imatinib

Consistent with prior preclinical studies, we demonstrate that dasatinib and ponatinib, unlike SRC sparing TKIs (imatinib, nilotinib), antagonize blinatumomab's T-cell engaging efficacy by potently inhibiting LCK Y394 phosphorylation, a critical step in proximal TCR signaling. We show that TKI-induced T-cell suppression and antagonism can be significantly improved by supplementing co-cultures with common gamma-chain cytokines, particularly IL-7. IL-7 robustly enhances human T-cell proliferation, reduces exhaustion, and significantly improves blinatumomab's cytotoxic efficacy in the presence of Src/BCRABL1 TKIs.

In vivo, both PDGFRα antibody neutralization and pharmacological inhibition with imatinib significantly attenuated DBP-induced hepatic fibrosis and inflammatory gene expression, confirming PDGFRα's central role in DBP toxicity...Collectively, these findings identify PDGFRα as a mechanistic nexus linking DBP and PS-NPs exposure to hepatic fibrosis and highlight its potential as a therapeutic target for environmentally induced liver disease. The results further underscore the importance of co-exposure paradigms in evaluating the health risks of complex contaminant mixtures.

Besides, bosutinib, dasatinib, imatinib, nilotinib, and radotinib were used as controls in the DockingServer program.The results displayed different types of aminoacid residues involved in the interaction of amide derivatives with the 1iep protein surface compared to the controls. Finally, the Ki for amide derivatives 1, 19, and 21 were lower compared with bosutinib, dasatinib, imatinib, and nilotinib.Theoretical data indicate that amide derivatives such as 1, 15, 16, 18, 19, and 21 might have a higher affinity for the 1iep protein surface. This phenomenon could be translated as c-Abl kinase inhibition, resulting in a decrease in cancer cell growth.

P=N/A, N=32, Not yet recruiting, Affiliated Hospital of Guilin Medical University; Affiliated Hospital of Guilin Medical University

High-risk patients were found to be more sensitive to treatment drugs ABT.263, AZD.0530, gefitinib, imatinib, PAC.1, and shikonin. The predictive model we constructed can independently predict the prognosis of patients with CRC. Further experimental validation and mechanistic studies are warranted to elucidate the precise role of OS-related lncRNAs in CRC pathogenesis.

We report a case of a 60-year-old male who developed intra-abdominal desmoid tumors five years after undergoing laparoscopy and endoscopy cooperative surgery (LECS) for gastric GIST, followed by adjuvant imatinib therapy...Histopathological confirmation remains crucial for accurate diagnosis. Surgical resection is the primary treatment for symptomatic desmoid tumors, but given their high recurrence rate, long-term follow-up and a multidisciplinary approach are essential for optimal management.

Percentage cost variation ranged from 8% (Bosutinib) to 14,774.74% (Midostaurin), with corresponding cost ratios up to 148.75...Absolute savings versus median branded costs ranged from ₹2,968 (Dasatinib) to ₹25,270 (Lapatinib), while percentage savings ranged from 58.89% (Dasatinib) to 91.32% (Imatinib)...However, limited PMBJP coverage restricts their overall benefit. Expanding Janaushadhi availability, improving price regulation, and encouraging rational prescribing are crucial to ensure equitable access to targeted cancer therapies in India.

Combination strategies, such as vorinostat with ponatinib, provide complementary therapeutic avenues...Hybrid molecules derived from approved TKIs, including GNF-7, olverembatinib, and HG-7-85-01, exemplify rational design trends that balance efficacy with improved safety. Molecular modeling continues to deepen understanding of ligand engagement within the T315I-mutated active site, supporting the development of next-generation inhibitors. In this review, we summarized recent progress in the design, optimization, and biological evaluation of small molecules targeting the BCR-ABLT315I mutation.

Patients with conditions that could confound MCV (hydroxyurea exposure, megaloblastic anemia, hypothyroidism, chronic liver disease, alcoholism) were excluded. MCV elevation during imatinib therapy is associated with deeper molecular response and reduced need for treatment modification. MCV dynamics may serve as an inexpensive pharmacodynamic marker to support risk assessment and guide monitoring in chronic-phase CML.

This allowed for targeted therapy with a tyrosine kinase inhibitor (TKI), leading to molecular remission monitored by RT-qPCR. This case highlights how a multidisciplinary approach can identify atypical transcripts in MPN, guiding targeted therapy with TK inhibitors, thus resulting in effective treatment and molecular remission.

The remaining patient had an unresectable tumor and received tyrosine kinase inhibitor therapy; however, sequential treatment with imatinib and sunitinib was clinically ineffective. However, their clinical behavior differs: D842Y-mutant GISTs consistently present as large, hypervascular tumors associated with acute complications. The therapeutic efficacy of tyrosine kinase inhibitors remains unclear, underscoring the need for further case accumulation to better define the clinical course and determine optimal treatment strategies for this rare subtype.

Imatinib and rosuvastatin were discontinued, and the patient was managed with intravenous fluids and supportive care. This case represents one of the most severe reported instances of imatinib-induced rhabdomyolysis. Early recognition and discontinuation are essential to prevent life-threatening sequelae.