Results 121 to 130 of about 871,767 (407)

Small molecule tyrosine kinase inhibitors in pancreatic cancer

open access: yesBiologics: Targets & Therapy, 2008
Sachin Gupta, Bassel F El-RayesDepartment of Hematology/Oncology, Karmanos Cancer Institute, Wayne State University, MI, USAAbstract: Pancreatic cancer has proven to be chemo-resistant, with gemcitabine being the only cytotoxic agent approved for ...
Sachin Gupta, Bassel F El-Rayes
doaj  

Ibrutinib Displays Atrial-Specific Toxicity in Human Stem Cell-Derived Cardiomyocytes

open access: yesStem Cell Reports, 2019
Summary: Ibrutinib (IB) is an oral Bruton's tyrosine kinase (BTK) inhibitor that has demonstrated benefit in B cell cancers, but is associated with a dramatic increase in atrial fibrillation (AF).
Sanam Shafaattalab   +11 more
doaj   +1 more source

Inhibition of c-Kit by tyrosine kinase inhibitors

open access: yesHaematologica, 2015
Several small molecule tyrosine kinase inhibitors (TKIs) inhibit c-Kit, an effect associated with myelosuppression and hair depigmentation. We studied a panel of approved and investigational TKIs for inhibitory activity against FLT3 and c-Kit, and on ...
A. Galanis, M. Levis
semanticscholar   +1 more source

Targeting Oncogenic BRAF: Past, Present, and Future. [PDF]

open access: yes, 2019
Identifying recurrent somatic genetic alterations of, and dependency on, the kinase BRAF has enabled a "precision medicine" paradigm to diagnose and treat BRAF-driven tumors.
Bivona, Trever G   +2 more
core   +1 more source

Integrative miRNOMe profiling reveals the miR‐195‐5p–CHEK1 axis and its impact on luminal breast cancer outcomes

open access: yesMolecular Oncology, EarlyView.
In luminal (ER+) breast carcinoma (BC), miRNA profiling identified miR‐195‐5p as a key regulator of proliferation that targets CHEK1, CDC25A, and CCNE1. High CHEK1 expression correlates with worse relapse‐free survival after chemotherapy, especially in patients with luminal A subtype.
Veronika Boušková   +14 more
wiley   +1 more source

SÍNTESES E PROPRIEDADES DE FÁRMACOS INIBIDORES DA TIROSINA QUINASE BCR-ABL, UTILIZADOS NO TRATAMENTO DA LEUCEMIA MIELOIDE CRÔNICA

open access: yesQuímica Nova
The chronic myeloid leukemia (CML) is characterized by presence of the Philadelphia chromosome (Ph), originated from the translocation between chromosomes 9 and 22.
Liviane D. de Azevedo   +3 more
doaj   +1 more source

Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer. [PDF]

open access: yes, 2019
Although targeted therapies often elicit profound initial patient responses, these effects are transient due to residual disease leading to acquired resistance.
A Hübner   +66 more
core   +1 more source

Unveiling unique protein and phosphorylation signatures in lung adenocarcinomas with and without ALK, EGFR, and KRAS genetic alterations

open access: yesMolecular Oncology, EarlyView.
Proteomic and phosphoproteomic analyses were performed on lung adenocarcinoma (LUAD) tumors with EGFR, KRAS, or EML4–ALK alterations and wild‐type cases. Distinct protein expression and phosphorylation patterns were identified, especially in EGFR‐mutated tumors. Key altered pathways included vesicle transport and RNA splicing.
Fanni Bugyi   +12 more
wiley   +1 more source

Outcome of 82 chronic myeloid leukemia patients treated with nilotinib or dasatinib after failure of two prior tyrosine kinase inhibitors

open access: yesHaematologica, 2013
There have been few reports of a response to dasatinib or nilotinib after failure of two prior sequential tyrosine kinase inhibitors. We report the outcome of 82 chronic phase patients who received nilotinib or dasatinib as third-line alternative ...
Antonella Russo Rossi   +19 more
doaj   +1 more source

Ubiquitylation in immune disorders and cancer: from molecular mechanisms to therapeutic implications [PDF]

open access: yes, 2012
Conjugation of ubiquitin to proteins (ubiquitylation) has emerged to be one of the most crucial post-translational modifications controlling virtually all cellular processes.
Fulda, Simone   +2 more
core   +1 more source

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