Yanchu Li

Glioblastoma (GBM) is a highly aggressive malignancy with a poor prognosis. Despite advanced molecular characterization, the traditional tumor-centric model ignores the patient’s systemic body condition, which significantly influences disease progression and therapeutic outcomes. This review aims to elucidate the interactions between GBM and systemic comorbidities, focusing on metabolic, immune, and vascular networks. A key feature is activity-dependent gliomagenesis, in which neuronal firing via Neuroligin-3 (NLGN3) and glutamatergic signaling fuels tumor growth. This process confers a substantial cognitive reserve, thereby attenuating or masking early clinical manifestations via functional compensatory mechanisms; however, it may concomitantly promote rapid tumor proliferation. Overall, combined diabetes, glutamine-induced and hyperglycemia or dexamethasone-induced hyperglycemia may trigger tumor aggressive. The prothrombotic nature of GBM complicates the use of anti-angiogenic therapies. Thus, GBM and its comorbidities can be seen as metabolic-immune and vascular-cardiovascular cycles. Furthermore, chronic Hepatitis B (HBV) infection poses a unique risk of fatal reactivation during therapy in endemic regions, such as China. Consequently, real-world GBM management requires a shift from an isolated oncological to a patient-centric approach. Addressing systemic health disparities and the intrinsic interplay of comorbidities is essential to optimize treatment protocols and improve patient survival.

Background: Histiocytic sarcoma originates in various tissues, including the skin, lymph nodes, gastrointestinal tract, lungs, bone marrow, and central nervous system. Primary central nervous system histiocytic sarcoma (PCNSHS) is exceptionally rare, known for its aggressive behavior and poor prognosis. This report describes a case of PCNSHS in the cerebellum treated with surgery and radiotherapy.Case presentation: A 30-year-old woman presented with progressive dizziness and headache. Magnetic resonance imaging scans showed right cerebellar neoplastic lesions approximately 3.6 cm*3.0 cm with cerebral edema and fourth ventricle and brainstem compression. The patient underwent surgical debulking, and the pathological diagnosis was PCNSHS. Two months after the surgery, the patient underwent adjuvant radiotherapy at a dose of 60 Gy. No tumor progression has been observed during the one-year follow-up period.Conclusions: This case report provides an example of effective central nervous system control using resection and radiation therapy. A review of the literature confirms that surgery alone or combined concurrent or sequential treatment of radiotherapy and chemotherapy is often used; however, the best treatment plan remains unclear. Moreover, the prognosis is poor, with a median survival of six months. Thus, ongoing research aims to better understand the biology of histiocytic sarcomas and find more effective strategies.

Breast cancer is the most prevalent form of cancer in women. Despite significant advances in conventional treatment, additional safer complementary treatment options are needed. Recently, ozone therapy has been considered as a type of medical adjunctive treatment that could inhibit cancer cell survival and reduce chemoresistance. However, only a few studies have been conducted on its use in breast cancer, and the optimal dosage and time of administration are unknown. Currently, preclinical studies suggest that ozone alone or in combination with chemotherapy is an effective method for inhibiting breast cancer cell growth. However, rather than investigating the effects of ozone as an antitumor therapy, current clinical trials have generally assessed its effect as an adjunctive therapy for reducing chemotherapy-induced side effects, increasing oxygen tension, normalizing blood flow, restoring blood lymphocytes more rapidly, and reducing fatigue symptoms. In this article, the use of ozone as a medical adjunctive treatment for breast cancer and its role in integrative therapy are summarized and discussed.

High-grade gliomas (grades III and IV) are highly malignant and aggressive brain tumors that present significant treatment challenges. Despite advances in surgery, chemotherapy, and radiation therapy, the prognosis for patients with glioma remains poor, with a median overall survival (mOS) range of 9–12 months. Therefore, exploring new and effective therapeutic strategies to improve glioma prognosis is of utmost importance and ozone therapy is a viable option. Ozone therapy has been used in various cancers, such as colon, breast, and lung, yielding significant results in preclinical studies and clinical trials. Only a few studies have been conducted on gliomas. Furthermore, since the metabolism of brain cells involves aerobic glycolysis, ozone therapy may improve the oxygen condition and enhance glioma radiation treatment. However, understanding the correct ozone dosage and optimal time of administration remains challenging. Herein, we hypothesize that ozone therapy should be more effective in gliomas compared with other tumors. This study provides an overview of the use of ozone therapy in high-grade glioma, including mechanisms of action, preclinical data, and clinical evidence.

Aims: The transport of patients suspected of having COVID-19 requires careful consideration. Using paths selected at random and not accounting for person flow along the path are risk factors for infection spread. Intrahospital transportation (IHT) protocols and guidelines should be used to help reduce the risk of secondary virus transmission during transport. This study aimed to propose optimal IHT for patients with an infectious disease presenting in an out-patient area.Design: The map of a West China Hospital was used. We also used field investigation findings and simulated person flow to establish pathway length and transportation time. We identified three optimum pathways and estimated safety boundary marks, including a patient transportation border (PTB) and safety transportation border (STB). Finally, IHT, PTB, and STP formed a virtual transport pipeline (VTP) and a traceable IHT management system, which can generate a virtual isolation space.Results: The three pathways met efficiency, accessibility, and by-stander flow criteria. No facility characteristic modification was required.Conclusions: Using virtual models to identify pathways through out-patient hospital areas may help reduce the risk of infection spread.

Role of Estrogen Receptor-Positive/Negative Ratios in Regulating Breast Cancer: The alpha estrogen receptor (ERα) contributes to breast cancer progression and recent guidelines define ER positivity as 1 stained cells, and a few tumor tissues show no ERα expression at all or are at 100. Although ER and aromatase inhibitors are widely used to treat hormone receptor-positive (HR+) breast cancer, their effect on tumor activity at different ERα levels remains unclear. Therefore, we investigated the role of ERα+/ERα ratios in determining the ERα level. We used ERα stably transfected and wild-type MDA-MB-231 cells (MDA-MB-231^Trans−ER and MDA-MB-231^WT, respectively) as represented ER+ and ER cells, respectively, and MCF-7 cells were the positive control. MDA-MB-231^Trans−ER and MDA-MB-231^WT cells were mixed and cocultured at a ratio of 0, 20, 40, 70, and 100. Migration and invasion functions at different cell ratios were evaluated in vitro using the Transwell and scratch test. In a xenograft mouse model, the polarization of the tumor-associated (M2) macrophage and the expression of breast cancer gene 1 (BRCA1), human epidermal growth factor receptor 2 (HER2), vascular endothelial growth factor (VEGF), and tumor necrosis factor (TNF)-α were measured. The results showed that the cell invasion and migration were significantly higher at 40 and 70 than they were at other ratios. Additionally, in vivo, the 70 ERα+/ERα-ratio was a critical indicator of cell activity and cytokine expression. The highest M2 level and expression of VEGR, TNF-α, BRCA1, and HER2 were shown at a ratio of 70. Moreover, the effects of ERα were not linear in breast cancer, indicating that the ERα status requires continuous monitoring during long-term endocrine treatment. These results indicate that during HR+ breast cancer treatment, the ERα+/ERα ratio may be a useful predictor and should be evaluated further.

Background. Plant polyphenols, which contain phenolic acids such as chlorogenic acid (CGA), can be used for the treatment of gastrointestinal cancer and have gained increasing attention in recent years. In this study, we explored a novel CGA-containing herbal medicine named LAS^NB, which was extracted from Lonicera japonica Thunb., Agrimonia eupatoria L., and Scutellaria barbata D.Don. Methods. CGA in LAS^NB was analyzed using high-performance liquid chromatography (HPLC). The biological functions and molecular mechanisms of LAS^NB were investigated in colon cancer cell lines (HCT116, HCT15, and CT26), a normal colon cell line (NCM460), and a CT26 xenograft model. To assess safety, hematological toxicity and pathology of the liver, kidney, and lung were evaluated. Results. LAS^NB suppressed HCT116, HCT15, and CT26 colon cancer progression by inhibiting proliferation capacity, promoting cell apoptosis, and suppressing cell migration both in vitro and in vivo. Investigation into the underlying molecular mechanism indicated that LAS^NB suppressed the activation of receptor tyrosine kinase- (RTK-) MEK-ERK and NF-κB pathways. With regard to safety, slight interstitial vascular congestion in the lung was observed, but no severe pathological or hematological toxicity was detected. Conclusions. We found that LAS^NB suppressed the progression of colon cancer via the RTK-MEK-ERK and NF-κB pathways, with no severe toxicity observed. Therefore, LAS^NB has the potential to be used as a supplementary herbal medicine for the treatment of colon cancer.

Background: Triple-negative breast cancer (TNBC) is a type of highly invasive breast cancer with poor prognosis. Recently, massive data reveal that long non-coding RNAs (lncRNAs) play important roles in cancer progress. Recently, although the role of lncRNAs in breast cancer has been well documented, few focused on TNBC. In this study, we aimed to systematically identify functional lncRNAs and to explore its molecular mechanism on TNBC progress.Methods: The recurrence of lncRNAs and their target genes were validated with TNBC biopsies and cell lines. Total one hundred and thirteen TNBC biopsies, including nineteen patient-matched samples, were collected. The profile of TNBC-related lncRNAs and their target genes were characterized by RNA sequencing (RNA-seq) and bioinformatic analysis. Tumor specific lncRNAs, which also showed biological function correlated with TNBC, were identified as potential candidates; and the target genes, which regulated by the identified lncRNAs, were predicted by the analysis of expression correlation and chromosome colocalization. Cross bioinformatic validation was performed with TNBC independent datasets from the cancer genome atlas (TCGA). The biological functions and molecular mechanism were investigated in TNBC model cell lines by cell colony forming assay, flow cytometry assay, western-blot, RNA Fluorescence in situ Hybridization assay (RNA FISH) and chromatin immunoprecipitation-qPCR (ChIP-qPCR).Results: Abundant Lnc-BTG3-7:1, which targets gene C21ORF91, was specifically observed in TNBC biopsies and cell lines. Knockdown of Lnc-BTG3-7:1 or C21ORF91 strongly inhibited cell proliferation, promoted cell apoptosis and cell cycle G1-arrested. Meanwhile, investigation of molecular mechanism indicated that Lnc-BTG3-7:1, cooperated with transcription factor JUND, cis-regulated the transcription of C21ORF91 gene, and down-regulation of Lnc-BTG3-7:1/C21ORF91 suppressed GRB2-RAS-RAF-MEK-ERK and GRB2-PI3K-AKT-GSK3β-β-catenin pathways.Conclusions: In this study, we identified a TNBC specific lncRNA Lnc-BTG3-7:1, which sustained tumor progress. Up-regulation of Lnc-BTG3-7:1 promoted the transcription of oncogene C21ORF91 and activated PI3K-AKT-GSK3β-β-catenin and MAPK pathways. Taken together, our results not only identified a biomarker for diagnosis but also provided a potential therapeutic target against TNBC.

Purpose: To determine the M1 sub-staging in synchronous metastatic nasopharyngeal carcinoma (smNPC) and to examine the effect of nasopharyngeal-neck radiotherapy (RT) and local treatment of metastases on overall survival (OS) of smNPC patients. Patients and Methods: A total of 150 patients with smNPC were included. Metastatic characteristics associated with their potential prognostic significance were analyzed. Then, a stratification system of the M1 sub-staging in smNPC was provided according to metastatic features. Moreover, the OS of patients with or without nasopharyngeal-neck RT was compared by Log rank test. The OS of patients who received or did not receive local treatment of metastases was also analyzed. Results: We successfully divided the M1 stage into three sub-staging: M1a (a single site with a single lesion), M1b (a single site with multiple lesions), and M1c (multiple sites with multiple lesions). The median OS was 53.2, 25.8, and 18.9 months for M1a, M1b, and M1c, respectively (p < 0.001). Nasopharyngeal-neck RT plus systematic chemotherapy (CT) significantly improved OS compared to systematic CT (median OS, 34.0 vs 15.2 months, p = 0.002). However, incorporation of local treatment of metastases did not bring survival benefit to smNPC patients who received nasopharyngeal-neck RT plus systematic CT (median OS, 25.8 vs 35.1 months, p = 0.374). Conclusion: The sub-staging of the M1 stage in smNPC had promising prognostic value. Adding nasopharyngeal-neck RT on the basis of systematic CT markedly improved the survival of smNPC patients, while addition of local treatment of metastases to nasopharyngeal-neck RT plus systematic CT for smNPC needed further exploration.