P=N/A, N=46, Completed, Tanta University

Our study establishes a novel multi-gene diagnostic signature for oxaliplatin resistance through integrative bioinformatics and machine learning approaches. The comprehensive molecular characterization and identification of potential therapeutic candidates provide new insights into resistance mechanisms and clinical management strategies for oxaliplatin-resistant colorectal cancer.

Combining cytokine mRNA immunotherapy with cytotoxic killing and immune checkpoint blockade can reactivate antitumour immunity, offering a promising strategy for treating advanced PDAC.

Cell lines representing DLBCL subtypes were treated with varying concentrations of the XPO1 inhibitor selinexor (XPO1i), cisplatin (CDDP), and oxaliplatin (OXA), alone or in combination. In OCI-Ly8 and OCI-Ly1 cells, OXA alone inhibited phosphorylation of AKT and mTOR while increasing phosphorylation of JNK, ATM, and p53, and expression of γH2AX; these effects were potentiated by the combination of XPO1i and OXA. XPO1 inhibition enhances platinum-induced cytotoxicity in GCB-DLBCL, supporting clinical evaluation of XPO1i-platinum combinations as salvage therapy.

P2, N=128, Not yet recruiting, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine

To address these issues, we developed a mild PTT (mPTT) nanoparticle based on mesoporous polydopamine (MPDA), loaded with oxaliplatin (OXP) and manganese dioxide (MnO2), and coated with tumor cell membranes to enhance the targeting capability...The activation of both adaptive and innate immune responses triggers a potent antitumor immune reaction, which, combined with chemotherapy and enhanced mPTT, significantly suppresses tumor growth, metastasis and recurrence. This strategy not only enhances the targeting of chemotherapeutic drugs but also provides new possibilities for expanding the field of immunotherapy in gastric cancer by regulating tumor metabolism and enhancing mPTT.

CPhG alleviates oxaliplatin-induced peripheral neuropathy by dual mechanisms: reducing neuroinflammation via IL-6 suppression and promoting neuronal survival and regeneration through AKT activation and m6A-dependent epitranscriptomic regulation. Compared with duloxetine, CPhG demonstrated superior neuroprotective and anti-inflammatory effects, supporting its potential as a novel therapeutic agent for OIPN.

HQGZWWT significantly ameliorated CINP by increasing sciatic nerve conduction velocity, reducing oxidative stress and inflammatory responses, and inhibiting ferroptosis. Both HQGZWWT and its active monomeric component paeoniflorin protect neurons by suppressing ferroptosis, thereby exerting preventive and therapeutic effects against CINP. These findings provide new insights into the clinical treatment of CINP with HQGZWWT. Inhibiting ferroptosis by regulating the p38/c-FOS/NF-κB pathway through HQGZWWT and its primary monomeric component paeoniflorin represents a promising therapeutic strategy for preventing and treating oxaliplatin-induced CINP.

P=N/A, N=30, Not yet recruiting, Tongde Hospital of Zhejiang Province; Tongde Hospital of Zhejiang Province

P=N/A, N=150, Recruiting, Linyi Tumor Hospital; Linyi Tumor Hospital

P2, N=30, Recruiting, Beijing Cancer Hospital; Beijing Cancer Hospital

P2, N=106, Recruiting, Jiangsu Hengrui Medicine Co., Ltd.; The First Affiliated Hospital of Nanchang University