scholarly journals The expression of HOXA13 in lung adenocarcinoma and its clinical significance: A study based on The Cancer Genome Atlas, Oncomine and reverse transcription‑quantitative polymerase chain reaction

2018 ◽  
Author(s):  
Yun Deng ◽  
Rongquan He ◽  
Rui Zhang ◽  
Binliang Gan ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Lung Adenocarcinoma ◽  
Clinical Significance ◽  
Reverse Transcription ◽  
Quantitative Polymerase Chain Reaction ◽  
The Cancer Genome Atlas ◽  
Chain Reaction ◽  
Cancer Genome Atlas ◽  
Polymerase Chain ◽  
Genome Atlas

Phosphatase and Tensin Homolog Is a Potential Target for Ovarian Cancer Sensitization to Cytotoxic Agents

2016 ◽  
Vol 26 (4) ◽  
pp. 632-639 ◽  
Author(s):  
Aiste McCormick ◽  
Eleanor Earp ◽  
Charlotte Leeson ◽  
Michelle Dixon ◽  
Rachel O’Donnell ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Polymerase Chain Reaction ◽  
The Cancer Genome Atlas ◽  
Chain Reaction ◽  
Phosphatase And Tensin Homolog ◽  
Atlas Data ◽  
Tensin Homolog ◽  
Cancer Genome Atlas ◽  
Polymerase Chain ◽  
Genome Atlas

ObjectivesThe phosphatase and tensin homolog (PTEN) tumor suppressor protein has been found to be inactivated or mutated in various human malignancies and to play a role in cisplatin and poly(ADP-ribose) polymerase inhibitor sensitivity. In this study, we assessed the association of PTEN loss with homologous recombination (HR) deficiency and increased chemosensitivity.Materials and MethodsThe PTEN knockdown models were created using MISSION shRNA lentiviral transduction particles in cell lines derived from normal ovarian surface epithelium and a mixed endometrioid/clear-cell carcinoma. Sensitivity to common therapeutics was assessed using sulforhodamine B assay. Twenty-eight unselected primary epithelial ovarian cancer cultures derived from ascitic fluid collected at the time of surgery and matched genomic DNA were assessed for PTEN mutations using polymerase chain reaction amplification and Sanger sequencing and for mRNA expression using quantitative reverse transcription-polymerase chain reaction; HR was determined using γH2AX/RAD51 assay. The Cancer Genome Atlas data were analyzed using cBioPortal.ResultsIn the carcinoma cell line, the PTEN knockdown enhanced sensitivity to cisplatin, rucaparib, doxorubicin, camptothecin, paclitaxel, and irradiation. In the primary ovarian cancer cultures, 2 point mutations were found (1105T>TG, 25L>L in 6 cultures and 1508G>GA, 159R>R in 4 cultures). The PTEN mRNA expression varied over 40-fold between the cultures, but did not correlate with HR status or in vitro sensitivity to cisplatin or rucaparib. The Cancer Genome Atlas data showed a rate of 8% alteration in PTEN and a trend toward improved survival in PTEN-mutated cases.ConclusionsThese data indicate that although PTEN mutations in ovarian cancer are rare, PTEN inhibition results in therapeutic sensitization. Therefore, PTEN may be an important therapeutic target, in at least some cancers.

scholarly journals Clinical value of miR-452-5p expression in lung adenocarcinoma: A retrospective quantitative real-time polymerase chain reaction study and verification based on The Cancer Genome Atlas and Gene Expression Omnibus databases

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770575 ◽  
Author(s):  
Xiao-ning Gan ◽  
Jie Luo ◽  
Rui-xue Tang ◽  
Han-lin Wang ◽  
Hong Zhou ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Gene Expression Omnibus ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Chain Reaction ◽  
Clinical Value ◽  
Node Metastasis ◽  
Cancer Genome Atlas ◽  
Polymerase Chain ◽  
Genome Atlas

The role and mechanism of miR-452-5p in lung adenocarcinoma remain unclear. In this study, we performed a systematic study to investigate the clinical value of miR-452-5p expression in lung adenocarcinoma. The expression of miR-452-5p in 101 lung adenocarcinoma patients was detected by quantitative real-time polymerase chain reaction. The Cancer Genome Atlas and Gene Expression Omnibus databases were joined to verify the expression level of miR-452-5p in lung adenocarcinoma. Via several online prediction databases and bioinformatics software, pathway and network analyses of miR-452-5p target genes were performed to explore its prospective molecular mechanism. The expression of miR-452-5p in lung adenocarcinoma in house was significantly lower than that in adjacent tissues (p < 0.001). Additionally, the expression level of miR-452-5p was negatively correlated with several clinicopathological parameters including the tumor size (p = 0.014), lymph node metastasis (p = 0.032), and tumor–node–metastasis stage (p = 0.036). Data from The Cancer Genome Atlas also confirmed the low expression of miR-452 in lung adenocarcinoma (p < 0.001). Furthermore, reduced expression of miR-452-5p in lung adenocarcinoma (standard mean deviations = −0.393, 95% confidence interval: −0.774 to −0.011, p = 0.044) was validated by a meta-analysis. Five hub genes targeted by miR-452-5p, including SMAD family member 4, SMAD family member 2, cyclin-dependent kinase inhibitor 1B, tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein epsilon, and tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein beta, were significantly enriched in the cell-cycle pathway. In conclusion, low expression of miR-452-5p tends to play an essential role in lung adenocarcinoma. Bioinformatics analysis might be beneficial to reveal the potential mechanism of miR-452-5p in lung adenocarcinoma.

Expression of DNA repair genes in oral squamous cell carcinoma using reverse transcription-quantitative polymerase chain reaction

2020 ◽  
Vol 130 (3) ◽  
pp. 298-305
Author(s):  
Mônica Ghislaine Oliveira Alves ◽  
Natália da Silva Miguel ◽  
Camila Cristina Panisello Ferreira ◽  
Elis Ribeiro Alvarenga ◽  
Bruna Manzanares Tonon ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Squamous Cell Carcinoma ◽  
Dna Repair ◽  
Oral Squamous Cell Carcinoma ◽  
Reverse Transcription ◽  
Quantitative Polymerase Chain Reaction ◽  
Dna Repair Genes ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Repair Genes
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