Molecular biological analysis for apoptosis induction and variation of cytoskeltons ＆ adhesion molecules in malignant melanoma

恶性黑色素瘤细胞凋亡诱导及细胞骨架和粘附分子变化的分子生物学分析

• 批准号: 12670815
• 负责人: TAKAGI Hajime
• 金额: $ 2.56万
• 依托单位: Gifu University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2000
• 资助国家: 日本
• 起止时间: 2000 至 2001
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12670815/
• 关键词: apoptosis; cytoskeltons; adhesion molecules; 悪性黒色腫; 抗腫瘍剤

Basic research1. Immunohistochemically we confirmed sequential bioimmunochemotherapy induced apoptosis for mouse melanoma cells. 2. We checked drug sensitivity of cultured human melanoma cells by FACScan. 3. Variation of cytoskelton, especially vimentin, were examined with immunofluorescent technique. But analysis was not enough, because of technical trouble. 4. Animal experiments were not done. We did not prepare to a favorable environment. 5. We compared extent of multidrug-resistance-associated protein between before and after chemotherapy. 6. We have been trying establish cell line of drug resistant melanoma cells.Clinical research1. We refer to the apoptosis cells, apoptosis- related gene/protein, and adhesion molecules by melanoma patients specimens immunohistochemically. 2. We measured melanoma inhibitory activity by ELISA method, and checked with association of the value and clinical course. 3. We evaluated of combination chemotherapy (DAC-Tam) for advanced malignant melanoma.SummaryWe cannot show enough results in this periods, but we got some promising products. We will keep this projects going on some experiments.

基础研究1。免疫组化证实序贯生物免疫化疗诱导小鼠黑色素瘤细胞凋亡。2.我们通过FACScan检查培养的人黑素瘤细胞的药物敏感性。3.用免疫荧光技术检测细胞凋亡，尤其是波形蛋白的变化。但由于技术问题，分析是不够的。4.没有进行动物实验。我们没有准备好一个有利的环境。5.比较化疗前后多药耐药相关蛋白的表达情况。6.我们一直在尝试建立耐药黑色素瘤细胞系。本研究以恶性黑色素瘤患者标本为研究对象，通过免疫组化的方法，对细胞凋亡、凋亡相关基因/蛋白、粘附分子等进行了研究。2.我们用ELISA法测定了黑色素瘤抑制活性，并检查了其值与临床病程的关系。3.我们对联合化疗（DAC-Tam）治疗晚期恶性黑色素瘤进行了评价。我们将继续这个项目进行一些实验。

项目成果

Kubo H, Matsumoto K, Funahashi M, Takagi H, Kitajima Y, Taniguchi S and Saida T: "Sequential chemoimmunotherapy with cisplatin, interferon-beta and interleukin-2 inhibits the growth of B16-F1 melanoma in cyngeneic mice"Melanoma Research. 10. 223-229 (2000

Kubo H、Matsumoto K、Funahashi M、Takagi H、Kitajima Y、Taniguchi S 和 Saida T：“使用顺铂、干扰素-β 和白细胞介素 2 的序贯化学免疫疗法抑制新生小鼠中 B16-F1 黑色素瘤的生长”黑色素瘤研究。

Kamiya H, Kanoh H, Ichihashi N, Ichiki Y, Takagi H, and Kitajima Y: "Evaluations of combination chemotherapy (DAC-Tam) for advanced malignant melanoma"Nishinihon J Dermatol. 63. 561-568 (2002)

Kamiya H、Kanoh H、Ichihashi N、Ichiki Y、Takagi H 和 Kitajima Y：“晚期恶性黑色素瘤联合化疗 (DAC-Tam) 的评估”Nishinihon J Dermatol。

神谷秀喜他: "進行期悪性黒色腫に対するDAC-Tam 療法の使用経験"西日皮膚. 63. 561-568 (2001)

Hideki Kamiya 等人：“DAC-Tam 治疗晚期恶性黑色素瘤的经验”Nishinichi Skin 63. 561-568 (2001)。

H.Kubo et al.: "Sequential chemoimmuno therapy with cisplatin, interferon-β and interleukin-2 inhibits the growth of B16-F1 melanoma in syngeneic mice"Melanoma Research. 10. 223-229 (2000)

H. Kubo 等人：“使用顺铂、干扰素-β 和白介素-2 的序贯化学免疫疗法抑制同系小鼠中 B16-F1 黑色素瘤的生长”Melanoma Research 10. 223-229 (2000)。