Breast cancer is the most frequent malignancy in women worldwide and is curable in ~70–80% of patients with early-stage, non-metastatic disease. Advanced breast cancer with distant organ metastases is considered incurable with currently available therapies. Vascular endothelial cell growth factor (VEGF) and VEGF receptor 2 (VEGFR2) are closely related to angiogenesis in Breast cancer. Main functions of VEGFR2 include increasing the expression of VEGF and inducing tumor angiogenesis. In addition, VEGF plays a role in promoting vascular endothelial cell division and angiogenesis through VEGFR2 and is also involved in promoting the aggressive growth of tumors. Previous research has revealed that genetic mutations and polymorphisms are closely related to disease susceptibility and can lead to different responses to environmental factors and drugs. Therefore, we conducted this meta-analysis to evaluate the association of rs2305948 with Breast cancer and to obtain a stronger conclusion. Many studies have reported a relationship between the vascular endothelial growth factor receptor 2 single nucleotide polymorphism (SNP) rs2305948 and Breast cancer, but their conclusions have been controversial. A meta-analysis was performed to assess the association between rs2305948 and Breast cancer susceptibility

Numerous studies have evaluated the association between the matrix metalloproteinase 9 (MMP-9) and prostate cancer (PCA) risk. However, these studies have yielded conflicting results. As one of the most widely investigated matrix metalloproteinases (MMPs), MMP-9 is a significant protease which plays vital roles in many biological processes. MMP-9 can cleave many extracellular matrix (ECM) proteins to regulate ECM remodelling. It can also cleave many plasma surface proteins to release them from the cell surface. MMP-9 has been widely found to relate to the pathology of cancers, including but not limited to invasion, metastasis and angiogenesis. Some recent research evaluated the value of MMP-9 as biomarkers to various specific cancers. Besides, recent research of MMP-9 biosensors discovered various novel MMP-9 biosensors to detect this enzyme. In our findings provide further evidence that the expression of MMP-9 contribute to PCA risk. MMP-9 protein overexpression was found in prostate cancers, low expression in any of the normal tissues or in benign prostatic tissue. MMP-9 is potentially an important prostate tumor marker. Such research could ultimately contribute to more personalized and effective treatment strategies for patients with prostate cancer.

Alzheimer's disease (AD) is marked by cognitive decline and involves complex pathophysiology, including neuroinflammation. Interleukin-18 (IL-18), a proinflammatory cytokine, is linked to AD's progression, with elevated levels found in patients. IL-18's role in neuroinflammation, including its production by microglia and effects on other immune cells, contributes to AD's pathology. This study explores the role of Interleukin-18 (IL-18) levels in the progression of Alzheimer's Disease (AD) using the Enzyme-Linked Immunosorbent Assay (ELISA) methodology. It investigates the complex pathophysiology of AD, highlighting the significance of neuroinflammation and the contribution of IL-18 as a proinflammatory cytokine in the disease's progression. The study employed ELISA to quantitatively measure IL-18 levels in 20 patient samples and 20 healthy control samples, providing insights into the correlation between IL-18 expression and AD severity. Results revealed a marked elevation of IL-18 in AD patients (59.38) compared to controls (14.38), underscoring the cytokine's potential role as a biomarker for AD progression and its involvement in the disease's inflammatory processes. These findings suggest that IL-18 could be a target for therapeutic intervention, offering new avenues for AD management and treatment.

Alzheimer’s disease (AD) is a devastating condition with no known effective treatment. AD is characterized by memory loss as well as impaired locomotor ability, reasoning, and judgment. Emerging evidence suggests that the innate immune response plays a major role in the pathogenesis of AD. In AD, the accumulation of β-amyloid (Aβ) in the brain perturbs physiological functions of the brain, including synaptic and neuronal dysfunction, microglial activation, and neuronal loss. Serum levels of soluble ST2 (sST2), a decoy receptor for interleukin (IL)-33, increase in patients with mild cognitive impairment, suggesting that impaired IL-33/ST2 signaling may contribute to the pathogenesis of AD. Therefore, we investigated the potential therapeutic role of IL-33 in AD. Our results demonstrate a potential therapeutic role for IL-33 in AD. The elevated levels of IL-33 in Alzheimer’s disease patients highlight a promising area of research that could have significant implications for the understanding and management of the disease.