Aim: To investigate c-met expression during early pancreatic carcinogenesis.
Methods: We used 46 bulk tissues and 36 micro-dissected samples, including normal pancreas, chronic pancreatitis, and pancreatic cancer, for quantitative real-time reverse transcription-polymerase chain reaction.
Results: In bulk tissue analyses, pancreatic cancer tissues expressed significantly higher levels of c-met than did chronic pancreatitis and normal pancreas tissues. c-met levels did not differ between chronic pancreatitis and normal pancreas tissues. In microdissection-based analyses, c-met was expressed at higher levels in microdissected pancreatic cancer cells and pancreatitis-affected epithelial cells than in normal ductal epithelial cells (both, P < 0.01). Interestingly, pancreatitis-affected epithelial cells expressed levels of c-met similar to those of pancreatic cancer cells.
Conclusion: Overexpression of c-met occurs during the early stage of pancreatic carcinogenesis, and a single alteration of c-met expression is not sufficient for progression of chronic pancreatitis-affected epithelial cells to pancreatic cancer cells.
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http://dx.doi.org/10.3748/wjg.v12.i24.3878 | DOI Listing |
World J Surg Oncol
January 2025
Department of Hepatobiliary Surgery, Guangzhou Red Cross Hospital of Jinan University, Tongfu Roud 396, Guangzhou, 510220, Guangdong, China.
Schwannomas are tumors that originate from the glial cells of the nervous system and can occur on myelinated nerve fibers throughout the body, especially in the craniofacial region. However, pancreatic schwannomas are extremely rare. We report a case of a pancreatic schwannoma that was difficult to differentiate from other pancreatic tumors preoperatively.
View Article and Find Full Text PDFBMC Cancer
January 2025
Department of Medical Oncology, Cancer Centre of Excellence, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
Background: Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, with limited treatment options yielding poor outcomes. This study aimed to evaluate the real-world clinical characteristics, treatment patterns, and outcomes of patients with locally advanced unresectable and de-novo metastatic PDAC in Saudi Arabia, providing regional data to compare with international benchmarks.
Methods: This is a retrospective, multicentre study involving 350 patients diagnosed with unresectable locally advanced or de-novo metastatic PDAC between January 2015 and November 2023.
BMC Cancer
January 2025
Department of General Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Peking, Beijing, 100023, People's Republic of China.
Background: Pancreatic cancer is a highly aggressive neoplasm characterized by poor diagnosis. Amino acids play a prominent role in the occurrence and progression of pancreatic cancer as essential building blocks for protein synthesis and key regulators of cellular metabolism. Understanding the interplay between pancreatic cancer and amino acid metabolism offers potential avenues for improving patient clinical outcomes.
View Article and Find Full Text PDFNat Med
January 2025
Department of Medicine, Memorial Sloan Kettering Cancer Center, New York City, NY, USA.
Nearly all pancreatic adenocarcinomas (PDAC) are genomically characterized by KRAS exon 2 mutations. Most patients with PDAC present with advanced disease and are treated with cytotoxic therapy. Genomic biomarkers prognostic of disease outcomes have been challenging to identify.
View Article and Find Full Text PDFCommun Biol
January 2025
Translational Inflammation Research, Medical Faculty, Otto von Guericke University (OvGU), Magdeburg, Magdeburg, Germany.
Extrinsic apoptotic network is driven by Death Ligand (DL)-mediated activation of procaspase-8. Recently, we have developed the first-in class small molecule, FLIPinB, which specifically targets the key regulator of extrinsic apoptosis, the protein c-FLIP, in the caspase-8/c-FLIP heterodimer. We have shown that FLIPinB enhances DL-induced caspase-8 activity and apoptosis.
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