scholarly journals Thymidylate synthetase and dihydropyrimidine dehydrogenase mRNA levels in esophageal cancer

2010 ◽  
Vol 2 (2) ◽  
pp. 297-301 ◽  
Author(s):  
MASAHIRO KIMURA ◽  
YOSHIYUKI KUWABARA ◽  
AKIRA MITSUI ◽  
HIDEYUKI ISHIGURO ◽  
NOBUYOSHI SUGITO ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Dihydropyrimidine Dehydrogenase ◽  
Thymidylate Synthetase ◽  
Mrna Levels

High intratumoral dihydropyrimidine dehydrogenase mRNA levels in pancreatic cancer associated with a high rate of response to S-1

2008 ◽  
Vol 63 (1) ◽  
pp. 85-89 ◽  
Author(s):  
Hidekazu Kuramochi ◽  
Kazuhiko Hayashi ◽  
Kazumi Uchida ◽  
Go Nakajima ◽  
Takashi Hatori ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Dihydropyrimidine Dehydrogenase ◽  
High Rate ◽  
Mrna Levels ◽  
Rate Of Response

Use of DNA repair proteins translated from biomarker screening to predict overall survival in patients with esophageal cancer treated with oxaliplatin chemotherapy.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e13587-e13587
Author(s):  
Ricky A Sharma ◽  
Tom Macgregor ◽  
Richard Gillies ◽  
Stephanie Hatch ◽  
Lonnie Swift ◽  
...  
Keyword(s):  
Overall Survival ◽  
Esophageal Cancer ◽  
Dna Repair ◽  
Cho Cells ◽  
Univariate Analysis ◽  
S Phase ◽  
Mrna Levels ◽  
Oxaliplatin Treatment ◽  
Response To Chemotherapy ◽  
Dna Repair Proteins

e13587 Background: Oxaliplatin is first-line chemotherapy for colorectal, gastric, and esophageal cancers. Aim was to identify key determinants of oxaliplatin sensitivity and optimise these biomarkers to select patients for chemotherapy. Methods: High-throughput screening of oxaliplatin sensitivity was performed in a Schizosaccharomyces pombe deletion library of 229 DNA repair strains and Chinese Hamster Ovary (CHO) cell lines with mutations in specific proteins. Biopsies were taken from 50 patients with esophageal cancer, who then received two cycles of oxaliplatin and fluorouracil chemotherapy prior to surgery. Levels of DNA repair proteins were quantified by immunohistochemistry and by qRT-PCR. Results: Twelve lead biomarkers were identified from the preclinical models. In CHO cells, XPF and ERCC1 mutants were approximately 30 times more sensitive than the WT cells (p<0.01). In comparison to WT CHO cells, XPF-deficient cells had prolonged delay in mid-late S-phase after oxaliplatin treatment, and persistence of double strand breaks for at least 48 hours. Modified Comet assay confirmed persistence of inter-strand crosslinks created by oxaliplatin. Cells deficient in DNA polymerase eta (pol eta) also accumulated in S-phase and were 3-fold more sensitive (p<0.01) to oxaliplatin treatment than pol eta-complemented cells. Knockdown of XPF, ERCC1 or pol eta sensitised both oxaliplatin-resistant and oxaliplatin-sensitive HCT116 cells to oxaliplatin. In patients with esophageal cancer, low or absent XPF protein expression predicted complete pathological response to chemotherapy with a sensitivity of 58% and specificity of 72%. Cyclin A protein levels (univariate analysis, p<0.005) and pol eta mRNA levels (multivariate analysis, P<0.005) in pre-treatment esophageal biopsies correlated with overall survival. Conclusions: Results suggest that inter-strand DNA cross-links are the principal cytotoxic lesions created by oxaliplatin. Homologous recombination and damage checkpoint proteins are leading biomarkers for patient selection. In patients with esophageal cancer, XPF and pol eta predict response to oxaliplatin chemotherapy.

Carvacrol Induces Cell Apoptosis in Human Esophageal Squamous Carcinoma the Human Esophageal Squamous Carcinoma Cell Line (KYSE-150) Cells

2021 ◽  
Vol 11 (9) ◽  
pp. 1844-1847
Author(s):  
DaoBin Lin ◽  
Zhangkai Yang ◽  
YiHua Su ◽  
YaWei Cheng
Keyword(s):  
Cell Proliferation ◽  
Esophageal Cancer ◽  
Cell Apoptosis ◽  
Squamous Carcinoma ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Anti Cancer ◽  
Esophageal Squamous Carcinoma Cell ◽  
Esophageal Squamous Carcinoma ◽  
Squamous Carcinoma Cell

Carvacrol is a natural phenol with antioxidant, antimicrobials, and anti-cancer activities. The present study aimed to explore the anti-cancer activity of carvacrol in human esophageal squamous carcinoma KYSE-150 cells. Cell proliferation and apoptosis were measured using WST-1 assay and cell death detection ELISA kit respectively. Caspase activities were determined with caspase fluorometric assay kits. WST-1 assay revealed that carvacrol suppressed KYSE-150 cell proliferation in both dose and time-dependent manner. Carvacrol could increase cell apoptosis in a dose-dependent manner through caspase-3 and caspase-9 activation. In addition, Bcl-2 mRNA levels were significantly decreased by carvacrol treatment. This study delivers that carvacrol exerts a favorable anti-cancer action against esophageal cancer via inhibiting cell proliferation and inducing cell apoptosis. These discoveries suggest that carvacrol is deserved to be further studied and developed as a chemotherapeutic agent for esophageal cancer.

Phase I Study of Capecitabine With Concomitant Radiotherapy for Patients With Locally Advanced Pancreatic Cancer: Expression Analysis of Genes Related to Outcome

2005 ◽  
Vol 23 (34) ◽  
pp. 8679-8687 ◽  
Author(s):  
M. Wasif Saif ◽  
Mohammaed A. Eloubeidi ◽  
Suzanne Russo ◽  
Adam Steg ◽  
Jennifer Thornton ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Dihydropyrimidine Dehydrogenase ◽  
Locally Advanced ◽  
Three Dimensional ◽  
Advanced Pancreatic Cancer ◽  
Needle Aspiration ◽  
Mrna Levels ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Grade 3

Purpose To establish the feasibility of capecitabine with concurrent radiotherapy (XRT) in patients with locally advanced (LA) pancreatic cancer and evaluate the effect of XRT on thymidine phosphorylase (TP), dihydropyrimidine dehydrogenase (DPD), and tumor necrosis factor-alpha (TNF-α). Patients and Methods Fifteen patients with LA pancreatic cancer received three-dimensional conformal XRT to a dose of 50.4 Gy with capecitabine at escalating doses from 600 to 1,250 mg/m2 bid (Monday through Friday). Following chemo-XRT, stable and responding patients were treated with capecitabine 2,000 mg/m2 orally bid for 14 days every 21 days. Tumor specimens were procured with endoscopic ultrasound–guided fine-needle aspiration 1 week before and 2 weeks after chemo-XRT to evaluate TP, DPD, and TNF-α mRNA levels. Results Dose-limiting grade 3 diarrhea was observed in two of six patients treated at a capecitabine dose of 1,000 mg/m2 with XRT. Three patients (20%) achieved partial response. Mean percent difference in TP pre- and post-XRT was 119.2% (P = .1934). There was no significant differences in mean TNF-α, or DPD levels pre- and post-XRT (P = .1934 and .4922, respectively). TP and TNF-α levels were not significantly correlated both at pre- and post-XRT (P = .670 and P < .154, respectively). Median value of TP:DPD ratios at baseline was 2.65 (range, 0.36 to 11.08). No association between TP:DPD ratio and efficacy of capecitabine or severity of toxicities was identified. Conclusion The recommended dose for phase II evaluation is capecitabine 800 mg/m2 bid (Monday through Friday) with concurrent XRT. This approach offers an easy alternative to intravenous fluorouracil as a radiosensitizer in these patients. Role of TP and TP:DPD ratio warrants further investigation in a larger clinical trial.

scholarly journals RNA-Binding Proteins CLK1 and POP7 as Biomarkers for Diagnosis and Prognosis of Esophageal Squamous Cell Carcinoma

2021 ◽  
Vol 9 ◽  
Author(s):  
Xiuping Yang ◽  
Baoai Han ◽  
Zuhong He ◽  
Ya Zhang ◽  
Kun Lin ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Cancer ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Risk Group ◽  
Mrna Levels ◽  
Worse Prognosis

The abnormality of RNA-binding proteins (RBPs) is closely related to the tumorigenesis and development of esophageal squamous cell carcinoma (ESCC), and has been an area of interest for research recently. In this study, 162 tumors and 11 normal samples are obtained from The Cancer Genome Atlas database, among which 218 differentially expressed RBPs are screened. Finally, a prognostic model including seven RBPs (CLK1, DDX39A, EEF2, ELAC1, NKRF, POP7, and SMN1) is established. Further analysis reveals that the overall survival (OS) rate of the high-risk group is lower than that of the low-risk group. The area under the receiver operating characteristic (ROC) curve (AUC) of the training group and testing group is significant (AUCs of 3 years are 0.815 and 0.694, respectively, AUCs of 5 years are 0.737 and 0.725, respectively). In addition, a comprehensive analysis of seven identified RBPs shows that most RBPs are related to OS in patients with ESCC, among which EEF2 and ELCA1 are differentially expressed at the protein level of ESCC and control tissues. CLK1 and POP7 expressions in esophageal cancer tumor samples are undertaken using the tissue microarray, and show that CLK1 mRNA levels are relatively lower, and POP7 mRNA levels are higher compared with non-cancerous esophageal tissues. Survival analysis reveals that a higher expression of CLK1 predicts a significant worse prognosis, and a lower expression of POP7 predicts a worse prognosis in esophageal cancer. These results suggest that CLK1 may promote tumor progression, and POP7 may hinder the development of esophageal cancer. In addition, gene set enrichment analysis reveals that abnormal biological processes related to ribosomes and abnormalities in classic tumor signaling pathways such as TGF-β are important driving forces for the occurrence and development of ESCC. Our results provide new insights into the pathogenesis of ESCC, and seven RBPs have potential application value in the clinical prognosis prediction of ESCC.

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