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- the writing point of a pen (同)pen nib
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- ペン先 / (一般的に)とがった部分,先端(tip) / (鳥の)くちばし
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/04/11 14:06:55」(JST)
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- 1. 若年成人における急性骨髄性白血病に対する導入療法 induction therapy for acute myeloid leukemia in younger adults
- 2. 再発性または難治性の急性骨髄性白血病の治療 treatment of relapsed or refractory acute myeloid leukemia
- 3. 急性骨髄性白血病の予後 prognosis of acute myeloid leukemia
- 4. 血液学の最新情報 whats new in hematology
- 5. Acute myeloid leukemia in children and adolescents
English Journal
- Perturbation of the mutated EGFR interactome identifies vulnerabilities and resistance mechanisms.
- Li J, Bennett K, Stukalov A, Fang B, Zhang G, Yoshida T, Okamoto I, Kim JY, Song L, Bai Y, Qian X, Rawal B, Schell M, Grebien F, Winter G, Rix U, Eschrich S, Colinge J, Koomen J, Superti-Furga G, Haura EB.Author information Department of Thoracic Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.AbstractWe hypothesized that elucidating the interactome of epidermal growth factor receptor (EGFR) forms that are mutated in lung cancer, via global analysis of protein-protein interactions, phosphorylation, and systematically perturbing the ensuing network nodes, should offer a new, more systems-level perspective of the molecular etiology. Here, we describe an EGFR interactome of 263 proteins and offer a 14-protein core network critical to the viability of multiple EGFR-mutated lung cancer cells. Cells with acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) had differential dependence of the core network proteins based on the underlying molecular mechanisms of resistance. Of the 14 proteins, 9 are shown to be specifically associated with survival of EGFR-mutated lung cancer cell lines. This included EGFR, GRB2, MK12, SHC1, ARAF, CD11B, ARHG5, GLU2B, and CD11A. With the use of a drug network associated with the core network proteins, we identified two compounds, midostaurin and lestaurtinib, that could overcome drug resistance through direct EGFR inhibition when combined with erlotinib. Our results, enabled by interactome mapping, suggest new targets and combination therapies that could circumvent EGFR TKI resistance.
- Molecular systems biology.Mol Syst Biol.2013 Nov 5;9:705. doi: 10.1038/msb.2013.61.
- We hypothesized that elucidating the interactome of epidermal growth factor receptor (EGFR) forms that are mutated in lung cancer, via global analysis of protein-protein interactions, phosphorylation, and systematically perturbing the ensuing network nodes, should offer a new, more systems-level per
- PMID 24189400
- Increased reactive oxygen species production and p47phox phosphorylation in neutrophils from myeloproliferative disorders patients with JAK2 (V617F) mutation.
- Hurtado-Nedelec M, Csillag-Grange MJ, Boussetta T, Belambri SA, Fay M, Cassinat B, Gougerot-Pocidalo MA, Dang PM, El-Benna J.Author information jamel.elbenna@inserm.fr.AbstractMyeloproliferative disorders are associated with increased risk of thrombosis and vascular complications. The pathogenesis of these complications is not completely known. Reactive oxygen species produced by the neutrophil NADPH oxidase could have a role in this process. The aim of this study was to evaluate reactive oxygen species production by neutrophils of myeloproliferative disorder patients. Patients with or without the JAK2 V617F mutation were characterized. Reactive oxygen species production was assessed by chemiluminescence, and phosphorylation of the NADPH oxidase subunit p47phox was analyzed by Western blots. In a comparison of controls and myeloproliferative disorder patients without the JAK2 V617F mutation, reactive oxygen species production by neutrophils from patients with the JAK2 V617F mutation was dramatically increased in non-stimulated and in stimulated conditions. This increase was associated with increased phosphorylation of the p47phox on Ser345 and of the uspstream kinase ERK1/2. In neutrophils from healthy donors, JAK2 can be activated by GM-CSF. GM-CSF-induced p47phox phosphorylation and priming of reactive oxygen species production are inhibited by the selective JAK2 inhibitors AG490 and lestaurtinib (CEP-701), supporting a role for JAK2 in the upregulation of NADPH oxidase activation. These findings show an increase in reactive oxygen species production and p47phox phosphorylation in neutrophils from myeloproliferative disorder patients with the JAK2 V617F mutation, and demonstrate that JAK2 is involved in GM-CSF-induced NADPH oxidase hyperactivation. As neutrophil hyperactivation could be implicated in the thrombophilic status of patients with myeloproliferative disorders, aberrant activation of JAK2 V617F, leading to excessive neutrophil reactive oxygen species production might play a role in this setting.
- Haematologica.Haematologica.2013 Oct;98(10):1517-24. doi: 10.3324/haematol.2012.082560. Epub 2013 Aug 23.
- Myeloproliferative disorders are associated with increased risk of thrombosis and vascular complications. The pathogenesis of these complications is not completely known. Reactive oxygen species produced by the neutrophil NADPH oxidase could have a role in this process. The aim of this study was to
- PMID 23975181
- New agents: great expectations not realized.
- Lancet JE.Author information Oncologic Sciences, University of South Florida, Tampa, USA; Department of Malignant Hematology, Moffitt Cancer Center, 12902 Magnolia Drive, Tampa, FL 33612, USA. Electronic address: Jeffrey.lancet@moffitt.org.AbstractA number of new agents in acute myeloid leukemia (AML) have held much promise in recent years, but most have failed to change the therapeutic landscape. Indeed, with the exception of gemtuzumab ozogamicin (which was subsequently voluntarily withdrawn from the commercial market), no new agent has been approved for acute myeloid leukemia (AML) beyond the 7 + 3 regimen, which was has been in use for over 40 years. This review touches upon the potential reasons for these failures and explores the newer therapeutic approaches being pursued in AML.
- Best practice & research. Clinical haematology.Best Pract Res Clin Haematol.2013 Sep;26(3):269-74. doi: 10.1016/j.beha.2013.10.007. Epub 2013 Oct 16.
- A number of new agents in acute myeloid leukemia (AML) have held much promise in recent years, but most have failed to change the therapeutic landscape. Indeed, with the exception of gemtuzumab ozogamicin (which was subsequently voluntarily withdrawn from the commercial market), no new agent has bee
- PMID 24309529
Japanese Journal
- JAK2変異による骨髄増殖性疾患発症機構とJAK2阻害剤開発の現状 (特集 血液疾患における病態解析研究の進歩)
- 松永 卓也,下田 和哉
- 血液・腫瘍科 60(2), 149-156, 2010-02
- NAID 40019064611
Related Links
- Lestaurtinib (rINN, codenamed CEP-701) is a tyrosine kinase inhibitor structurally related to staurosporine, and is being ... "A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid ...
- 一般名： lestaurtinib(CEP701),tandutinib (MLN518),Sunitinib(SU11248） ... これ までにレスタウルチニブ（lestaurtinib, CEP701）タンヅチニブ（tandutinib, MLN518）、 PKC412など数種のFLT3阻害薬の臨床治験が報告されている。CEP701は合成 化合物 ...
Related Pictures
★リンクテーブル★
| リンク元 | 「nib」 |
「nib」
- 受容体のリガンド結合部を標的とした小分子化合物。
nib
- アキシチニブ axitinib
- ボスチニブ bosutinib
- ブリバニブ brivanib
- カネルチニブ canertinib
- セジラニブ cediranib
- ダサチニブ dasatinib チロシンキナーゼ阻害薬 イマチニブ抵抗性の慢性骨髄性白血病、再発又は難治性のフィラデルフィア染色体陽性急性リンパ性白血病
- エルロチニブ erlotinib
- ゲフィチニブ gefitinib
- イマチニブ imatinib チロシンキナーゼ阻害薬 CML、CKIT(CD117)陽性消化管間質腫瘍、
- ラパチニブ lapatinib
- レスタウルチニブ lestaurtinib
- リニファニブ linifanib
- ロナファーニブ lonafarnib
- ネラチニブ neratinib
- ニブリン nibrin
- ニロチニブ nilotinib チロシンキナーゼ阻害薬 イマチニブ抵抗性の慢性期又は移行期の慢性骨髄性白血病
- パゾパニブ pazopanib
- ペガプタニブ pegaptanib
- ラニビズマブ ranibizumab
- セマキシニブ semaxinib
- ソラフェニブ sorafenib
- スニチニブ sunitinib VEGFRやPDGFRチロシンキナーゼ阻害薬 イマチニブ抵抗性の消化管間質腫瘍、根治切除不能又は転移性の腎細胞癌
- ティピファニブ tipifarnib
- バンデタニブ vandetanib
- バタラニブ vatalanib