Department of Clinical Pathomorphology, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Sklodowskiej-Curie Str. 9, 85-094, Bydgoszcz, Poland.
Department of Pathomorphology, Military Clinical Hospital, Bydgoszcz, Poland.
Mol Biol Rep. 2019 Dec;46(6):6629-6645. doi: 10.1007/s11033-019-05058-1. Epub 2019 Sep 5.
Pancreatic cancer (PC) is the fourth most common cause of death among all cancers. Poor prognosis of PC may be caused by a prevalence of cancer stem cells (CSCs). CSCs are a population of cancer cells showing stem cell-like characteristics. CSCs have the ability to self-renew and may initiate tumorigenesis. PC CSCs express markers such as CD133, CD24, CD44, DCLK1, CXCR4, ESA, Oct4 and ABCB1. There is a wide complexity of interaction and relationships between CSC markers in PC. These markers are negative prognostic factors and are connected with tumor recurrence and clinical progression. Additionally, PC CSCs are resistant to treatment with gemcitabine. Thus, most current therapies for PC are ineffective. Numerous studies have shown, that targeting of these proteins may increase both disease-free and overall survival in PC.
胰腺癌（PC）是所有癌症中第四种最常见的死亡原因。PC 预后不良可能是由于癌症干细胞（CSC）的普遍存在造成的。CSC 是一群具有干细胞样特征的癌细胞。CSC 具有自我更新的能力，并可能引发肿瘤发生。PC CSC 表达 CD133、CD24、CD44、DCLK1、CXCR4、ESA、Oct4 和 ABCB1 等标志物。在 PC 中，CSC 标志物之间存在广泛的相互作用和关系复杂性。这些标志物是不良预后因素，与肿瘤复发和临床进展有关。此外，PC CSCs 对吉西他滨治疗具有耐药性。因此，目前大多数 PC 治疗方法均无效。大量研究表明，针对这些蛋白的治疗可能会提高 PC 的无病生存率和总生存率。
