scholarly journals Clinicopathological features and outcomes of progression of CLL on the BCL2 inhibitor venetoclax

Blood ◽  
2017 ◽  
Vol 129 (25) ◽  
pp. 3362-3370 ◽  
Author(s):  
Mary Ann Anderson ◽  
Constantine Tam ◽  
Thomas E. Lew ◽  
Surender Juneja ◽  
Manu Juneja ◽  
...  
Keyword(s):  
Risk Factors ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Clinicopathological Features ◽  
Complex Karyotype ◽  
Prior Therapy ◽  
Key Points ◽  
Bruton Tyrosine Kinase

Key Points Complex karyotype and fludarabine refractoriness are key risk factors for progression of CLL on venetoclax. Bruton tyrosine kinase inhibitors are active in patients with CLL after prior therapy with venetoclax.

scholarly journals Oral Bruton tyrosine kinase inhibitors selectively block atherosclerotic plaque–triggered thrombus formation in humans

Blood ◽  
2018 ◽  
Vol 131 (24) ◽  
pp. 2605-2616 ◽  
Author(s):  
Kristina Busygina ◽  
Janina Jamasbi ◽  
Till Seiler ◽  
Hans Deckmyn ◽  
Christian Weber ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Atherosclerotic Plaque ◽  
Kinase Inhibitors ◽  
Thrombus Formation ◽  
Drug Dosing ◽  
Key Points ◽  
Bruton Tyrosine Kinase ◽  
Platelet Thrombus ◽  
Btk Inhibitors

Key Points Btk inhibitors specifically block platelet thrombus formation on atherosclerotic plaque but spare physiologic hemostasis. Irreversible Btk inactivation in platelets incapable of enzyme resynthesis allows low intermittent drug dosing for antiatherothrombosis.

scholarly journals Oral Bruton tyrosine kinase inhibitors block activation of the platelet Fc receptor CD32a (FcγRIIA): a new option in HIT?

2019 ◽  
Vol 3 (23) ◽  
pp. 4021-4033 ◽  
Author(s):  
Luise Goldmann ◽  
Rundan Duan ◽  
Thorsten Kragh ◽  
Georg Wittmann ◽  
Christian Weber ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Platelet Activation ◽  
Kinase Inhibitors ◽  
Fc Receptor ◽  
Cross Linking ◽  
Key Points ◽  
Bruton Tyrosine Kinase

Key Points Six different BTKi’s blocked platelet activation in blood after FcγRIIA stimulation by cross-linking, anti-CD9 antibodies, or HIT serum. Established oral irreversible and novel reversible BTKi’s may offer a new option to treat HIT.

scholarly journals Antiangiogenic Tyrosine Kinase Inhibitors: Occurrence and Risk Factors of Hemoptysis in Refractory Thyroid Cancer

2016 ◽  
Vol 101 (7) ◽  
pp. 2733-2741 ◽  
Author(s):  
Livia Lamartina ◽  
S. Ippolito ◽  
M. Danis ◽  
F. Bidault ◽  
I. Borget ◽  
...  
Keyword(s):  
Risk Factors ◽  
Thyroid Cancer ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors

scholarly journals Impact of BCR-ABL transcript type on outcome in patients with chronic-phase CML treated with tyrosine kinase inhibitors

Blood ◽  
2016 ◽  
Vol 127 (10) ◽  
pp. 1269-1275 ◽  
Author(s):  
Preetesh Jain ◽  
Hagop Kantarjian ◽  
Keyur P. Patel ◽  
Graciela Nogueras Gonzalez ◽  
Rajyalakshmi Luthra ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Treatment Modality ◽  
Kinase Inhibitors ◽  
Chronic Phase ◽  
Key Points ◽  
Transcript Type

Key Points Patients with e13a2 transcripts have inferior outcomes with imatinib 400; e14a2 has favorable outcomes regardless of treatment modality. Multivariate analysis showed that the expression of e14a2 or both e14a2 and e13a2 predicts optimal ELN responses and longer EFS and TFS.

scholarly journals MicroRNA-486 regulates normal erythropoiesis and enhances growth and modulates drug response in CML progenitors

Blood ◽  
2015 ◽  
Vol 125 (8) ◽  
pp. 1302-1313 ◽  
Author(s):  
Li-Sheng Wang ◽  
Ling Li ◽  
Liang Li ◽  
Su Chu ◽  
Keh-Dong Shiang ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Drug Response ◽  
Kinase Inhibitors ◽  
Erythroid Progenitors ◽  
Growth And Survival ◽  
Key Points

Key Points miR-486-5p is expressed in megakaryocyte-erythroid progenitors and regulates growth and survival by regulating FOXO1 and AKT. miR-486-5p is overexpressed in CML progenitors and enhances their growth, survival, and response to tyrosine kinase inhibitors.

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