Andersson Roland, Aho Ursula, Nilsson Bo I, Peters Godefridus J, Pastor-Anglada Marçal, Rasch Wenche, Sandvold Marit L
Department of Surgery, Clinical Sciences Lund, Lund University Hospital, Sweden.
Scand J Gastroenterol. 2009;44(7):782-6. doi: 10.1080/00365520902745039.
Ductal pancreatic adenocarcinoma is associated with a very poor prognosis and most patients are given palliative care. Chemotherapy in the form of gemcitabine has been found to reduce disease-related pain, and the otherwise frequently occurring weight changes, to increase Karnofsky performance status and quality of life and has also resulted in a modest improvement in survival time. The intracellular uptake of gemcitabine is dependent on nucleoside transporters, predominantly human equilibrative nucleoside transporter-1 (hENT-1), which is over-expressed in human pancreatic adenocarcinoma cells. Cellular resistance to gemcitabine can be intrinsic or acquired during gemcitabine treatment. One of the mechanisms is a decrease in hENT-1 expression. Modifications of gemcitabine not rendering it dependent on the nucleoside transporter may be a successful future mode of chemotherapy treatment, and determination of the nucleoside receptor status at the time of diagnosis could potentially also contribute to a more targeted therapy in the future.
胰腺导管腺癌的预后非常差，大多数患者接受姑息治疗。已发现吉西他滨形式的化疗可减轻与疾病相关的疼痛以及其他常见的体重变化，提高卡氏功能状态和生活质量，还使生存时间有适度延长。吉西他滨的细胞内摄取依赖于核苷转运体，主要是人类平衡核苷转运体-1（hENT-1），其在人类胰腺腺癌细胞中过度表达。细胞对吉西他滨的耐药性可以是内在的，也可以在吉西他滨治疗期间获得。其中一种机制是hENT-1表达降低。对吉西他滨进行修饰使其不依赖核苷转运体可能是未来成功的化疗治疗模式，并且在诊断时确定核苷受体状态可能也有助于未来更有针对性的治疗。
