A bibliometric analysis of radiation-induced brain injury: a research of the literature from 1998 to 2023.

BACKGROUND: Radiation-induced brain injury (RIBI) is a debilitating sequela after cranial radiotherapy. Research on the topic of RIBI has gradually entered the public eye, with more innovations and applications of evidence-based research and biological mechanism research in the field of that. This was the first bibliometric analysis on RIBI, assessing brain injury related to radiation articles that were published during 1998-2023, to provide an emerging theoretical basis for the future development of RIBI. METHODS: Literature were obtained from the Web of Science Core Collection (WOSCC) from its inception to December 31, 2023. The column of publications, author details, affiliated institutions and countries, publication year, and keywords were also recorded. RESULTS: A total of 2543 journal articles were selected. The annual publications on RIBI fluctuated within a certain range. Journal of Neuro-oncology was the most published journal and Radiation Oncology was the most impactful one. LIMOLI CL was the most prolific author with 37 articles and shared the highest h-index with BARNETT GH. The top one country and institutions were the USA and the University of California System, respectively. Clusters analysis of co-keywords demonstrated that the temporal research trends in this field primarily focused on imaging examination and therapy for RIBI. CONCLUSION: This study collects, visualizes, and analyzes the literature within the field of RIBI over the last 25 years to map the development process, research frontiers and hotspots, and cutting-edge directions in clinical practice and mechanisms related to RIBI.

Identification and validation of COL6A1 as a novel target for tumor electric field therapy in glioblastoma.

BACKGROUND: Glioblastoma multiforme (GBM) is the most aggressive primary brain malignancy. Novel therapeutic modalities like tumor electric field therapy (TEFT) have shown promise, but underlying mechanisms remain unclear. The extracellular matrix (ECM) is implicated in GBM progression, warranting investigation into TEFT-ECM interplay. METHODS: T98G cells were treated with TEFT (200 kHz, 2.2 V/m) for 72 h. Collagen type VI alpha 1 (COL6A1) was identified as hub gene via comprehensive bioinformatic analysis based on RNA sequencing (RNA-seq) and public glioma datasets. TEFT intervention models were established using T98G and Ln229 cell lines. Pre-TEFT and post-TEFT GBM tissues were collected for further validation. Focal adhesion pathway activity was assessed by western blot. Functional partners of COL6A1 were identified and validated by co-localization and survival analysis. RESULTS: TEFT altered ECM-related gene expression in T98G cells, including the hub gene COL6A1. COL6A1 was upregulated in GBM and associated with poor prognosis. Muti-database GBM single-cell analysis revealed high-COL6A1 expression predominantly in malignant cell subpopulations. Differential expression and functional enrichment analyses suggested COL6A1 might be involved in ECM organization and focal adhesion. Western blot (WB), immunofluorescence (IF), and co-immunoprecipitation (Co-IP) experiments revealed that TEFT significantly inhibited expression of COL6A1, hindering its interaction with ITGA5, consequently suppressing the FAK/Paxillin/AKT pathway activity. These results suggested that TEFT might exert its antitumor effects by downregulating COL6A1 and thereby inhibiting the activity of the focal adhesion pathway. CONCLUSION: TEFT could remodel the ECM of GBM cells by downregulating COL6A1 expression and inhibiting focal adhesion pathway. COL6A1 could interact with ITGA5 and activate the focal adhesion pathway, suggesting that it might be a potential therapeutic target mediating the antitumor effects of TEFT.

Advanced tumor electric fields therapy: A review of innovative research and development and prospect of application in glioblastoma.

BACKGROUND: Glioblastoma multiforme (GBM) is an aggressive malignant tumor with a high mortality rate and is the most prevalent primary intracranial tumor that remains incurable. The current standard treatment, which involves surgery along with concurrent radiotherapy and chemotherapy, only yields a survival time of 14-16 months. However, the introduction of tumor electric fields therapy (TEFT) has provided a glimmer of hope for patients with newly diagnosed and recurrent GBM, as it has been shown to extend the median survival time to 20 months. The combination of TEFT and other advanced therapies is a promising trend in the field of GBM, facilitated by advancements in medical technology. AIMS: In this review, we provide a concise overview of the mechanism and efficacy of TEFT. In addition, we mainly discussed the innovation of TEFT and our proposed blueprint for TEFT implementation. CONCLUSION: Tumor electric fields therapy is an effective and highly promising treatment modality for GBM. The full therapeutic potential of TEFT can be exploited by combined with other innovative technologies and treatments.

Use of the Disposcope endoscope for awake orotracheal intubation in an elderly patient with a large vocal cord polyp -a case report.

BACKGROUND: Vocal cord polyps are commonly encountered in the otorhinolaryngology department. The risk of anesthesia is high in patients with large vocal cord polyps. Awake intubation with appropriate airway tools provides a favorable safety profile. CASE: We present the case of a 60-year-old male patient who had been suffering from a large vocal cord polyp for 16 years. Electronic laryngoscopy revealed that the vocal cord polyp was approximately 1.5 cm in diameter. The polyp had a pedicle and demonstrated synchronous motion with respiratory excursion. It covered almost the entire glottic area during inspiration and moved away from the glottis during expiration. A Disposcope endoscope was used for awake tracheal intubation, and the surgery was completed successfully. CONCLUSIONS: The Disposcope endoscope can be a useful option for awake orotracheal intubation in cases of anticipated difficult intubation and difficult facemask ventilation.

Erratum: PFKFB4 promotes angiogenesis via IL-6/STAT5A/P-STAT5 signaling in breast cancer: Erratum.

[This corrects the article DOI: 10.7150/jca.66773.].

Hemoglobin-to-Red Cell Distribution Width Ratio is Associated with All-Cause Mortality in Critically Ill Patients with Traumatic Brain Injury.

BACKGROUND: Hemoglobin-to-red cell distribution width ratio (HRR) has shown good prognostic value in various cancers. However, the relationship between HRR and outcomes in critically ill patients with traumatic brain injury (TBI) remains unclear. This study aimed to investigate the association between HRR and mortality among critically ill patients with TBI. METHODS: The Medical Information Mart for Intensive Care-IV (MIMIC-IV) database was utilized to conduct this retrospective cohort study. TBI patients were divided into four quartiles according to their HRR values. The primary outcome was 30-day mortality, whereas the secondary outcomes were 60-day and 120-day mortality. Univariable and multivariable Cox proportional risk models were performed to evaluate the hazard ratio (HR) and 95% confidence interval (CI) for the relationship between HRR and mortality. Receiver operating characteristic (ROC) curves were conducted to assess the prognostic value of HRR. RESULTS: For 30-day mortality, after adjustment for all potential covariates, the relationship remained significant with HRR treated as a continuous variable (HR, 95% CI: 0.87 [0.81, 0.92]; p < 0.001). In the fully adjusted model, the HR with 95% CI for the second, third, and fourth quartile groups were 0.67 (0.5, 0.9), 0.65 (0.46, 0.94), and 0.5 (0.32, 0.79), respectively, compared to the first quartile group. A similar relationship was also observed for 60-day mortality and 120-day mortality. HRR had a better predictive value than hemoglobin and red cell distribution width (RDW). CONCLUSIONS: A lower level of HRR is significantly associated with higher all-cause mortality among critically ill patients with TBI.

PTPN2 in the Immunity and Tumor Immunotherapy: A Concise Review.

PTPN2 (protein tyrosine phosphatase non-receptor 2), also called TCPTP (T cell protein tyrosine phosphatase), is a member of the PTP family signaling proteins. Phosphotyrosine-based signaling of this non-transmembrane protein is essential for regulating cell growth, development, differentiation, survival, and migration. In particular, PTPN2 received researchers' attention when Manguso et al. identified PTPN2 as a cancer immunotherapy target using in vivo CRISPR library screening. In this review, we attempt to summarize the important functions of PTPN2 in terms of its structural and functional properties, inflammatory reactions, immunomodulatory properties, and tumor immunity. PTPN2 exerts synergistic anti-inflammatory effects in various inflammatory cells and regulates the developmental differentiation of immune cells. The diversity of PTPN2 effects in different types of tumors makes it a potential target for tumor immunotherapy.

PFKFB4 promotes angiogenesis via IL-6/STAT5A/P-STAT5 signaling in breast cancer.

Breast cancer has become the most newly-diagnosed cancer and the 5th leading cause of cancer death worldwide. The 5-year survival rate of breast cancer is about 90%. However, the 5-year survival rate drops to <30% when metastasis to distant sites occurs. The blood vessel formation (i.e., angiogenesis) plays a crucial role during the metastatic process. In this study, we investigated the role of PFKFB4 in angiogenesis of breast cancer. Employing in vitro HUVEC tube formation or in vivo orthotopic mouse model, and gene editing or specific small inhibitors strategy, and utilizing qPCR, western blot, ELISA, or immunofluorescent/immunohistochemistry staining methods, we found the following: 1) PFKFB4 upregulates IL-6 expression via NF-κB signaling in breast cancer cells; 2) PFKFB4-induced lactate secretion contributes to NF-κB activation in breast cancer cells; 3) IL-6 elicits angiogenesis via STAT5A/P-STAT5 in HUVEC; 4) 5-MPN (a specific PFKFB4 inhibitor) suppresses angiogenesis in vitro and in vivo. Our findings suggest a potential strategy whereby 5-MPN may lead to an improved therapeutic outcome for breast cancer patients.

MCP-1 targeting: Shutting off an engine for tumor development.

A large amount of research has proven that monocyte chemotactic protein-1 (MCP-1) is associated with different types of disease, including autoimmune, metabolic and cardiovascular diseases. In addition, several studies have found that MCP-1 is associated with tumor development. MCP-1 expression level in the tumor microenvironment is associated with tumor development, including in tumor invasion and metastasis, angiogenesis, and immune cell infiltration. However, the precise mechanism involved is currently being investigated. MCP-1 exerts its effects mainly via the MCP-1/C-C motif chemokine receptor 2 axis and leads to the activation of classical signaling pathways, such as PI3K/Akt/mTOR, ERK/GSK-3ß/Snail, c-Raf/MEK/ERK and MAPK in different cells. The specific mechanism is still under debate; however, target therapy utilizing MCP-1 as a neutralizing antibody has been found to have a detrimental effect on tumor development. The aim of the present review was to examine the effect of MCP-1 on tumor development from several aspects, including its structure, its involvement in signaling pathways, the participating cells, and the therapeutic agents targeting MCP-1. The improved understanding into the structure of MCP-1 and the mechanism of action may facilitate new and practical therapeutic agents to achieve maximum performance in the treatment of patients with cancer.