BACKGROUND: Malignant ascites is one of the severe complications of hepatocellular carcinoma, which can be regarded as a unique tumor microenvironment of hepatocellular carcinoma. The identification of novel biomarkers in malignant ascites could be crucial to differentiate patients with hepatocellular carcinoma and cirrhotic ascites.
OBJECTIVE: The study aimed to distinguish the metabolomics of malignant ascites in patients with hepatocellular carcinoma from that of non-malignant ascites (cirrhotic ascites).
METHODS: Liquid chromatography-mass spectrometry was performed to analyze the differentially distributed biomarkers in patients with malignant ascites and hepatocellular carcinoma (n = 39), as well as in patients with cirrhotic ascites, which were taken as controls (n = 36).
RESULTS: A total of 20 differential metabolites associated with malignant ascites were identified, of which 8 metabolites were upregulated and 12 metabolites were downregulated (ratio < 0.5 or > 1.5, respectively). Moreover, pathway and enrichment analyses revealed nitrogen metabolism, urea cycle, phenylalanine, and tyrosine metabolism to be implicated in the formation of malignant ascites in patients with hepatocellular carcinoma.
CONCLUSIONS: Our results suggest that the key factors associated with pathways, such as arachidonic acid, phenylalanine, and glutamic acid pathways, are potential ascitic fluidbased biomarkers for differentiating hepatocellular carcinoma with cirrhosis ascites; the results also provide a clinical pathophysiological interpretation of biomarkers and metabolic pathways relevant to disease status.

BACKGROUND: Prolactinomas are the most common type of pituitary gland tumors that secrete overly prolactin. They account for approximately 60% of all hormone-secreting hypophysis tumors.
OBJECTIVE: This study aims to analyze gender differences in patients with prolactinomas who were operated on transsphenoidal surgery and conduct a single-center retrospective analysis of patient data.
METHODS: This study evaluated the medical records of 109 patients (61 females and 48 males) from 2009 to 2019 at Feofaniya Clinical Hospital of the State Administration of Affairs in Kyiv, Ukraine. The primary criterion for including patients was a Serum Prolactin (PRL) level of over 100 ng/ml and the presence of a pituitary adenoma (PA) as observed on MRI. Additionally, the histological examination needed to confirm the presence of Prolactin-Secreting Pituitary Adenomas (PSPAs) without plurihormonal activity through both microscopy and immunohistochemical (IHC) staining.
RESULTS: Significant differences in preoperative PRL levels were not observed. However, males had significantly larger tumor sizes and prevalence of macroadenomas. In male patients, the preoperative PLR levels showed a weak negative correlation with age (r=-0.304, p < 0.036) and a positive correlation with tumor size (r=0.555, p < 0.001) and cavernous sinus invasion (r=0.339, p < 0.018). In females, preoperative PRL was significantly associated only with tumor size and Knosp grade.
CONCLUSIONS: Prolactin-Secreting Pituitary Adenomas (PSPAs) are more common in women than men and are characterized by larger and more invasive tumors with high PRL levels at diagnosis. The PRL level and tumor size before surgery can predict early biochemical remission in both males and females with an accuracy of 58.3% and 68.8%, respectively.

BACKGROUND: Primary pulmonary meningioma (PPM) is an extremely rare primary tumor of the lung. The diagnosis should first exclude metastasis of central nervous system MPM by using imaging, and the final diagnosis depends mainly on the tissue pathology and immunohistochemical results. Malignant PPM is even rarer, and a clear pathological definition to distinguish between benign and malignant PPM is lacking.
METHODS: A 47-year-old woman was admitted to the hospital after a lung mass was found during a physical examination one month earlier. The imaging findings for this patient showed a large mass in the lower lobe of the left lung with bronchial invasion. A contrast-enhanced MRI of the brain was normal. Bronchoscopy shows a mass at the opening of the left lower basal branch, with mucosal infiltration, protrusion, and stenosis of the opening. The patient underwent radical left lung cancer surgery, and the pathology specimens stained with hematoxylin-eosin demonstrated tumor cells with the focal invasion of the bronchial cartilage. Immunohistochemical staining was positive for epithelial membrane antigen(EMA), somatostatin receptor 2 (SSTR2), progesterone receptor (PR), Ki-67 (5%-10%), CD34, and D2-40 and weakly positive for p53.The pathologic diagnosis was primary pulmonary meningioma (PPM). The tumor marker CA-125 had significantly increased in the 2 months after surgery.
CONCLUSIONS: Malignant PPM is rarer, and a clear pathological definition to distinguish between benign and malignant PPM is lacking. Potential cases should be comprehensively evaluated based on imaging, laboratory, and pathology results. A long-term regular follow-up will be required to rule out metastasis or recurrence of PPM.

Background: Ginsenoside, the main active constituent of traditional Chinese medicine Ginseng, has been shown to play an important role in the prevention and treatment of cancer. However, the literature as well as the antitumor mechanisms of ginsenosides has not yet been systematically studied. Methods: We screened all relevant literature on ginsenosides and tumors from Web of Science during 2001-2021 and analyzed the extracted terms of these publications by VOSviewer and CiteSpace. DAVID online tool was used to perform Gene Ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathways analysis of ginsenoside-related genes. Cytoscape and String software were used to construct the interaction networks of ginsenoside-related genes and corresponding proteins. Results: A total of 919 publications were included in the study. A total of 122 identified keywords were mainly divided into 3 clusters: \"pharmacological function research\", \"functional validation in animal models\" and \"anti-tumor efficacy and mechanism\". The keywords of \"oxidative stress\" had the strongest citation burst in the past 5 years. A total of 50 genes were identified as ginsenoside-related genes in tumors. They have the function of regulating gene expression and apoptosis, and they are closely related to signaling pathways in cancers. Ginsenoside-related genes form a complex interactional network, in which TP53 and IL-6 are centrally located. Conclusions: We explored and revealed research hotspots related to the ginsenosides and tumors. More precise anti-tumor mechanism research will be promising in the future. TP53 and IL-6 may be the key points to comprehending the anti-tumor mechanism of ginsenosides.

In recent years, dysregulation of the notch pathway has been associated with the development and progression of various cancers. Notch signaling is involved in several cellular processes, such as proliferation, differentiation, apoptosis, and angiogenesis, and its abnormal activation can lead to uncontrolled cell growth and tumorigenesis. In various human cancers, the Notch pathway has been shown to have both tumor-promoting and tumor-suppressive effects, depending on the context and stage of cancer development. Notch signaling has been implicated in tumor initiation, cancer cell proliferation, cell migration and maintenance of cancer stem cells in several human cancers, including leukemia, breast, pancreatic and lung cancer. Understanding the role of the Notch pathway in cancer development and progression may provide new opportunities for the development of potent targeted therapies for cancer treatment. Several drugs targeting the Notch pathway are currently in preclinical or clinical development and may hold promise for anticancer therapy in the future.

OBJECTIVE: We aimed to develop a prognostic model with stemness-correlated genes to evaluate prognosis and immunotherapy responsiveness in gastric cancer (GC).
BACKGROUND: Tumor stemness is related to intratumoral heterogeneity, immunosuppression, and anti-tumor resistance. We developed a prognostic model with stemness-correlated genes to evaluate prognosis and immunotherapy responsiveness in GC.
OBJECTIVE: We aimed to develop a prognostic model with stemness-correlated genes to evaluate prognosis and immunotherapy responsiveness in GC.
METHODS: We downloaded single-cell RNA sequencing (scRNA-seq) data of GC patients from the Gene-Expression Omnibus (GEO) database and screened GC stemness- related genes using CytoTRACE. We characterized the association of tumor stemness with immune checkpoint blockade (ICB) and immunity. Thereafter, a 9-stemness signature-based prognostic model was developed using weighted gene co-expression network analysis (WGCNA), univariate Cox regression analysis, and the least absolute shrinkage and selection operator (LASSO) regression analysis. The model predictive value was evaluated with a nomogram.
RESULTS: Early GC patients had significantly higher levels of stemness. The stemness score showed a negative relationship to tumor immune dysfunction and exclusion (TIDE) score and immune infiltration, especially T cells and B cells. A stemness-based signature based on 9 genes (ERCC6L, IQCC, NKAPD1, BLMH, SLC25A15, MRPL4, VPS35, SUMO3, and CINP) was constructed with good performance in prognosis prediction, and its robustness was validated in GSE26942 cohort. Additionally, nomogram and risk score exhibited the most powerful ability for prognosis prediction. High-risk patients exhibited a tendency to develop immune escape and low response to PD-L1 immunotherapy.
CONCLUSIONS: We developed a stemness-based gene signature for prognosis prediction with accuracy and reliability. This signature also helps clinical decision-making of immunotherapy for GC patients.

The theory of cancer stem cells is a breakthrough discovery that offers exciting possibilities for comprehending the biological behavior of tumors. More and more evidence suggests that retinoblastoma cancer stem cells promote tumor growth and are likely to be the origin of tumor formation, drug resistance, recurrence, and metastasis. At present, some progress has been made in the verification, biological behavior, and drug resistance mechanism of retinoblastoma cancer stem cells. This article aims to review the relevant research and explore future development direction.

BACKGROUND: Gefitinib, an Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor (EGFR-TKI), frequently causes side effects when used to treat non-small cell lung cancer.
OBJECTIVE: The purpose of this experiment was to investigate the side effect of gefitinib on the skin and colon of mice.
METHODS: Male Balb/c nu-nu nude mice aged 4-5 weeks were used as xenograft tumor models, and gefitinib at 150 mg/kg and 225 mg/kg was started at 9 days after the xenograft tumor grew out. The mice\'s weights and tumor volumes were tracked concurrently, and the mouse skin adverse reactions and diarrhea were observed during the treatment. The animal tissues were subjected to biochemical and pathological evaluations after 14 days.
RESULTS: Gefitinib effectively decreased the size and weight of transplanted tumors in nude mice, while also lowering body weight and raising indexes of the liver and spleen. Gefitinib could cause skin adverse reactions and diarrhea in mice. Further pathological investigation revealed tight junction- related markers in the mice\'s skin and colon to be reduced and macrophages and neutrophils to be increased after gefitinib treatment.
CONCLUSIONS: The findings imply that gefitinib has negative effects on the skin and colon. Gefitinib- induced skin and colon adverse reactions in mice have been successfully modeled in this study.

Pancreatic cancer is one of the highly malignant gastrointestinal tumors in humans, and patients suffer from cancer pain in the process of cancer. Most patients suffer from severe pain in the later stages of the disease. The latest studies have shown that the main cause of pain in patients with pancreatic cancer is neuroinflammation caused by tumor cells invading nerves and triggering neuropathic pain on this basis, which is believed to be the result of nerve invasion. Peripheral nerve invasion (PNI), defined as the presence of cancer cells along the nerve or in the epineurial, perineural, and endoneurial spaces of the nerve sheath, is a special way for cancer to spread to distant sites. However, due to limited clinical materials, the research on the mechanism of pancreatic cancer nerve invasion has not been carried out in depth. In addition, perineural invasion is considered to be one of the underlying causes of recurrence and metastasis after pancreatectomy and an independent predictor of prognosis. This article systematically reviewed the neural invasion of pancreatic cancer through bioinformatics analysis, clinical manifestations and literature reviews.

Flavonoids are classified into subclasses of polyphenols, a multipurpose category of natural compounds which comprises secondary metabolites extracted from vascular plants and are plentiful in the human diet. Although the details of flavonoid mechanisms are still not realized correctly, they are generally regarded as antimicrobial, anti-fungal, anti-inflammatory, anti-oxidative; anti-mutagenic; anti-neoplastic; anti-aging; anti-diabetic, cardio-protective, etc. The anti-cancer properties of flavonoids are evident in functions such as prevention of proliferation, metastasis, invasion, inflammation and activation of cell death. Tumors growth and enlargement expose cells to acidosis, hypoxia, and lack of nutrients which result in endoplasmic reticulum (ER) stress; it triggers the unfolded protein response (UPR), which reclaims homeostasis or activates autophagy. Steady stimulation of ER stress can switch autophagy to apoptosis. The connection between ER stress and cancer, in association with UPR, has been explained. The signals provided by UPR can activate or inhibit anti-apoptotic or apoptotic pathways depending on the period and grade of ER stress. In this review, we will peruse the link between flavonoids and their impact on the endoplasmic reticulum in association with cancer therapy.