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ABL相关的网络例句
与 ABL 相关的网络例句 [注:此内容来源于网络,仅供参考]

Objective:To study on frequencies of bcr/abl fusion gene in chronic myelogenous leukemia,polycythemia vera and their clinical significance.

目的:探讨慢性粒细胞白血病和真性红细胞增多症bcr/abl融合基因出现的频率及临床意义。

Two patients had priapism, their m-bcr/abl being negative.

有2例患者阴茎异常勃起,均为m-bcr/abl阴性CML患者。

The laboratory findings of a typical CCML patient comprised of peripheral blood leukocytosis, basophilia and eosinophilia,myeloid differentiation in different stages, and increased megakaryocytes. The immunohistochemical features of the CCML consisted of highly positive MPO and CD68, significant lowering of neutrophil alkaline phosphatase, positive for Philadel- phia chromosome or chimeric BCR/ABL gene, etc. But in most cases of juvenile CCML, the Philadelphia chromosome could not be detected.

临床表现以乏力、低热、贫血、肝脾及淋巴结肿大为主要特点;典型儿童慢性髓细胞白血病的实验室特点有白细胞计数高、嗜酸和嗜碱性粒细胞增多、骨髓不同阶段髓细胞分化和巨核细胞增多;免疫组化提示CD68,髓过氧化物酶,中性粒细胞碱性磷酸酶积分明显减低,Ph染色体或BCR/ABL融合基因阳性,而幼年型CCML的Ph染色体常为阴性。

It is concluded that the value of routine cytogenetical and molecular biological analysis in diagnosis for potential CML cases,which mimicked ET as in this presentation,is very distinctive,and the importance is magnified by the recent availability of imatinib,a specific inhibitor of the bcr/abl tyrosine kinase produced by the Philadelphia chromosome.Every case of

对血小板明显增多的患者应及时进行Ph染色体及bcr/abl融合基因表达水平的检测,这对于ET及CML的诊断和鉴别诊断极为重要,以避免误诊、误治。

Imatinib, a BCR-ABL tyrosine kinase inhibitor, is able to induce a complete cytogenetic response in more than 85% of patients with CML. However, the researchers note that patients with a complete cytogenic response tend to relapse when imatinib is discontinued, and less than 10% of patients achieve a molecular remission, defined by an undetectable residual disease using real-time quantitative–polymerase chain reaction.

Imatinib是一种BCR-ABL酪胺酸激酶抑制物,可以在85%以上的CML病患诱导完整的细胞生成反应;不过,研究者指出,完整细胞生成反应的病患倾向在停用imatinib时复发,不到10%的病患达到分子生物学上的缓解,其定义为以即时定量聚合酶连锁反应侦测不出残余疾病。

Imatinib, a BCR-ABL tyrosine kinase inhibitor, is able to induce a complete cytogenetic response in more than 85% of patients with CML. However, the researchers note that patients with a complete cytogenic response tend to relapse when imatinib is discontinued, and less than 10% of patients achieve a molecular remission, defined by an undetectable residual disease using real-time quantitative–polymerase chain reaction.

Imatinib是一种BCR-ABL酪胺酸激酶抑制物,可以在85%以上的CML病患诱导完整的细胞生成反应;不过,研究者指出,完整细胞生成反应的病患倾向在停用imatinib时復发,不到10%的病患达到分子生物学上的缓解,其定义为以即时定量聚合酶连锁反应侦测不出残餘疾病。

BCR-ABL and mutant JAK2 inhibit the Bcl-x deamidation pathway and the apoptotic response to DNA damage in primary cells from patients with CML or polycythemia vera.

BCR-ABL和突变的JAK2可抑制CML或真性红细胞增多症患者Bcl -×的脱酰胺途径和原代细胞DNA损伤诱导的凋亡反应。

METHODS: We searched for abnormalities of the proapoptotic Bcl-x deamidation pathway in primary cells from patients with chronic myeloid leukemia or polycythemia vera, myeloproliferative disorders associated with the BCR-ABL fusion kinase and the Janus tyrosine kinase 2 (JAK2) V617F mutation, respectively.

我们分别对来自慢性粒细胞白血病或真性红细胞增多症、骨髓增生性疾病相关的BCR-ABL融合蛋白激酶及Janus酪氨酸激酶2 (JAK2) V617F突变体患者原代细胞凋亡前Bcl-x脱酰胺途径的异常情况进行研究。

IM-induced autophagy did not involve c-Abl or Bcl-2 activity but was associated with ER stress and was suppressed by depletion of intracellular Ca2+, suggesting it is mechanistically nonoverlapping with IM-induced apoptosis.

IM诱导的自噬与c-Abl 或 Bcl-2活性无关,但与内质网应激相关并受细胞内Ca2+缺失抑制,提示其与IM诱导的细胞凋亡机制不同。

Aim Chronic myelogenous leukemia bcr abl fusion gene cDNA was cloned and expressed in COS 7 cells.

目的克隆慢性髓系白血病融合基因bcr abl的cDNA序列,并在真核细胞中表达。

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