Results 61 to 70 of about 486,983 (268)

Advancements in research on the cardiovascular toxicity caused by TEC family kinases inhibitors

Frontiers in Pharmacology
The tyrosine kinase expressed in hepatocellular carcinoma (TEC) family kinases (TFKs) are a subfamily of non-receptor protein tyrosine kinases (PTKs) that include five members: TEC, bruton’s tyrosine kinase (BTK), interleukin 2-inducible T-cell kinase ...
Yi Zhang, Huangxi Fu, Xingchen Kang, Zixuan Qiu, Hao Yan, Qiaojun He, Qiaojun He, Qiaojun He, Bo Yang, Bo Yang, Bo Yang, Zhifei Xu, Peihua Luo, Peihua Luo   +13 more
doaj   +1 more source

Transcriptional network analysis of PTEN‐protein‐deficient prostate tumors reveals robust stromal reprogramming and signs of senescent paracrine communication

Molecular Oncology, EarlyView.
Combining PTEN protein assessment and transcriptomic profiling of prostate tumors, we uncovered a network enriched in senescence and extracellular matrix (ECM) programs associated with PTEN loss and conserved in a mouse model. We show that PTEN‐deficient cells trigger paracrine remodeling of the surrounding stroma and this information could help ...
Ivana Rondon‐Lorefice, Jose I. Lopez, Aitziber Ugalde‐Olano, Maite Zufiaurre, Ianire Astobiza, Natalia Martin‐Martin, Laura Bozal‐Basterra, Saioa Garcia‐Longarte, Amaia Zabala‐Letona, Sofia Rey, Aida Santos‐Martin, Miguel Unda, Ana Loizaga‐Iriarte, Mariona Graupera, Paolo Nuciforo, Arkaitz Carracedo, Isabel Mendizabal   +16 more
wiley   +1 more source

Tyrosine kinase inhibitor-induced carotid stenosis: A case report

Leukemia Research Reports, 2019
Tyrosine kinase inhibitors are considered as highly effective and relatively safe drugs for the treatment of chronic myeloid leukemia. If several side effects on short and long term are well known and described, their involvement in the development of ...
Jeanne Hersant, Martine Gardembas, Georges Leftheriotis, Patrick Vandeputte, Pierre Abraham, Samir Henni   +5 more
doaj   +1 more source

Potential therapeutic targeting of BKCa channels in glioblastoma treatment

Molecular Oncology, EarlyView.
This review summarizes current insights into the role of BKCa and mitoBKCa channels in glioblastoma biology, their potential classification as oncochannels, and the emerging pharmacological strategies targeting these channels, emphasizing the translational challenges in developing BKCa‐directed therapies for glioblastoma treatment.
Kamila Maliszewska‐Olejniczak, Karolina Pytlak, Sandra Jaworowska, Bogusz Kulawiak, Piotr Bednarczyk   +4 more
wiley   +1 more source

Recent Advances and Prospect of Advanced Non-small Cell Lung Cancer Targeted 
Therapy: Focus on Small Molecular Tyrosine Kinase Inhibitors

Chinese Journal of Lung Cancer, 2017
At present the treatment of advanced non-small cell lung cancer enters a targeted era and develops rapidly. New drugs appear constantly. Small molecular tyrosine kinase inhibitors have occupied the biggest piece of the territory, which commonly have a ...
Guowei ZHANG, Huijuan WANG, Zhiyong MA
doaj   +1 more source

ATF4‐mediated stress response as a therapeutic vulnerability in chordoma

Molecular Oncology, EarlyView.
We screened 5 chordoma cell lines against 100+ inhibitors of epigenetic and metabolic pathways and kinases and identified halofuginone, a tRNA synthetase inhibitor. Mechanistically halofuginone induces an integrated stress response, with eIF2alpha phosphorylation, activation of ATF4 and its target genes CHOP, ASNS, INHBE leading to cell death ...
Lucia Cottone, James Dunford, Eleanor Calcutt, Vicki Gamble, Filiz Senbabaoglu Aksu, Lorena Ligammari, Georgina Wherry, Giorgia Gaeta, John C. Christianson, Adrienne M. Flanagan, Udo Oppermann, Adam P. Cribbs   +11 more
wiley   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

Molecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala, Sini Ahonen, Sara Peltola, Aura Tuohisto‐Kokko, Olaya Esparta, Peppi Suominen, Anne Jokilammi, Iman Farahani, Deepankar Chakroborty, Nikol Dibus, Steffen Boettcher, Tomi T. Airenne, Mark S. Johnson, Lisa D. Eli, Klaus Elenius, Kari J. Kurppa   +15 more
wiley   +1 more source

Second-generation tyrosine kinase inhibitors improve the survival of patients with chronic myeloid leukemia in whom imatinib therapy has failed

Haematologica, 2011
Background It has not been clearly established whether second-generation tyrosine kinase inhibitors actually improve the survival of patients with chronic myeloid leukemia in chronic phase who are given nilotinib or dasatinib therapy after treatment ...
Amr R. Ibrahim, Richard E. Clark, Tessa L. Holyoake, Jenny Byrne, Pat Shepherd, Jane F. Apperley, Dragana Milojkovic, Richard Szydlo, John Goldman, David Marin   +9 more
doaj   +1 more source

Dammarenediol II enhances etoposide‐induced apoptosis by targeting O‐GlcNAc transferase and Akt/GSK3β/mTOR signaling in liver cancer

Molecular Oncology, EarlyView.
Etoposide induces DNA damage, activating p53‐dependent apoptosis via caspase‐3/7, which cleaves PARP1. Dammarenediol II enhances this apoptotic pathway by suppressing O‐GlcNAc transferase activity, further decreasing O‐GlcNAcylation. The reduction in O‐GlcNAc levels boosts p53‐driven apoptosis and influences the Akt/GSK3β/mTOR signaling pathway ...
Jaehoon Lee, Byung‐Cheol Han, Gi‐Bang Koo, Jihye Park, Mijin Kwon, Young Bin Park, Jae‐Mun Choi, Seung‐Ho Lee, Sangho Roh   +8 more
wiley   +1 more source

Insulin receptor has tyrosine kinase activity toward Shc in rat liver

Brazilian Journal of Medical and Biological Research, 1998
Insulin induces tyrosine phosphorylation of Shc in cell cultures and in insulin-sensitive tissues of the intact rat. However, the ability of insulin receptor (IR) tyrosine kinase to phosphorylate Shc has not been previously demonstrated.
E.V. Páez-Espinosa, C.R.O. Carvalho, L.A. Velloso, M.J.A. Saad   +3 more
doaj   +1 more source