Dear editor, we have read with great interest the basic research paper entitled in the journal (1)

Dear editor, we have read with great interest the basic research paper entitled in the journal (1). 93% of the resected chronic pancreatitis human specimens, especially at the ductal level and less significant in the acinar compartments (1). Loncle revealed that transition from chronic pancreatitis to pancreatic malignancy is promoted by the Il 17, using as a downstream pathway REG3-JAK2-STAT3 inflammatory pathway (12). CA19-9 expression is associated with hyperactivation of the epidermal growth factor receptor (EGFR) signaling. CA19-9 expression was associated with elevated levels of endogenous fibulin-3 (FBLN3), a glycoprotein with five EGF-like domains, which activated the EGFR pathway (1). Administration of antibodies directed against CA19-9 reduced the inflammatory process of the pancreas, the serum amylase and lipase levels, and decrease the hyperactivation of the EGFR pathway (1). Given the presence of gene mutation in more than 90% of patients with pancreatic malignancy, the role of EGFR, Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/mTORC1/GSK-3, Janus kinase/Transmission Transducer and Activator of Transcription pathways were extensively Zofenopril calcium analyzed for a better understating of disease pathogenesis (13). The EGFR family of receptors are significantly involved in malignant transformation processes, such as prevention of apoptosis, drug resistance, malignancy stem cells and metastasis (13,14). Increasing evidence supports that EGRF signaling is usually involved the metaplasia process, which converts the acinar cells in progenitor-like ductal cells. This process of acinar to ductal metaplasia may be observed in pancreatic malignancy initiation in oncogenic and patients with chronic pancreatitis (15,16). EGFR inhibitors, such as gefitinib (Iressa) and erlotinib (Tarceva) block the epithelial-to mesenchymal transition, decreasing the metastatic potential of pancreatic malignancy cells (14). Some drugs that sensitize the pancreatic cancers cells to EGRF inhibitors were described, such as rhein Zofenopril calcium (17) or alantolactone (18). Inhibition of PI3K significantly reduced acinar cells injury and necrosis in a murine model of AP (19). Karki revealed that gene transcription and protein accumulation were significantly reduced during the process of acinar-to-ductal metaplasia found in patients with AP (20). Constitutive mice with expression of Cre-inducible transgene (oncogene, generates aggressive types of pancreatic cancers, with anaplastic principal tumors and popular metastases, connected with reduced median success (202 versus 460 times) (1). There’s a combination chat between EGFR and Ras downstream pathways, UBCEP80 which appears to have essential role in generating metastasis (13). Today’s evidence uncovered constructed anti-CA 19-9 antibodies, created with desire to to specifically focus on pancreatic tumors and raise the Zofenopril calcium Zofenopril calcium precision of imagistic methods (21-23). In a murine study, the authors developed three specifically antibodies (89Zr-ssDFO-5B1, ssFL-5B1, and 89Zr-ssdual-5B1), directed against CA 19-9 for Positron Emission Tomography (PET), near-infrared fluorescent optical imaging and multimodal imaging of pancreatic cancers (24). Currently, a phase 1 study evaluates 89Zr-DFO-HuMab-5B1 (MVT-2163) and HuMab-5B1 (MVT-5873) for tumor imaging using PET scanning in patients with pancreatic malignancy and other CA 19-9 positive malignancies (25). Targeted therapies using 225Ac-labeled tetrazine radioligand and a Trans-cyclooctene-bearing anti CA 19-9 antibodies (5B1) were explained for -radioimmunotherapy of pancreatic ductal adenocarcinoma, reducing hematotoxicity while maintaining the therapeutic effects (26). Human monoclonal antibodies to sialyl-Lewisa were generated and characterized from blood lymphocytes of people immunized with sLea-KLH vaccine (27). The 5B1 and 7E3 antibodies increased the median survival of animals engrafted with Colo205 tumor cells. Treatment with 5B1 antibodies cured 40C60% of mice, while the mortality was 100% in untreated mice within 155 days. Both antibodies offered increased activity through a complement-dependent cytotoxicity mechanism; the 5B1 antibody offered also an increased antibody-dependent cytotoxicity (27). In conclusion, further basic and clinical research is needed in the area of pancreatology, due to the severity of pancreatic diseases and their increased morbidity and mortality. The recent findings revealed the genetic pathways and epigenetic factors involved in pathogenesis of acute pancreatitis, chronic pancreatitis and pancreatic malignancy, offering the hope for more precise and effective treatments in patients with pancreatic diseases. Acknowledgments None. Notes This is an invited article commissioned by the Section Editor Dr. Le Li (Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University or college, Harbin Medical University or college, Harbin, China). em Conflicts appealing /em : zero issues are had with the writers appealing to declare..