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本文引用的文献

1
miRNA analysis in pancreatic cancer: the Dartmouth experience.胰腺癌中的miRNA分析:达特茅斯的经验
Clin Chem Lab Med. 2017 May 1;55(5):755-762. doi: 10.1515/cclm-2017-0046.
2
Novel Diagnostic and Predictive Biomarkers in Pancreatic Adenocarcinoma.胰腺腺癌中的新型诊断和预测生物标志物
Int J Mol Sci. 2017 Mar 20;18(3):667. doi: 10.3390/ijms18030667.
3
Pivotal role of high-mobility group box 1 (HMGB1) signaling pathways in glioma development and progression.高迁移率族蛋白B1(HMGB1)信号通路在胶质瘤发生发展中的关键作用。
J Mol Med (Berl). 2016 Aug;94(8):867-74. doi: 10.1007/s00109-016-1435-y. Epub 2016 Jun 4.
4
Mesenchymal-epithelial signalling in tumour microenvironment: role of high-mobility group Box 1.肿瘤微环境中的间充质-上皮信号传导:高迁移率族蛋白盒1的作用
Cell Tissue Res. 2016 Aug;365(2):357-66. doi: 10.1007/s00441-016-2389-7. Epub 2016 Mar 16.
5
MicroRNA Targeted Therapeutic Approach for Pancreatic Cancer.胰腺癌的微小RNA靶向治疗方法
Int J Biol Sci. 2016 Jan 28;12(3):326-37. doi: 10.7150/ijbs.15017. eCollection 2016.
6
Reactive oxygen species and synthetic antioxidants as angiogenesis modulators: Clinical implications.活性氧物质与合成抗氧化剂作为血管生成调节剂:临床意义
Pharmacol Rep. 2016 Apr;68(2):462-71. doi: 10.1016/j.pharep.2015.10.002. Epub 2015 Oct 23.
7
Reactive Oxygen Species and Targeted Therapy for Pancreatic Cancer.活性氧与胰腺癌的靶向治疗
Oxid Med Cell Longev. 2016;2016:1616781. doi: 10.1155/2016/1616781. Epub 2016 Jan 3.
8
HMGB1 enhances the protumoral activities of M2 macrophages by a RAGE-dependent mechanism.高迁移率族蛋白B1(HMGB1)通过一种依赖于晚期糖基化终末产物受体(RAGE)的机制增强M2巨噬细胞的促肿瘤活性。
Tumour Biol. 2016 Mar;37(3):3321-9. doi: 10.1007/s13277-015-3940-y. Epub 2015 Oct 6.
9
The Role of HMGB1 Signaling Pathway in the Development and Progression of Hepatocellular Carcinoma: A Review.HMGB1信号通路在肝细胞癌发生发展中的作用:综述
Int J Mol Sci. 2015 Sep 17;16(9):22527-40. doi: 10.3390/ijms160922527.
10
Molecular Targeted Intervention for Pancreatic Cancer.分子靶向干预治疗胰腺癌。
Cancers (Basel). 2015 Aug 10;7(3):1499-542. doi: 10.3390/cancers7030850.

胰腺癌发展过程中发现的病症:早期有效诊断和治疗的潜在机会。

Disorders noticed during development of pancreatic cancer: potential opportunities for early and effective diagnostics and therapy.

作者信息

Bałan Barbara Joanna, Zygmanowska Ewa, Radomska-Leśniewska Dorota Magdalena

机构信息

Department of Immunology, Biochemistry and Nutrition, Medical University of Warsaw, Poland.

Department of Histology and Embryology, Biostructure Centre, Medical University of Warsaw, Poland.

出版信息

Cent Eur J Immunol. 2017;42(4):377-382. doi: 10.5114/ceji.2017.68698. Epub 2017 Dec 30.

DOI:10.5114/ceji.2017.68698
PMID:29472816
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5820973/
Abstract

Pancreatic cancer, with a total five-year survival rate below 5%, represents a disease with a high level of malignancy. Some of the pancreatic cancer bad prognosis factors are nutrition disorders. Malnutrition, neither recognized nor properly referred to by the healthcare system, leads to well-documented negative health consequences in hospitalized patients including their impaired immunity, delayed post-surgery wound healing, a high risk of infectious complications, morbidity and mortality. There are numerous factors contributing to the development of pancreatic cancer, including telomerases, inflammation, angiogenesis, epigenetics and genetics factors, miRNA, pancreatic cancer stem cells. On the basis of molecular analyses, it has been established that precursor injuries may trigger pancreatic cancer when added to genetic alterations. Perhaps, combination of few presently used methods, like signal transduction modulated by K-ras, STAT3 activation, HMGB1 releasing, presence of oxidative stress and free radicals secretion, genes for proangiogenic growth factors activation or tissue-specific miRNA genes expression - will solve the problem of inadequate diagnostics.

摘要

胰腺癌的总体五年生存率低于5%,是一种恶性程度很高的疾病。胰腺癌的一些不良预后因素是营养紊乱。医疗系统既未认识到营养不良,也未对其进行恰当提及,这在住院患者中会导致有充分文献记载的负面健康后果,包括免疫力受损、术后伤口愈合延迟、感染并发症风险高、发病率和死亡率增加。导致胰腺癌发生的因素众多,包括端粒酶、炎症、血管生成、表观遗传学和遗传学因素、微小RNA、胰腺癌干细胞。基于分子分析,已确定前驱性损伤与基因改变共同作用时可能引发胰腺癌。或许,将目前使用的几种方法结合起来,如由K-ras调节的信号转导、STAT3激活、HMGB1释放、氧化应激和自由基分泌的存在、促血管生成生长因子激活基因或组织特异性微小RNA基因表达,将解决诊断不足的问题。