<?0.05), and was inversely correlated with the degree of cell differentiation and clinical stages of lung cancer (both P?<?0.05). Additionally, the expression of miR-181b was significantly lower in adenocarcinoma compared with squamous cell carcinoma in the lungs (P?<?0.05). Overexpression of miR-181b significantly decreased the protein level of Sox6 and significantly suppressed the cell proliferation and metastasis (both P?<?0.05); this effect was also observed in A549 cells transfected with si-Sox6. The luciferase activity of a Sox6 3′-untranslated region-based reporter construct was significantly lower when transfected with miR-181b (P?<?0.05), which suggests that Sox6 is a direct target of miR-181b.Conclusion
The results of the present study suggest that miR-181b may function as a tumor inhibitor in the development of lung cancer via targeting Sox6 to decrease the proliferation and metastasis of lung cancer cells. 相似文献15.
Zhiming Ma 《Pathology, research and practice》2018,214(3):356-360
Background
SETD8 (named PR-SET7 or KMT5a) has been reported to regulate various biological processes including carcinogenesis. However, the role of SETD8 in glioma progression has not been investigated.Method
qPCR and western blot were used to detect the expression levels of miR-382 and SETD8. MTT and wound healing assay used to detect the cell proliferation and migratory capability. A predicted target of miR-382 (SETD8) was first validated using a luciferase assay.Results
In this study, we found that SETD8 expression was evidently upregulated in glioma tissues and glioma cells, compared with the adjacent normal tissues and normal human astrocytes (NHA). Next, we showed that SETD8 evidently induced cell proliferation and migration in vitro and in vivo. In addition,dual-luciferase assays revealed that miR-382 directly regulates oncogenic SETD8 expression in U87 and U251 cells. Finally a statistically significant inverse correlation of miR-382 and SETD8 expression was observed in 30 glioma patients.Conclusion
These data indicated that oncogenic SETD8 was regulated by miR-382 and involved glioma progression, revealing new therapeutic targets for glioma cancer. 相似文献16.
Binnari Kim Yun-jeong Jang Sujin Park Jung-Il Lee Hong Kwan Kim Joungho Han 《Pathology, research and practice》2019,215(4):807-815
Background
Studies have shown that 30–50% of non-small cell lung cancer (NSCLC) patients develop brain metastasis (BM). Since BM shortens overall survival and decreases the quality of life, early detection and treatment of BM are vital. While data are available for clinical risk factors of NSCLC with BM, histopathological factors are not well understood. Therefore, we evaluated the histopathological related factors which will help early detection and selection of effective treatment options.Materials and methods
A total of 117 surgical lung specimens diagnosed as NSCLC with BM were included as a study group. We included 237 cases without BM as a control group. One pathologist reviewed H&E slides and analyzed the histopathologic factors of all cases.Results
In pulmonary adenocarcinoma, vascular invasion, N stage, micropapillary pattern and necrosis were significantly associated with BM in multivariate analysis (vascular invasion, p?=?0.009; micropapillary pattern, p?=?0.024; others, p?<?0.001). Tumor with extensive necrosis had higher hazard ratio and shorter time to BM (p?<?0.001).Conclusion
Our findings suggest that necrosis is a new predictive factor of BM in pulmonary adenocarcinoma. Short term follow-up is needed especially when extensive necrosis is present. 相似文献17.
Kamuran Ibis Sezer Saglam Esra Kaytan Saglam Pinar Firat Dilek Yilmazbayhan Alper Toker Berker Ozkan Veysel S. Hancer Murat Buyukdogan Rian Disci Kezban Nur Pilanci 《Pathology, research and practice》2018,214(9):1291-1296
Background
To assess the prognostic importance of carbonic anhydrase IX (CA IX), a hypoxic biomarker, after neoadjuvant treatment in Stage III non-small cell lung cancer (NSCLC) patients.Methods
Tissue CA IX expression was examined after surgical resection in 77 patients who had undergone neoadjuvant treatment. The effects of CA IX overexpression and other clinical factors on disease-free survival and overall survival were investigated.Results
In multivariate analysis, number of neoadjuvant chemotherapy (CT) courses and gender emerged as significant independent predictors for disease-free survival, where administration of 2–3 courses of neoadjuvant chemotherapy (CT) (HR, 3.2 [95% CI 1.3–7.6], p?=?0.009) and female gender were associated with poor survival (HR, 3.2 [95% CI 1.3–7.7], p?=?0.009). The only significant independent predictor for overall survival was recurrence (HR, 5.6 [95% CI 2.4–12.8], p?<?0.001). On the other hand, CA IX overexpression was not associated with disease free survival (p?=?0.560) or overall survival (p?=?0.799).Discussion
Our results do not suggest a prognostic role for CA IX overexpression in stage III NSCLC patients who received neoadjuvant treatment. 相似文献18.
Wen-Jing Liu Li Zhou Zhi-Yong Liang Wei-Xun Zhou Lei You Tai-Ping Zhang Yu-Pei Zhao 《Pathology, research and practice》2018,214(2):228-232
Background
It was found that G-protein-coupled receptor kinase 3 (GRK3) played key biological roles in some cancers. However, its associations with clinicopathologic features and prognosis in pancreatic ductal adenocarcinoma (PDAC) remain unknown.Methods and methods
Expression of GRK3 was detected, using tissue microarray-based immunohistochemistry, in paired formalin-fixed paraffin-embedded tumor and non-tumor samples from 165 patients with PDAC after curative resection, and was further correlated with clinicopathologic parameters and cancer-specific survival (CSS).Results
It was shown that GRK3 expression was much lower in tumor than in non-tumor tissues. Moreover, expression of GRK3 in tumor tissues was significantly associated with gender and T stage. Univariately, high GRK3 expression was predictive for favorable CSS, along with some conventional clinicopathologic variables. In multivariate Cox regression test, GRK3 expression remained to be a significant prognostic marker for PDAC. Finally, combination of GRK3 with some clinicopathologic variables, especially N stage, obtained more precise prediction for CSS.Conclusions
Our data suggested that expression of GRK3 was down-regulated in PDAC and was an independent prognostic factor. 相似文献19.
Evaluation of NCAM and c-Kit as hepatic progenitor cell markers for intrahepatic cholangiocarcinomas
Jing Xu Yanhong Tan Xiaoxia Shao Cuiming Zhang Yanling He Jie Wang Yanfeng Xi 《Pathology, research and practice》2018,214(12):2011-2017
Background
Intrahepatic cholangiocarcinomas (ICCs) are primary liver malignancies and are the second most common type of malignancy after hepatocellular carcinoma. ICCs are heterogeneous in clinical features, genotype, and biological behavior, suggesting that ICCs can initiate in different cell lineages.Aim
We investigated intrahepatic cholangiocarcinoma RBE cell lines for the markers neural cell adhesion molecule (NCAM) and c-Kit, which possess hepatic progenitor cells properties.Methods
NCAM?+?c-Kit?+?cells were tested for hepatic progenitor cell properties including proliferation ability, colony formation, spheroid formation, and invasiveness in NOD/SCID mice. The Agilent Whole Human Genome Microarray Kit was used to evaluate differences in gene expression related to stem cell signaling pathways between NCAM?+?c-Kit?+?and NCAM-c-Kit- subset cells. Microarray results were further confirmed by real-time RT-PCR.Results
NCAM?+?c-Kit?+?cells showed hepatic progenitor cell-like traits including the abilities to self-renew and differentiate and tumorigenicity in NOD/SCID mice. Differences were observed in the expression of 421 genes related to stem cell signaling pathways (fc ≥ 2 or fc ≤ 0.5), among which 231 genes were upregulated and 190 genes were downregulated.Conclusion
NCAM?+?c-Kit?+?subset cells in RBE may have properties of hepatic progenitor cells. NCAM combined with c-Kit may be a valuable marker for isolating and purifying ICC stem/progenitor cells. 相似文献20.
Yoon Jin Cha Hyo Sup Shim Joungho Han Yong Soo Choi 《Pathology, research and practice》2018,214(12):2093-2098