TMB-L

Understanding these resistance mechanisms is crucial for developing effective combination strategies and improving patient outcomes. Advances in molecular profiling and immune modulation present promising opportunities to broaden the application of ICIs in the treatment of CRC.

We identified the LINC01272-FUS axis as a critical regulatory pathway in TGCTs progression, providing mechanistic insights for developing liquid biopsy biomarkers and RNA-targeted therapies.

Case 1 received osimertinib combined with savolitinib, had 33 months of follow-up, and achieved a partial response. Case 2 received furmonertinib and achieved a complete response. NTRK2 fusion coexisting with EGFR mutations is a rare molecular characteristic of non-small cell lung cancer, accompanied by positive PD-L1 expression, and may serve as a promising biomarker for targeted therapy.

Cell experiments revealed that interference of UBE2Q1-AS1 significantly inhibited the proliferation and migration of 786-O cells. The migrasome-associated lncRNA model accurately predicts ccRCC patient prognosis, offering new insights for immunotherapy and clinical applications.

It highlights the importance of understanding tumour-immune interactions in their full biological context, and explores current thinking on how to reshape the immune landscape of solid tumours. By addressing both immunological and physical barriers, future approaches may broaden the benefit of immunotherapy beyond its current scope, ultimately improving outcomes for patients with traditionally treatment-resistant cancers.

pDCs appear to exert a tumor-promoting, immune-evasive role, suggesting that DC function depends on their programming and tumor context. Selective targeting of DC subsets may offer novel therapeutic opportunities in TP53-mutated, low-TMB cancers.

We demonstrate that optimal efficacy requires biomarker-guided patient selection integrating genetic and TME features, precise sequencing, and a mechanistic understanding of drug-specific immunomodulatory effects. The integration of platform trial designs (I-SPY2, CheckMate-7FL) with composite biomarker algorithms represents a paradigm shift toward precision neoadjuvant immunotherapy, offering a conceptual framework for transforming outcomes in molecularly defined HR+ breast cancer subsets.

In vitro experiments demonstrated that GAB3 overexpression inhibited cancer cell proliferation and migration, while siRNA-mediated knockdown of GAB3 promoted these processes, suggesting its role as a tumor suppressor gene. In conclusion, GAB3 and IL16 are key prognostic markers, providing insights into STING-related immunotherapy strategies for LUAD.

Importantly, knockdown of IGF2BP1 along with anti-GD2 immunotherapy induced a synergistic immunogenic effect and achieved a potent antitumor response in an HR-NB mouse model, with increased accumulation of effector CD8+ T cells and CD86+  macrophages but decreased MDSC numbers in the tumor microenvironment. Thus, disrupting NB cancer cell IGF2BP1-mediated immunosuppression is a potential approach for improving the efficacy of anti-GD2 immunotherapy towards HR-NBs.

This case highlights that a definitive distinction between WDPMT and malignant mesothelioma is paramount, as it dictates a radically different management strategy. Integration of immunohistochemistry (particularly BAP1) and molecular profiling is essential for accurate diagnosis and can prevent overtreatment. For appropriately selected patients with WDPMT, conservative management with active surveillance represents a safe and effective approach, underscoring the value of precision medicine in guiding patient-centric care.

While the biological and molecular determinants underlying the response rates observed in the NICHE-2 trial remain to be fully elucidated, the work by Tan et al. suggests that biomarker-guided neoadjuvant immunotherapy could represent a valuable strategy to achieve pathological responses in early-stage pMMR CC, despite its clinical relevance requiring further evaluation.

SULmax is an independent predictor of both PD-L1-Pos and TMB-High in ADC. The clinical-SULmax combined models effectively predicted PD-L1-Pos and TMB-High status, as well as PD-L1-Neg and TMB-Low status in ADC, indicating the clinical utility in patient selection and immunotherapy response stratification.