Aim: Assessment of mast cells density expression in oral premalignant and malignant lesions by histochemical analysis.
Materials And Methods: The study used a total of 120 tissue blocks that were formalin-fixed and paraffin-embedded. These blocks consisted of 40 cases of oral squamous cell carcinoma (OSCC), 40 cases of oral epithelial dysplasia, and 40 cases of normal oral mucosa (NOM).
Results: In the current investigation, a comparison was made between toluidine blue stained sections of normal oral mucosa, oral epithelial dysplasia and OSCC. The resultant value was determined to be statistically insignificant in all three categories, namely, oral epithelial dysplasia, oral squamous cell carcinoma (OSCC), and normal oral mucosa. The resultant values, calculated using an unpaired -test, were shown to be extremely significant ( = 0.001).
Conclusion: Research indicates that mast cells could be a significant marker for increased angiogenesis, which in turn could be used to predict carcinogenesis, its progression, and the prognosis of malignant lesions.
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http://dx.doi.org/10.4103/jpbs.jpbs_920_24 | DOI Listing |
Endocr Metab Immune Disord Drug Targets
March 2025
Colorectal Surgery, Shanxi Province Cancer Hospital/Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences/Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan, 030000, China.
Aim: The purpose of this study was to identify molecular subtypes and hub genes in fibromyalgia [FM] based on immune-related genes [IRGs].
Background: FM is a chronic disease featuring widespread pain, and the immune system may be involved in the FM progression.
Objective: The objectives of this study are as follows: 1] To identify the molecular subtypes of FM based on IRGs.
J Neuroinflammation
March 2025
College of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan, 430061, China.
Chronic urticaria (CU) arises from a multifaceted interplay of immunological, neurological, and psychological components. Immune dysregulation, mediated through both immunoglobulin E (IgE)-dependent and IgE-independent pathways, plays a pivotal role in CU pathogenesis, involving key effector cells such as mast cells (MCs), basophils, and eosinophils. This dysregulation culminates in the release of histamine, prostaglandins, and other mediators, which precipitate pruritus.
View Article and Find Full Text PDFBMC Pharmacol Toxicol
March 2025
Department of Cardiology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, 121000, China.
Objective: The aim of this study was to investigate AMD1 cardiotoxicity function for Maduramicin (Mad).
Methods: SD rats were divided into control (Control) group and Mad treatment (3.5 mg/kg) group (Mad).
Cancer Cell
March 2025
Massachusetts General Hospital Cancer Center, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA; Ludwig Center at Harvard, Boston, MA 02115, USA. Electronic address:
In this issue of Cancer Cell, Zhang et al. use single-cell RNA sequencing to compare immune cell dynamics in triple-negative breast cancers treated with the PD-L1 inhibitor atezolizumab plus paclitaxel or nab-paclitaxel. They identify distinct T cell activation patterns and highlight mast cells' role in immune activation exclusively in the nab-paclitaxel combination.
View Article and Find Full Text PDFNat Commun
March 2025
Department of Gastroenterology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Overcoming immunosuppression in the tumor microenvironment (TME) is crucial for developing novel cancer immunotherapies. Here, we report that IL-16 administration enhances the polarization of T helper 1 (Th1) cells by inhibiting glutamine catabolism through the downregulation of glutaminase in CD4 T cells and increases the production of Th1 effector cytokine IFN-γ, thus improving anti-tumor immune responses. Moreover, we find that establishing an IL-16-dependent, Th1-dominant TME relies on mast cell-produced histamine and results in the increased expression of the CXCR3 ligands in tumor-associated macrophages (TAM), thereby improving the therapeutic effectiveness of immune checkpoint blockade (ICB).
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