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bcl-2 anti-apoptotic oncoprotein suppresses angiogenesis in non-small cell lung cancer: implications in resistance to photodynamic treatment?

机译:bcl-2抗凋亡癌蛋白抑制非小细胞肺癌的血管生成:对光动力治疗的抵抗性有何影响?

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Abstract: PDT cytotoxicity is likely to occur throughphotooxidative reactions. In that way mechanisms thatdefine poor oxygenation should be involved in definingresistance to photo-dynamic treatment (PDT). On theother hand bcl-2 anti- apoptotic protein has been shownto delay cell death and protect cells from toxicoxidative products. We examined 134 specimens fromT1,2-NO,1 staged patients treated with surgery alone.Specimens were immunohistochemically examined forvascular grade using the JC70 MoAb, and bcl-2oncoprotein expression. Bcl-2 expression correlatedwith low vascular grade. Only 3/27 of bcl2$PLU case hadhigh angiogenesis vs. 34/107 of cases without bcl-2expression. In the present study we provide evidencethat bcl-2 overexpression directly suppressesangiogenesis in non-small cell lung cancer, whichobviously results in decreased blood supply andoxygenation. This finding implies that reducedintratumoral angiogenesis and immortalizing oncoproteinoverexpression are linked to each other and may have arole in defining tumors resistant to PDT. !9
机译:摘要:PDT的细胞毒性很可能通过光氧化反应发生。以此方式,应在定义对光动力治疗(PDT)的抗性中涉及定义不良氧合作用的机制。另一方面,bcl-2抗凋亡蛋白已被证明可延迟细胞死亡并保护细胞免受毒性氧化产物的侵害。我们检查了134例来自T1,2-NO,1阶段仅接受手术治疗的患者的标本。使用JC70 MoAb和bcl-2癌蛋白表达对标本进行了免疫组织化学检查,以检查其血管级别。 Bcl-2表达与低血管分级有关。 bcl2 $ PLU病例中只有3/27的血管发生较高,而无bcl-2表达的病例为34/107。在本研究中,我们提供证据表明bcl-2过表达直接抑制非小细胞肺癌中的血管生成,这显然导致血液供应和氧合减少。这一发现暗示着减少的肿瘤内血管生成和永生化的癌蛋白过度表达相互关联,并且在确定对PDT具有抗性的肿瘤中可能具有假说。 !9

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