关键词: Adjacent normal tissue Angiogenesis C-Kit receptor Endothelial area Mast cells Microvascular density Pancreatic tumor tissue Tryptase

Mesh : Humans Pancreatic Neoplasms / pathology metabolism immunology Mast Cells / metabolism immunology Tumor Microenvironment / immunology Neovascularization, Pathologic Carcinoma, Pancreatic Ductal / pathology immunology metabolism Pancreas / pathology immunology metabolism Animals Pancreatitis / metabolism pathology immunology Risk Factors Inflammation Mediators / metabolism Tryptases / metabolism Inflammation / metabolism

来  源:   DOI:10.3748/wjg.v30.i23.2927   PDF(Pubmed)

Abstract:
In this editorial, we focus specifically on the mechanisms by which pancreatic inflammation affects pancreatic cancer. Cancer of the pancreas remains one of the deadliest cancer types. The highest incidence and mortality rates of pancreatic cancer are found in developed countries. Trends of pancreatic cancer incidence and mortality vary considerably worldwide. A better understanding of the etiology and identification of the risk factors is essential for the primary prevention of this disease. Pancreatic tumors are characterized by a complex microenvironment that orchestrates metabolic alterations and supports a milieu of interactions among various cell types within this niche. In this editorial, we highlight the foundational studies that have driven our understanding of these processes. In our experimental center, we have carefully studied the mechanisms of that link pancreatic inflammation and pancreatic cancer. We focused on the role of mast cells (MCs). MCs contain pro-angiogenic factors, including tryptase, that are associated with increased angiogenesis in various tumors. In this editorial, we address the role of MCs in angiogenesis in both pancreatic ductal adenocarcinoma tissue and adjacent normal tissue. The assessment includes the density of c-Kit receptor-positive MCs, the density of tryptase-positive MCs, the area of tryptase-positive MCs, and angiogenesis in terms of microvascularization density.
摘要:
在这篇社论中,我们特别关注胰腺炎症影响胰腺癌的机制.胰腺癌仍然是最致命的癌症类型之一。胰腺癌的发病率和死亡率最高的是发达国家。胰腺癌发病率和死亡率的趋势在世界范围内差异很大。更好地了解病因和确定危险因素对于这种疾病的一级预防至关重要。胰腺肿瘤的特征在于复杂的微环境,其协调代谢改变并支持该生态位内的各种细胞类型之间的相互作用的环境。在这篇社论中,我们强调推动我们理解这些过程的基础研究。在我们的实验中心,我们仔细研究了胰腺炎症和胰腺癌的相关机制.我们专注于肥大细胞(MC)的作用。MC含有促血管生成因子,包括类胰蛋白酶,这与各种肿瘤的血管生成增加有关。在这篇社论中,我们探讨了MC在胰腺导管腺癌组织和邻近正常组织血管生成中的作用。评估包括c-Kit受体阳性MC的密度,类胰蛋白酶阳性MC的密度,类胰蛋白酶阳性MC的区域,和微血管密度方面的血管生成。
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