Bałan Barbara Joanna, Zygmanowska Ewa, Radomska-Leśniewska Dorota Magdalena
Department of Immunology, Biochemistry and Nutrition, Medical University of Warsaw, Poland.
Department of Histology and Embryology, Biostructure Centre, Medical University of Warsaw, Poland.
Cent Eur J Immunol. 2017;42(4):377-382. doi: 10.5114/ceji.2017.68698. Epub 2017 Dec 30.
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.
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。