Results 111 to 120 of about 857,410 (384)
Alectinib resistance in ALK+ NSCLC depends on treatment sequence and EML4‐ALK variants. Variant 1 exhibited off‐target resistance after first‐line treatment, while variant 3 and later lines favored on‐target mutations. Early resistance involved off‐target alterations, like MET and NF2, while on‐target mutations emerged with prolonged therapy.
Jie Hu+11 more
wiley +1 more source
Exploring receptor tyrosine kinases-inhibitors in Cancer treatments
Background Receptor tyrosine kinases (RTKs) are signaling enzymes responsible for the transfer of Adenosine triphosphate (ATP) γ-phosphate to the tyrosine residues substrates.
D. Samuel Metibemu+5 more
doaj +1 more source
B‐cell chronic lymphocytic leukemia (B‐CLL) and monoclonal B‐cell lymphocytosis (MBL) show altered proteomes and phosphoproteomes, analyzed using mass spectrometry, protein microarrays, and western blotting. Identifying 2970 proteins and 316 phosphoproteins, including 55 novel phosphopeptides, we reveal BCR and NF‐kβ/STAT3 signaling in disease ...
Paula Díez+17 more
wiley +1 more source
Drug−drug interactions (DDIs) occur when a patient's response to the drug is modified by administration or co‐exposure to another drug. The main cytochrome P450 (CYP) enzyme, CYP3A4, is implicated in the metabolism of almost all of the tyrosine kinase ...
Y. Teo, H. Ho, A. Chan
semanticscholar +1 more source
BCR-ABL residues interacting with ponatinib are critical to preserve the tumorigenic potential of the oncoprotein [PDF]
Patients with chronic myeloid leukemia in whom tyrosine kinase inhibitors (TKIs) fail often present mutations in the BCR-ABL catalytic domain. We noticed a lack of substitutions involving 4 amino acids (E286, M318, I360, and D381) that form hydrogen ...
Alessandro Pandini+11 more
core +1 more source
Tyrosine kinase inhibitors are known to cause pulmonary complications. We report a case of bosutinib related bilateral pleural effusions in a patient with chronic myeloid leukemia. Characteristics of the pleural fluid are presented. We also discuss other
Natalia I. Moguillansky, MD+2 more
doaj +1 more source
Ubiquitination of transcription factors in cancer: unveiling therapeutic potential
In cancer, dysregulated ubiquitination of transcription factors contributes to the uncontrolled growth and survival characteristics of tumors. Tumor suppressors are degraded by aberrant ubiquitination, or oncogenic transcription factors gain stability through ubiquitination, thereby promoting tumorigenesis.
Dongha Kim, Hye Jin Nam, Sung Hee Baek
wiley +1 more source
Future therapeutic strategies: Implications for Brk targeting [PDF]
The official published article can be found at the link below - Copyright @ 2011 InTech. This Article has been provided by the Brunel Open Access Publishing Fund.Rajpal Burmi was supported by a Breast Cancer Campaign project ...
Burmi, RS, Harvey, AJ
core +2 more sources
Targeted protein degradation in oncology: novel therapeutic opportunity for solid tumours?
Current anticancer therapies are limited by the occurrence of resistance and undruggability of most proteins. Targeted protein degraders are novel, promising agents that trigger the selective degradation of previously undruggable proteins through the recruitment of the ubiquitin–proteasome machinery. Their mechanism of action raises exciting challenges,
Noé Herbel, Sophie Postel‐Vinay
wiley +1 more source
Inhibition of c-Kit by tyrosine kinase inhibitors
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