Drug sensitivity analysis suggested gefitinib, zebularine, and simvastatin as potential therapies for high-risk AML (p < 0.05). Notably, in vitro studies indicated that KCNMB1 facilitates AML progression. In conclusion, our robust PRG-based model elucidates the link between platelet biology, immune dysregulation, and therapeutic vulnerability in AML, offering clinical utility for risk stratification and treatment decisions.

Compounds 4c, 4e, 4f, 4h, 4i and 4j showed promising anticancer activities against MCF-7 cells, with lower IC50 values (IC50 = 5.65 μM to 7.51 μM) than erlotinib (IC50 = 10.50 μM)...In silico molecular modelling studies also indicated that the 4i-EGFR complex was less stable than the 4h-EGFR complex throughout the simulation time. Furthermore, the disruption of cellular redox homeostasis, as evidenced by reduced ROS generation, mitochondrial membrane depolarization, and the induction of apoptosis in treated cells, suggests a possible secondary anticancer mechanism.

P2, N=60, Not yet recruiting, University of Texas Southwestern Medical Center | Trial completion date: Dec 2030 --> Aug 2030 | Trial primary completion date: Dec 2030 --> Jun 2030

P2, N=118, Completed, Institut für Klinische Krebsforschung IKF GmbH at Krankenhaus Nordwest | Active, not recruiting --> Completed

These findings suggest that osimertinib crosses the placenta with a moderate tissue uptake, while alectinib and its metabolite M4 do not appear to be transferred to the fetus but accumulate significantly within the placental tissue. Further studies are needed to guide treatment selection for NSCLC in pregnant women.

Recent clinical trials have led to US Food and Drug Administration approval of osimertinib and alectinib as adjuvant treatments for resected pathologic stage II/III EGFR and ALK-mutated NSCLC; their use in the neoadjuvant setting remains subject to trials. These questions are the subject of two ongoing National Clinical Trials Network trials: CTIU2317-A082304-S2402-Perioperative versus Adjuvant Systemic Therapy in Patients with Resectable NSCLC (PROSPECT-Lung; ClinicalTrials.gov Identifier: NCT04267848)-and S2414-A Randomized Phase III Trial Incorporating Pathologic Response in Participants with Early-Stage NSCLC to Optimize Immunotherapy in the Adjuvant Setting (INSIGHT; ClinicalTrials.gov Identifier: NCT06498635). We discuss why there is sufficient equipoise to justify seeking answers to these two extremely important, patient-centered questions.

The mOS of the EGFR-TP53 co-mutant group who received second-line TKIs combined with platinum-containing double-drug chemotherapy and bevacizumab after the progression of first-line single-drug TKIs was 27.0 months versus 6.0 months compared with those who did not receive second-line therapy (P = .019). In first-line EGFR-TKIs monotherapy in patients with EGFR-TP53 co-mutation, osimertinib was clearly superior to gefitinib. In first-line EGFR-TKIs monotherapy progression, TKIs combined with chemotherapy and antiangiogenesis therapy could prolong patients' survival.

HHT has been identified as an impediment to cell invasion and metastasis in PC via the EphB4/SRI/EMT axis. Additionally, HHT enhances the efficacy of ERT in inhibiting the migration of PC cells.

The results suggest that carmofur and B13 are promising alternatives for therapeutic targets in drug-resistant lung cancer cells.

NSC265450 and NSC70845 were the most potent antiproliferative agents with IC50 < 4 nM against overexpressed EGFR-TK cancer cell lines, HeLa and A549, displayed significantly much greater potencies than NSC116555, erlotinib and doxorubicin. Furthermore, molecular docking and molecular dynamics results predicted the binding action of the series to the ATP binding site of EGFR-TK; intermolecular interactions to key regions of the protein and amino acid residues are described. Prediction of pharmacokinetic and toxicity profiles of the series, and calculations of known drug indexes suggest the molecules are pharmaceutically compatible as therapeutic drug candidates.

P1, N=42, Recruiting, Alpha Biopharma (Jiangsu) Co., Ltd. | Not yet recruiting --> Recruiting