P1, N=800, Active, not recruiting, University of Chicago | Trial completion date: Jan 2026 --> Jan 2028 | Trial primary completion date: Dec 2025 --> Dec 2027

Mechanistic studies reveal that 3N-DPQ-COF accumulates efficiently in resistant tumor cells and suppresses cancer stemness in 4T1 and CT26 models, outperforming doxorubicin...Remarkably, even without checkpoint blockade, 3N-DPQ-COF suppresses metastasis and recurrence in chemoresistant 4T1 tumors, achieving >90% tumor inhibition and cure rates exceeding 80%. This study highlights the potential of AIEgen-based COF nanomedicines for overcoming chemoresistance through concurrent modulation of tumor stemness, pyroptosis, and immune activation.

The OS benefit of CPX-351 observed in the trial was driven by AML-MR with no benefit of CPX-351 in TP53-AML, where the primary prognostic factor was allelic state. Clinical Trial Information: NCT01696084.

Additionally, bile acids induce biomolecular condensate formation in mutant p53, sequestering doxorubicin within these structures and suggesting a mechanism for chemoresistance. These findings highlight the role of bile acids in promoting mutant p53 aggregation and therapy resistance, suggesting potential new therapeutic targets for p53 mutant CRC.

In this context, the CAP regimen-comprising cyclophosphamide, adriamycin, and cisplatin-has demonstrated superior overall efficacy. Moreover, these tumors seem to be relatively resistant to radiation therapy.

Initial systemic therapy with doxorubicin achieved stable disease at three months. Based on the genomic findings identified following comprehensive genomic profiling, the patient was subsequently enrolled in the DESTINY-PanTumor02 clinical trial and transitioned to treatment with trastuzumab deruxtecan targeting the human epidermal growth factor receptor 2 (HER2) alteration...It illustrates the marked radiologic and clinicopathologic heterogeneity of IMT and emphasizes the importance of comprehensive histopathologic and molecular evaluation to guide management in aggressive disease variants. Close collaboration across cross-disciplinary diagnostic specialties is essential for the assessment and treatment of rare, multi-organ conditions.

Loss of breast cancer susceptibility gene 2 (BRCA2) function was found to exacerbate doxorubicin-mediated cardiomyocyte apoptosis and promote heart failure progression...These results indicated that upregulation of BRCA2 could improve hypertrophic cardiomyopathy. BRCA2 alleviated cardiac hypertrophy via attenuation of inflammation and apoptosis.

Our analyses reveal that Tan IIA regulates 13 core targets of Dox cardiotoxicity-with enrichment in pathways including canonical cancer and small cell lung cancer pathways-and that six of these targets exhibit high binding affinity for Tan IIA or Dox; notably, machine learning prioritized the histone methyltransferase EZH2 as the central target for Tan IIA's anti-TNBC activity, and we further show EZH2 is highly expressed in breast invasive carcinoma (BRCA) tissues and correlates positively with infiltration of immune cells (e.g., B cells, CD4⁺ T cells) and expression of immune-related molecules (including immunosuppressors and MHC-associated antigen-presenting molecules). Collectively, these findings demonstrate that Tan IIA may mitigate Dox cardiotoxicity via modulation of targets such as APAF1, AR, and TERT (and their associated signaling cascades) while targeting EZH2 to exert anti-TNBC effects, providing a mechanistic framework for repurposing Tan IIA to improve the safety and efficacy of Dox-based BC therapy.

Betamethasone and levofloxacin ophthalmic solutions were started on the same day. Molecular remission was achieved on day 161 after relapse. Three years later, the patient remains in remission on dasatinib therapy.

P=N/A, N=72, Not yet recruiting, The First Affiliated Hospital, College of Medicine, Zhejiang University; The First Affiliated Hospital of Zhejiang University School of Medicine

P=N/A, N=23, Recruiting, The Second Affiliated Hospital of Hainan Medical University; The Second Affiliated Hospital of Hainan Medical University

P=N/A, N=82, Not yet recruiting, Renji Hospital, Shanghai Jiao Tong University School of Medicine; Renji Hospital, Shanghai Jiao Tong University School of Medicine