Proteome of formalin-fixed paraffin-embedded pancreatic ductal adenocarcinoma and lymph node metastases

2012 ◽  
Vol 226 (5) ◽  
pp. 756-763 ◽  
Author(s):  
Kalnisha Naidoo ◽  
Richard Jones ◽  
Branko Dmitrovic ◽  
Nilukshi Wijesuriya ◽  
Hemant Kocher ◽  
...  
2017 ◽  
Vol 117 (12) ◽  
pp. 1874-1882 ◽  
Author(s):  
Vicente Morales-Oyarvide ◽  
Douglas A Rubinson ◽  
Richard F Dunne ◽  
Margaret M Kozak ◽  
Justin L Bui ◽  
...  

2020 ◽  
Vol 159 (2) ◽  
pp. 562-574
Author(s):  
Satoshi Nishiwada ◽  
Masayuki Sho ◽  
Jasjit K. Banwait ◽  
Kensuke Yamamura ◽  
Takahiro Akahori ◽  
...  

2021 ◽  
Vol 147 (5) ◽  
pp. 1341-1354
Author(s):  
Yutaka Endo ◽  
Mao Fujimoto ◽  
Nanako Ito ◽  
Yoriko Takahashi ◽  
Minoru Kitago ◽  
...  

AbstractPurposeThe present study was conducted to clarify the clinicopathological impacts of DNA methylation alterations on pancreatic ductal adenocarcinoma (PDAC).MethodsGenome-wide DNA methylation screening was performed using the Infinium HumanMethylation450 BeadChip, and DNA methylation quantification was verified using pyrosequencing. We analyzed fresh-frozen tissues from an initial cohort (17 samples of normal control pancreatic tissue [C] from 17 patients without PDAC, and 34 samples of non-cancerous pancreatic tissue [N] and 82 samples of cancerous tissue [T] both obtained from 82 PDAC patients) and formalin-fixed paraffin-embedded T samples from 34 patients in a validation cohort.ResultsThe DNA methylation profiles of N samples tended to differ from those of C samples, and 91,907 probes showed significant differences in DNA methylation levels between C and T samples. Epigenetic clustering of T samples was significantly correlated with a larger tumor diameter and early recurrence (ER), defined as relapse within 6 months after surgery. Three marker CpG sites, applicable to formalin-fixed paraffin-embedded surgically resected materials regardless of their tumor cell content, were identified for prediction of ER. The sensitivity and specificity for detection of patients belonging to the ER group using a panel combining these three marker CpG sites, including a CpG site in theCDK14gene, were 81.8% and 71.7% and 88.9% and 70.4% in the initial and validation cohorts, respectively.ConclusionThese findings indicate that DNA methylation alterations may have a clinicopathological impact on PDAC. Application of our criteria will ultimately allow prediction of ER after surgery to improve the outcome of PDAC patients.


Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 179
Author(s):  
Kristian Urh ◽  
Margareta Žlajpah ◽  
Nina Zidar ◽  
Emanuela Boštjančič

Significant progress has been made in the last decade in our understanding of the pathogenetic mechanisms of colorectal cancer (CRC). Cancer stem cells (CSC) have gained much attention and are now believed to play a crucial role in the pathogenesis of various cancers, including CRC. In the current study, we validated gene expression of four genes related to CSC, L1TD1, SLITRK6, ST6GALNAC1 and TCEA3, identified in a previous bioinformatics analysis. Using bioinformatics, potential miRNA-target gene correlations were prioritized. In total, 70 formalin-fixed paraffin-embedded biopsy samples from 47 patients with adenoma, adenoma with early carcinoma and CRC without and with lymph node metastases were included. The expression of selected genes and microRNAs (miRNAs) was evaluated using quantitative PCR. Differential expression of all investigated genes and four of six prioritized miRNAs (hsa-miR-199a-3p, hsa-miR-335-5p, hsa-miR-425-5p, hsa-miR-1225-3p, hsa-miR-1233-3p and hsa-miR-1303) was found in at least one group of CRC cancerogenesis. L1TD1, SLITRK6, miR-1233-3p and miR-1225-3p were correlated to the level of malignancy. A negative correlation between miR-199a-3p and its predicted target SLITRK6 was observed, showing potential for further experimental validation in CRC. Our results provide further evidence that CSC-related genes and their regulatory miRNAs are involved in CRC development and progression and suggest that some them, particularly miR-199a-3p and its SLITRK6 target gene, are promising for further validation in CRC.


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