Publications by authors named "Oier Azurmendi Senar"
Article Synopsis
- The study focused on mesopancreatic infiltration in patients with pancreatic ductal adenocarcinoma who had pancreatoduodenectomy, assessing the correlation between imaging findings and histopathology along with their impact on survival.
- A review of 149 patients from 2015 to 2021 showed that solid infiltration of mesopancreatic fat was present in 13.4% of patients, correlating with significantly lower survival rates compared to those with normal fat or fat stranding.
- The results indicate that solid infiltration is a negative prognostic factor for patient survival, with pathological tumor size also playing a critical role in overall and disease-free survival.
Pancreatic ductal adenocarcinoma (PDAC) represents a formidable challenge due to its aggressive nature and poor prognosis. The tumor microenvironment (TME) in PDAC, characterized by intense stromal desmoplastic reactions and a dominant presence of cancer-associated fibroblasts (CAFs), significantly contributes to therapeutic resistance. However, within the heterogeneous CAF population, fibroblast activation protein (FAP) emerges as a promising target for Gallium-68 FAP inhibitor positron emission tomography (Ga68FAPI-PET) imaging.
View Article and Find Full Text PDFPancreatic ductal adenocarcinoma is one of the most lethal malignant diseases, with a mortality rate being close to incidence. Due to its heterogeneity and plasticity, as well as the lack of distinct symptoms in the early phases, it is very often diagnosed at an advanced stage, resulting in poor prognosis. Traditional tissue biopsies remain the gold standard for making a diagnosis, but have an obvious disadvantage in their inapplicability for frequent sampling.
View Article and Find Full Text PDFPancreatic ductal adenocarcinoma (PDAC) is a fatal disease with poor prognosis. Gemcitabine is the first-line therapy for PDAC, but gemcitabine resistance is a major impediment to achieving satisfactory clinical outcomes. This study investigated whether methylglyoxal (MG), an oncometabolite spontaneously formed as a by-product of glycolysis, notably favors PDAC resistance to gemcitabine.
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