Nasopharyngeal Carcinoma

Among patients with heavily pretreated and immunotherapy-exposed recurrent or metastatic NPC, becotatug vedotin significantly improved ORR and PFS compared with chemotherapy, with comparable toxicity and encouraging but immature OS results.

In conclusion, LINC00312 increased PAX5 mRNA stability by recruiting PABPC1, which promoted LPLUNC1 transcription to regulate sensitivity of NPC to gemcitabine. Meanwhile, PAX5 in turn transcriptionally activated LINC00312 to form a feedback axis, which further increased gemcitabine sensitivity.

This study integrated multi-omics data with machine learning to develop a robust four-gene diagnostic model for NPC. The core genes (COL4A2, LAMB1, ACTA2, CCL2) are associated with tumor progression, prognosis, immune regulation, and distinct biological pathways. Our findings provide a valuable tool for the diagnosis and risk stratification of NPC and reveal potential therapeutic targets worthy of further investigation.

P1, N=60, Not yet recruiting, Memorial Sloan Kettering Cancer Center

P2, N=50, Suspended, National Cancer Institute (NCI) | Recruiting --> Suspended

ITGB1 knockdown partially mimicked the effects of rRGD3mu and reduced the additional cellular response to rRGD3mu treatment, supporting the substantial contribution of ITGB1-associated signaling. These findings provide preliminary mechanistic evidence that rRGD3mu suppresses malignant phenotypes in CNE2-based models, at least in part through modulation of ITGB1-associated FAK/AKT signaling.

Moreover, upstream regulators associated with EBV lytic activation, including p65, AP-1, HIF-1α, and SP1, were down-regulated following capsaicin treatment. Collectively, these findings demonstrate a multitarget inhibitory effect of capsaicin on EBV lytic reactivation and support its therapeutic potential against EBV-associated epithelial malignancies.

In conclusion, this study unveils the RNF138-hnRNPA0-WWOX axis as a driver of JAK2/STAT3 activation, leading to both chemoresistance and immune evasion in NPC. This work positions RNF138 as a valuable biomarker to guide individualized chemotherapy, and highlights JAK inhibitors as a potential targeted therapy for NPC patients.

Functionally, this axis suppresses NPC cell proliferation and migration. Our findings reveal a novel CLOCK-NBR1/p62-TRIM38-TAB2 pathway that links circadian gene to LLPS-driven tumor suppression in NPC, providing new insights into the role of circadian genes in cancer biology and pointing to a potential therapeutic target for this malignancy.

TQB2618 plus penpulimab combined with gemcitabine-cisplatin demonstrated encouraging antitumor activity and a manageable safety profile in treatment-naïve patients. However, the chemotherapy-free dual regimen showed limited efficacy in immunotherapy-refractory disease.

Moreover, miR-10b-3p levels were inversely correlated with ITGAV expression in NPC tissues. Collectively, these findings identify an EBV-regulated miR-10b-3p/ITGAV/STAT5-ERK1/2 axis in NPC and show that loss of miR-10b-3p promotes tumor growth and metastasis by relieving ITGAV repression, suggesting potential therapeutic targets for EBV-associated NPC.

Our findings contribute to a more nuanced understanding of LEL-ICC pathogenesis and highlight the potential synergistic role of viral co-infections. Further case accumulation and mechanistic studies are needed.