首页> 外文会议>NATO advanced research workshop on magnetic resonance in colloid and interface science >PHOSPHOLIPIDS' SERA AND MONONUCLEAR CELLS IN ACUTE LEUKEMIA, MALIGNANT LYMPHOMA AND MULTIPLE MYELOMA-EVALUATION BY ~(31)P MRS IN VITRO
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PHOSPHOLIPIDS' SERA AND MONONUCLEAR CELLS IN ACUTE LEUKEMIA, MALIGNANT LYMPHOMA AND MULTIPLE MYELOMA-EVALUATION BY ~(31)P MRS IN VITRO

机译:磷脂的血清和单核细胞在急性白血病,恶性淋巴瘤和多发性骨髓瘤 - 评估中由〜(31)PRS体外

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The experiences already achieved pointed out that ~(31)P spectra at present didn't allow for diagnosis of hematological disorders, but were of great importance in monitoring of therapy of the diseases under consideration. Moreover, the changes of concentrations of phospholipids in sera and cells in hematological cancers are probably due to the increased uptake of phospholipid metabolites in proliferating blast cells, and their disturbed transport through cell membranes. Mechanism of the changes of concentrations of the phospholipids in sera and cells in acute leukemia and disturbed transport of phospholipids through cell membranes remains unknown. It was suggested, that the pool involved in the SM cycle of signal trans-duction is localized to the intracellular portion of the human leukemia cells, most likely to the inner leaflet of the plasma membrane. It is very likely that observed reduction of the level of SM in blast cells' extraction is due to activation of sphingomyelinase (SMnase) by tumor necrosis factor (TNF). SMnase cleaves SM, generating choline phosphate and ceramide, that―among other things―mediate programmed cell death (apoptosis), induce differentiation and inhibit the growth of leukemia cells. As SM is an important participant of signal transduction pathway, the reason of reduced level of SM in the extracts of leukemia cells and changes concerning the CPLAS area observed by us needs further investigation.
机译:已经取得的经验指出,目前的〜(31)P光谱不允许诊断血液学疾病,但在监测所考虑的疾病的治疗方面具有重要意义。此外,血液癌中血清和细胞中磷脂浓度的变化可能是由于增殖喷射细胞中磷脂代谢物的摄取增加,以及通过细胞膜的干扰运输。血清血清中磷脂浓度变化的机制,急性白血病中的磷脂干扰通过细胞膜缺失仍然未知。有人建议,信号转导的SM循环中涉及的游泳池局部局限于人白血病细胞的细胞内部分,最有可能对质膜的内部瓣盖。观察到肿瘤萃取中SM水平的降低很可能是由于肿瘤坏死因子(TNF)的激活鞘氨酰胺酶(SMNase)。 Smnase切割SM,产生胆碱磷酸盐和神经酰胺,即其他次介质 - 介导的细胞死亡(凋亡),诱导分化并抑制白血病细胞的生长。由于SM是信号转导途径的重要参与者,但在白血病细胞提取物中减少SM水平的原因以及我们需要进一步调查的有关所观察到的CPLA区域的变化。

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