Epithelial ovarian carcinoma, the deadliest gynecological malignancy, frequently develops treatment resistance through polyploid giant cancer cells (PGCCs) that typically emerge after carboplatin-paclitaxel chemotherapy. Our findings establish that the cytoplasmic SIRT1/β-catenin axis contributes to PGCC stemness, elucidating a novel mechanism underlying chemoresistance. Therefore, targeting cytoplasmic SIRT1 represents a promising therapeutic strategy to overcome PGCC-mediated resistance in this lethal carcinoma.

The combination treatment inhibited PI3K, AKT, and STAT3 expressions, thereby suppressing proliferation and inducing proapoptotic protein expression in HGT-1 cells. Therefore, the combination of MRN and PTX could serve as a therapeutic approach for malignant GC treatment.

Inhibition of LDHAL6A combined with paclitaxel treatment markedly suppresses triple-negative breast cancer growth and metastasis. Collectively, our work not only establishes an advanced model for IVPL but also profiles ultimately exosomal actors in recipient organs for targeted therapy.

Pre-treatment biomarker levels were associated with greater KS tumor burden but not with KS response to chemotherapy + ART in people with advanced AIDS-KS. Differential levels of several serum biomarkers were noted on treatment in progressors and non-progressors, suggesting that increased tumor burden was associated with higher levels of inflammation and immune activation.

The combination of chemotherapy and immune checkpoint blockade therapy shows great potential in tumor treatment, but their integration remains a great challenge. Meanwhile‌, overexpression of programmed cell death ligand 1 (PD-L1) is suppressed by JQ1, thereby reversing PD-L1-mediated immune resistance to synergistically promote adaptive antitumor immune response. This hypoxia-sensitive versatile nanoplatform provides an elegant paradigm for precise tumor therapy.

The THAG regimen as preoperative therapy showed encouraging clinical activity with a manageable safety profile. Dynamic biomarker findings reveal potential for guiding precision treatment strategies with THAG.

Chemotherapy with gemcitabine and nab-paclitaxel was initiated, but the lesion persisted. Despite neoadjuvant chemotherapy, NTS occurred, indicating that this risk cannot be fully prevented. Surgical resection achieved disease control, underscoring the importance of vigilant follow-up and timely intervention in managing this rare but clinically significant complication.

This integrative bioinformatics approach prioritized functionally significant BCa-associated SNPs and identified promising candidates for biomarker development and drug repositioning. The nine high-scoring variants, including SLCO1B1 and ARHGEF38 emerge as biologically impactful genes, while MAPT's known drug interactions highlight its translational potential in repurposing existing anticancer agents.

To model acquired resistance, PC-9 cells were exposed to vinorelbine or paclitaxel for 18 weeks-approximating the clinical duration of four adjuvant chemotherapy cycles-and subsequent drug sensitivity and signaling pathway alterations were assessed using cell viability assays, RNA sequencing, and immunoblotting. These findings suggest that CaMKII plays a critical role in EGFR-TKI resistance. This study underscores the importance of optimizing the timing of EGFR-TKI administration in the therapeutic sequence for EGFR-mutated NSCLC.

By inhibiting FAK activation and upregulating PIK3IP1, Ifebemtinib and paclitaxel blocked the PI3K/Akt pathway, effectively suppressing TNBC proliferation and metastasis. Our findings suggest that FAK may serve as a potential therapeutic target for TNBC.

The expression of TRIM25 was negatively correlated with BRD7 expression, and the combined expression of TRIM25 and BRD7 might be a potential molecular marker for the prediction of malignant progression and prognosis of breast cancer. Our findings demonstrate that targeting the TRIM25/BRD7/YB1/Bcl-2 signal axis might be a potential therapeutic strategy for the treatment of breast cancer.

CRM1 also synergistically potentiated the cytotoxic efficacy of paclitaxel by co-targeting multiple cell death processes. Collectively, these results suggest CRM1 as a promising cytotoxic candidate with a multimodal mechanism of action in lung cancer cells.