eligibility_summary
Eligibility: Adults (>=18) with WHO 2016 DLBCL, Other molecular subtype by sequencing, MYC >=40% and BCL2 >=50% by IHC, measurable CT/MRI lesion (>=1.5 cm), ECOG <=2, adequate hepatic/renal function, and consent. Exclusions: concurrent trials, prior lymphoma therapy, other cancers, investigator judgment, severe psych/neuro illness, poor follow-up, pregnancy/lactation/no contraception, active infection or uncontrolled HBV/HCV.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: CR-CHOP (chidamide + R-CHOP) in newly diagnosed double-expressor DLBCL (Other subtype). Drugs and mechanisms: • Chidamide (tucidinostat): oral benzamide selective HDAC inhibitor (primarily class I/IIb). Epigenetic modulation leads to chromatin relaxation, tumor-cell apoptosis, cell-cycle arrest, and enhanced antigen presentation/immune killing, may counter MYC/BCL2-driven survival. • Rituximab: anti-CD20 monoclonal antibody causing B-cell depletion via CDC/ADCC/apoptosis. • Cyclophosphamide: alkylating agent creating DNA crosslinks. • Doxorubicin: anthracycline/topoisomerase II inhibitor and DNA intercalator generating ROS. • Vincristine: vinca alkaloid inhibiting microtubule polymerization. • Prednisone: glucocorticoid inducing lymphocyte apoptosis. Targets/pathways: CD20+ malignant B cells, MYC and BCL2 overexpression (proliferation/survival), epigenetic dysregulation, DNA damage/repair, microtubules, and glucocorticoid signaling.