酪氨酸激酶参与大多数癌症的发病机制。
Tyrosine kinases are involved in the pathogenesis of most cancers.
苏尼替尼是一种新型的多靶点酪氨酸激酶抑制剂。
Sunitinb is a novel multitargeted receptor tyrosine kinase inhibitor.
目的：研究酪氨酸激酶转染对鼻咽癌细胞成瘤的影响。
Objective To study the effects of transfection of tyrosine kinases on the tumorigenesis of nasopharyngeal carcinoma.
目的：对近年来酪氨酸激酶抑制剂的研究进展作以综述。
Objective: to review the progress in the research of tyrosine kinase inhibitors in recent years.
详细介绍了VEGF受体酪氨酸激酶抑制剂的研究进展。
The inhibitor of VEGF receptor tyrosine kinase was introduced in detail.
抑制BCR - ABL酪氨酸激酶可有效抑制肿瘤生长。
Inhibiting BCR-ABL tyrosine kinases can impede the growing progress of tumors.
属于酪氨酸激酶受体，可以传递表皮生长因子家族的信号。
The family of ErbB tyrosine kinase receptors can transmit signals derived from growth factor of epidermal growth factor family.
PDGF受体酪氨酸激酶抑制剂在胰腺癌中是否有作用？ ？
Is PDGF tyrosine kinase inhibitor effective in pancreatic cancer?
目的探讨蛋白酪氨酸激酶抑制剂抗肿瘤作用机理及其研究进展。
Objective To approach the mechanism of action of anticancer and the investigation progress of protein tyrosine kinase (PTK).
bcrabl；酪氨酸激酶；抑制剂；慢性粒细胞白血病；综述。
BCRABL; tyrosine kinases; inhibitors; chronic myelogenous leukemia; review.
目的探讨肺腺癌患者酪氨酸激酶传导通路的异常和临床预后的关系。
ObjectiveTo study the abnormity and clinical value of tyrosine kinase signaling pathway in lung adenocarcinoma.
结论GST可通过酪氨酸激酶途径抑制豚鼠结肠平滑肌l型钙通道。
CONCLUSION GST can block L-type calcium channel activity in guinea-pig colon smooth muscle cells via tyrosine kinase pathway.
继发性FLT3 - TKD突变与酪氨酸激酶抑制剂治疗失败有关。
Secondary FLT3-TKD mutations are associated with treatment failure with tyrosine kinase inhibitors.
结论AG490作为一种酪氨酸激酶抑制剂，能影响正常细胞的功能。
Conclusion As an inhibitor of JAK, AG490 can influence the function of normal cells.
本发明提供了使用抗egfr抗体治疗抗酪氨酸激酶抑制剂的癌症的方法。
The invention provides methods for the treatment of tyrosine kinase inhibitor resistant cancers with anti-EGFR antibodies.
本文介绍了第一、二代以及新近开发的BCR - ABL酪氨酸激酶抑制剂。
This paper introduces the first, second and some new BCR-ABL tyrosine kinases inhibitors.
目的：研究散发型甲状腺髓样癌酪氨酸激酶受体基因（RET）的突变情况。
Objective:To explore the mutation of receptor tyrosine kinase ( RET ) gene in sporadic medullary thyroid carcinoma.
酪氨酸激酶型受体、G蛋白偶联受体和离子通道型受体是细胞表面三类主要受体。
Receptor tyrosine kinases (RTK), G protein-coupled receptors (GPCR) and ion channel receptors are main cell surface receptors.
我认为一些酪氨酸激酶活化剂已经出现，但是我不确信它们要比胰岛素的效果好。
I think there are several tyrosine kinase activators already developed however I am not sure that they can perform better than insulin.
中国的非小细胞肺癌病人中吉非替尼敏感的表皮生长因子受体酪氨酸激酶区域的突变。
Gefitinib-sensitive mutations of the epidermal growth factor receptor tyrosine kinase domain in chinese patients with non-small cell lung cancer.
研究证实了源于颗粒细胞的酪氨酸激酶受体配体在卵母细胞生长过程中起重要作用。
It has been demonstrated that granular cell-derived kit ligand (KitL) plays important roles in oocyte growth.
结论：在苦参碱诱导K562细胞分化的过程中，涉及到蛋白酪氨酸激酶的活性改变。
Conclusions: the change of protein tyrosine kinase activity is involved in the differentiation of K562 cells induced by matrine.
这些药物的作用机制是阻断酪氨酸激酶启动信号级联反应，后者可以促进肿瘤细胞生长。
The drugs work by preventing an enzyme called tyrosine kinase from launching a signaling cascade that fuels tumor cell growth.
目的探讨胰岛素受体酪氨酸激酶(TK)活性变化在胰岛素抵抗(IR)发生中的作用。
Objective to investigate the change of insulin receptor tyrosine kinase (TK) activity in the pathogenesis of insulin resistance (IR).
大量的临床经验：酪氨酸激酶抑制剂治疗患有分化型甲状腺癌的患者：M。D。安德森经验。
Treatment with Tyrosine Kinase Inhibitors for Patients with Differentiated Thyroid Cancer: the M. D. Anderson Experience.
血管内皮细胞生长因子与其受体结合后通过酪氨酸激酶途径引起细胞的增殖及新生血管形成。
Vascular epithelial growth factor binding with its receptor leads to cell proliferation and new vascular formation by tyrosine kinase pathway.
目的：探讨表皮生长因子受体(EGFR)基因酪氨酸激酶域体细胞在肺腺癌患者中突变的相关因素。
Objective: to study Somatic mutation of the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR gene) in lung adenocarcinoma patients.
这可能解释以前的研究数据发现抑制酪氨酸激酶活性不足以诱导细胞死亡，或抑制EGFR的所有功能。
This may help to explain previous data indicating that inhibition of EGFR kinase activity is not sufficient to induce cell death, or to negate all of the functions of EGFR.
这可能解释以前的研究数据发现抑制酪氨酸激酶活性不足以诱导细胞死亡，或抑制EGFR的所有功能。
This may help to explain previous data indicating that inhibition of EGFR kinase activity is not sufficient to induce cell death, or to negate all of the functions of EGFR.
应用推荐