The patient completed six cycles of adjuvant chemotherapy with tegafur-gimeracil-oteracil (S-1) plus oxaliplatin, and routine follow-up examinations showed no evidence of recurrence...The patient was treated with SOX chemotherapy combined with the PD-1 inhibitor tislelizumab...This case highlights the importance of vigilance for rare metastatic sites, such as the adrenal gland, in patients with advanced gastric cancer even after standardized postoperative surveillance. Systemic chemotherapy combined with immunotherapy may represent an effective treatment strategy for selected patients with metastatic gastric cancer.

Both CHGA and UCHL1-activated transcription were regulated through the Rho/ERK/NF-κB signaling pathways by histone modifications of H3K4 trimethylation. In this study, Rho/ERK/NFκB signaling-mediated CHGA and UCHL1 expression, which is regulated through histone modifications and affects OXA-resistant CRC EMT outcomes, was assessed, and its potential as an early detection biomarker and prognostic indicator was explored with clinical applications.

Mechanism study discovered that activation of AMPK/Nrf2/HO-1 pathways participated in regulating the neuroprotective function of Eto in inflammatory response and oxidative stress response in OXA-treated mice and in C6 cells model. In conclusions, Eto improved OXA-induced neuropathic pain by regulating AMPK/Nrf2/HO-1 pathway.

These findings establish the COP1-LUZP1-MYL9 axis as a therapeutic target for CRLM and oxaliplatin-based chemoresistance. Clinically, COP1 expression profiling in PDOs from postoperative specimens enables a precision strategy for managing oxaliplatin-based chemoresistance, especially in the context of FOLFOX.

The research announced that Eto improved OXA-induced neuropathic pain by regulating AMPK/Nrf2/HO-1 pathway.

This study investigated the immunomodulatory effects of DAMPs released from HepG2 cells treated with standard chemotherapeutic agents, sorafenib and oxaliplatin. Although the cytokine profile was predominantly pro-inflammatory (TNF-α, IL-1β), the concurrent secretion of IL-10 suggests a complex, mixed activation state. By overriding M2 immunosuppression via an ERK-NLRP3-dependent pathway, sorafenib-derived DAMPs act as an immunological primer to convert cold to hot tumors, providing a molecular rationale for chemo-immunotherapy combinations.

Except for the blank control group, the remaining 48 mice underwent ectopic transplantation of gastric cancer cells into the axilla and were randomly divided into four groups (n=12 per group): the gastric cancer group, the CIPN model group, the modified Danggui buxue decoction group, and Duloxetine group. Conclusion Modified Danggui buxue decoction may ameliorate pathological damage and pain symptoms in the dorsal root ganglia of a mouse model of oxaliplatin-induced peripheral neurotoxicity following gastric cancer chemotherapy. The mechanism is likely associated with the inhibition of the NF-κB signaling pathway in the dorsal root ganglia and the down regulation of ATM, NF-κB, CCL21, TNF-α, IL-1β, and IL-6 expression.

Inhibiting miR-100-5p and FOXP3 down-regulates miR-100-5p expression, while increased CTDSPL expression contributed to reduced cell proliferation and promoted cell apoptosis in LoVoOXR CRC cells. miR-100-5p plays an oncogenic role in inducing chemoresistance through modulation of the CTDSPL/retinoblastoma protein (pRB)/E2F transcription factor 1 (E2F1) axis in CRC cells.

In vivo, OXA-OA Alb NPs achieved ~ 90% tumor inhibition in a TNBC mouse model, with minimal systemic toxicity, stable liver and kidney function, and reduced organ damage compared with other treatment groups. These findings suggest that OXA-OA Alb NPs offer a promising and safer approach for TNBC, with potential for further exploration in preventing metastasis and recurrence.

P3, N=304, Not yet recruiting, Shanghai Zhongshan Hospital

Combination treatment with mebendazole and oxaliplatin significantly enhanced chemosensitivity in ESCC cells. Collectively, these findings establish the USP5-IMPDH2-guanine axis as a critical driver of ESCC progression and highlight its potential as a promising therapeutic target for ESCC.

Molecular docking revealed higher binding affinities for both Idarubicin (- 9.98 kcal/mol) and Larotrectinib (- 9.42 kcal/mol) compared to the reference drug Erlotinib (-8.91 kcal/mol). Additionally, they demonstrated favorable predicted cytotoxicity against NSCLC cell lines. In conclusion, our integrated bioinformatics analysis identifies idarubicin and larotrectinib as putative candidates for drug repurposing targeting EGFR in NSCLC, providing a rational foundation for future experimental validation and further preclinical and clinical investigations.