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.

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 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 A phosphoproteomic signature in endothelial cells predicts vascular toxicity of tyrosine kinase inhibitors used in CML

2018 ◽  
Vol 2 (14) ◽  
pp. 1680-1684 ◽  
Author(s):  
Srila Gopal ◽  
Qing Lu ◽  
Joshua J. Man ◽  
Wendy Baur ◽  
Sitara P. Rao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Drug Development ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Screening Tool ◽  
Kinase Inhibitors ◽  
Vascular Toxicity ◽  
Key Points

Key Points Newer CML kinase inhibitors increase ischemia risk and are toxic to endothelial cells where they produce a proteomic toxicity signature. This phosphoproteomic EC toxicity signature predicts bosutinib to be safe, providing a potential screening tool for safer drug development.

scholarly journals BCR-ABL1 gene rearrangement as a subclonal change in ETV6-RUNX1–positive B-cell acute lymphoblastic leukemia

2016 ◽  
Vol 1 (2) ◽  
pp. 132-138 ◽  
Author(s):  
Karen A. Dun ◽  
Rob Vanhaeften ◽  
Tracey J. Batt ◽  
Louise A. Riley ◽  
Giuseppe Diano ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Tyrosine Kinase ◽  
B Cell ◽  
Tyrosine Kinase Inhibitors ◽  
Gene Rearrangement ◽  
Kinase Inhibitors ◽  
Lymphoblastic Leukemia ◽  
Rare Occurrence ◽  
Key Points ◽  
Cell Acute Lymphoblastic Leukemia

Key Points BCR-ABL1 rearrangement as a subclonal change in ETV6-RUNX1–positive B-ALL is a rare occurrence not previously reported. The prognosis of this rare subclonal change has not been determined, yet inclusion of tyrosine kinase inhibitors in treatment is ubiquitous.

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 BCR-ABL–specific T-cell therapy in Ph+ ALL patients on tyrosine-kinase inhibitors

Blood ◽  
2017 ◽  
Vol 129 (5) ◽  
pp. 582-586 ◽  
Author(s):  
Patrizia Comoli ◽  
Sabrina Basso ◽  
Giovanni Riva ◽  
Patrizia Barozzi ◽  
Ilaria Guido ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
T Cell ◽  
Cell Therapy ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
T Cell Therapy ◽  
Specific Ctls ◽  
Healthy Donors ◽  
Key Points

Key Points BCR-ABL–specific CTLs may be obtained by stimulation with peptides derived from BCR-ABL junctional region and alternative splicing. T-cell therapy with BCR-ABL–specific CTLs from healthy donors or patients mediates molecular or hematologic CR in patients with Ph+ ALL.

scholarly journals Autocrine TNF-α production supports CML stem and progenitor cell survival and enhances their proliferation

Blood ◽  
2013 ◽  
Vol 122 (19) ◽  
pp. 3335-3339 ◽  
Author(s):  
Paolo Gallipoli ◽  
Francesca Pellicano ◽  
Heather Morrison ◽  
Kamilla Laidlaw ◽  
Elaine K. Allan ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Cell Survival ◽  
Progenitor Cells ◽  
Tyrosine Kinase Inhibitors ◽  
Progenitor Cell ◽  
Kinase Inhibitors ◽  
Abl Kinase ◽  
Tnf Α ◽  
Key Points ◽  
Survival Signals

Key Points Autocrine TNF-α production by CML stem/progenitor cells is not BCR-ABL kinase-dependent and provides survival signals. Targeting TNF-α production by stem/progenitor cells might be exploited therapeutically, especially in combination with tyrosine kinase inhibitors.

scholarly journals Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases

Blood ◽  
2016 ◽  
Vol 127 (17) ◽  
pp. 2131-2143 ◽  
Author(s):  
Yashodhara Dasgupta ◽  
Mateusz Koptyra ◽  
Grazyna Hoser ◽  
Kanchan Kantekure ◽  
Darshan Roy ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Therapeutic Target ◽  
Kinase Activity ◽  
Kinase Inhibitors ◽  
Key Points ◽  
Human And Mouse ◽  
Stimulation Of

Key Points Normal ABL1 is a tumor suppressor in BCR-ABL1–induced leukemia. Allosteric stimulation of the normal ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors.

scholarly journals BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein

Blood ◽  
2014 ◽  
Vol 124 (22) ◽  
pp. 3260-3273 ◽  
Author(s):  
Anupriya Agarwal ◽  
Ryan J. Mackenzie ◽  
Arnaud Besson ◽  
Sophia Jeng ◽  
Alyssa Carey ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Key Points

Key Points Coordinated BCR-ABL1 kinase-dependent and -independent mechanisms convert p27 from a nuclear tumor suppressor to a cytoplasmic oncogene. Oncogenic functions of p27 that persist despite effective BCR-ABL1 inhibition may contribute to resistance to tyrosine kinase inhibitors.

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