Exploring the impact of ITGB2 on glioma progression and treatment: Insights from non-apoptotic cell death and immunotherapy.

In the realm of glioma treatment, our groundbreaking research has uncovered the pivotal role of Integrin Beta 2 (ITGB2) in non-apoptotic cell death and its profound implications for immunotherapy efficacy. Gliomas, known for their aggressive and infiltrative nature, demand innovative therapeutic strategies for improved patient outcomes. Our study bridges a critical gap by examining the interplay between non-apoptotic cell death and immunotherapy response in gliomas. Through comprehensive analysis of ten diverse glioma datasets, we developed a unique death enrichment score and identified ITGB2 as a significant risk marker. This study demonstrates that ITGB2 can predict immune activity, mutation characteristics, and drug response in glioma patients. We reveal that ITGB2 not only mediates glioma proliferation and migration but also crucially influences immunotherapy responses by modulating the interaction between gliomas and macrophages by single-cell sequencing analysis (iTalk and ICELLNET). Employing a variety of molecular and cellular methodologies, including in vitro models, our findings highlight ITGB2 as a potent marker in glioma biology, particularly impacting macrophage migration and polarization. We present compelling evidence of ITGB2's dual role in regulating tumor cell behavior and shaping the immune landscape, thereby influencing therapeutic outcomes. The study underlines the potential of ITGB2-targeted strategies in enhancing the efficacy of immunotherapy and opens new avenues for personalized treatment approaches in glioma management. In conclusion, this research marks a significant stride in understanding glioma pathology and therapy, positioning ITGB2 as a key biomarker and a promising target in the quest for effective glioma treatments.

Development of nomogram to predict in-hospital death for patients with intracerebral hemorrhage: A retrospective cohort study.

Aim: This study aimed to investigate the association between systemic immune-inflammation (SII) and the risk of in-hospital death for patients with intracerebral hemorrhage (ICH) in the intensive care units (ICU) and to further develop a prediction model related to SII in predicting the risk of in-hospital death for patients with ICH. Methods: In this retrospective cohort study, we included 1,176 patients with ICH from the Medical Information Mart for Intensive Care III (MIMIC-III) database. All patients were randomly assigned to the training group for the construction of the nomogram and the testing group for the validation of the nomogram based on a ratio of 8:2. Predictors were screened by the least absolute shrinkage and selection operator (LASSO) regression analysis. A multivariate Cox regression analysis was used to investigate the association between SII and in-hospital death for patients with ICH in the ICU and develop a model for predicting the in-hospital death risk for ICU patients with ICH. The receiver operator characteristic curve was used to assess the predicting performance of the constructed nomogram. Results: In the training group, 232 patients with ICH died while 708 survived. LASSO regression showed some predictors, including white blood cell count, glucose, blood urea nitrogen, SII, the Glasgow Coma Scale, age, heart rate, mean artery pressure, red blood cell, bicarbonate, red blood cell distribution width, liver cirrhosis, respiratory failure, renal failure, malignant cancer, vasopressor, and mechanical ventilation. A prediction model integrating these predictors was established. The area under the curve (AUC) of the nomogram was 0.810 in the training group and 0.822 in the testing group, indicating that this nomogram might have a good performance. Conclusion: Systemic immune-inflammation was associated with an increased in-hospital death risk for patients with ICH in the ICU. A nomogram for in-hospital death risk for patients with ICH in the ICU was developed and validated.

SOCS5 contributes to temozolomide resistance in glioblastoma by regulating Bcl-2-mediated autophagy.

Temozolomide (TMZ) is the primary chemotherapeutic drug for treating glioblastoma (GBM); however, the final clinical outcome is considerably limited by the poor response and resistance to TMZ. Although autophagy is thought to be associated with chemotherapy resistance and cancer cell survival, the precise molecular mechanisms underlying this process remain elusive. The suppressor of cytokine signaling (SOCS) family is widely distributed in vivo and exerts a range of effects on tumors; however, the expression pattern and role of SOCS in GBM remains unknown. In this study, we determined that high SOCS5 expression level was associated with poor prognosis and TMZ resistance in GBM. TMZ induced an increase in SOCS5 expression level and upregulated autophagy during the acquisition of drug resistance. The observed increase in the extent of autophagy was mediated by SOCS5. Mechanistically, SOCS5 enhances the transcription of Bcl-2. Knockdown of SOCS5 inhibited TMZ chemoresistance in GBM cells through the inhibition of Bcl-2 recruited autophagy; upregulation of Bcl-2 blocked this effect. In summary, our findings revealed the involvement and underlying mechanism of SOCS5 in TMZ resistance. SOCS5 plays a critical role in GBM chemoresistance and may serve as a novel prognostic marker and therapeutic target for chemotherapeutically treating drug-resistant GBM.