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標題: 自然發生之犬傳染性花柳性腫瘤於使用Vincristine治療後腫瘤微環境的變化
The microenvironmental changes in naturally occur-ring Canine transmissible venereal tumor after vin-cristine treatment
作者: 鄭玉均
Cheng, Yu-chung
關鍵字: 犬傳染性花柳性腫瘤
Canine transmissible venereal tumor (CTVT)
出版社: 獸醫學系暨研究所
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摘要: 犬傳染性花柳性腫瘤(Canine transmissible venereal tumor, CTVT) 於使用Vincristine (VCR)治療後,常可見明顯消退,僅少數病例對此藥物有抗性 (vincristine-resistant CTVT, VRTVT)。因此,CTVT可以作為探討腫瘤微環境的改變是如何影響化療結果,而造成腫瘤有效消退的模式。本研究探討於使用VCR治療後腫瘤內浸潤之淋巴球的數量、腫瘤細胞凋亡及表現主要組織相容複合體 (MHC class II)、黑色素細胞瘤抗原-A (MAGE-A protein) 及抗藥性蛋白(P-glycoprotein, P-gp)在CTVT細胞的表現與腫瘤消退之相關性。VRTVT 在化療後細胞組織學及細胞學之特徵與生長期中之CTVT相似,但消退中的腫瘤則與前二者差異很大。於使用VCR治療後消退中的CTVT,細胞學下可見淋巴球與漿細胞顯著增加;於免疫組織化學染色下則可見CD3+淋巴球,CD79a+淋巴球及MHC class II+腫瘤細胞也皆有顯著增加(p<0.05),凋亡之腫瘤細胞的比例也增加了。但於VRTVT,CD79a+淋巴球及凋亡之腫瘤細胞相較於化療前則無顯著增加。另一方面,CTVT化療後高表現腫瘤相關抗原MAGE-A的比例增加,VRTVT也顯示高表現此蛋白,且主要表現於細胞核。化療前較高比例之CTVT強表現P-gp,化療後強表現的比例減少,VRTVT則仍高表現此蛋白。VRTVT高表現P-gp可能使細胞擁有對抗VCR毒性的能力,因此無法消退,但為何CTVT化療前後的表現量有差異及為何CTVT可表現P-gp的詳細機制仍須進一步被釐清。此些結果顯示,VCR可誘發CTVT細胞之凋亡,此凋亡有能力引起免疫反應,而造成淋巴球聚集至腫瘤微環境中(特別是CD3+淋巴球),但缺少CD79a+淋巴球可能為VRTVT對VCR有抗性的原因。總結以上,足夠之CD3+與CD79a+淋巴球聚集治腫瘤微環境、MHC class II+腫瘤細胞增加、降低P-gp之表現及增加MAGE-A表現在VCR誘導CTVT消退中扮演著重要的角色。
Canine transmissible venereal tumor (CTVT) reveals effectively regression after vincristine treatment, and the resistance has been found only in a minority of CTVT. Thus, this tumor can be an informative tumor model for studying chemotherapy. The purpose of this study was to investigate association between the amounts of tumor infiltrating immunocytes, apoptosis fraction, the expression of MHC class II antigen, tumor-associated antigen (MAGE-A protein), drug efflux transporter P-glycoprotein (P-gp) in vincristine-induced regression and vincristine-resistance of naturally occurring CTVT. Histological and cytological examinations showed the characteristics of pro-gressive stage and vincristine-resistant CTVTs (VRTVTs) were very similar and differed from those in vincristine-induced regressive stage. In effectively regressed CTVTs, lymphocytes and plasma cells significantly increased (P<0.05) via cytological exami-nation; in addition, CD3 and CD79a positive lymphocytes, MHC II positive tumor cells significantly elevated (P<0.05) via immunohistochemical observations. However, CD79a positive lymphocytes and apoptotic fraction showed no significant increases in VRTVT compared with those regression ones; therefore, TVTs without increasing number of CD79a positive lymphocyte after chemotherapy treatment were likely to have resistant to vincristine. Higher ratio of CTVT expressed MAGE-A protein intensely after vincristine treatment, and mainly on the nucleus. Lower ratio of CTVT expressed P-gp intensely after VCR treatment. Without down- regulated P-gp, VRTVT cells survived from vincristine treatment. Taken together, sufficient CD3 and CD79a positive lym-phocytes appeared in tumor microenvironment, decrease expression of P-gp on cell membrane, and stronger expressed MAGE-A protein in tumor cell played a role in CTVT regression after vincristine treatment.
其他識別: U0005-1107201113133200
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