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1.
Arch Esp Urol ; 77(3): 229-234, 2024 Apr.
Article in English | MEDLINE | ID: mdl-38715162

ABSTRACT

BACKGROUND: This work aimed to investigate the potential role of abnormal lipid metabolism in the development of prostate cancer (PCa). METHODS: A retrospective study design was used. The clinical data of 520 patients who underwent rectal prostate biopsy in our hospital from January 2020 to June 2023 were analysed. The patients were enrolled and divided into the anterior PCa group including 112 patients and benign prostatic hyperplasia (BPH) group including 408 patients. Univariate and multivariate logistic regression analyses were performed for the two patient groups, and further comparisons were made according to the Gleason score and TNM staging. RESULTS: Low-density lipoprotein cholesterol (LDL-C) level may be an independent risk factor for PCa, and it was significantly associated with the risk of PCa (odds ratio (OR) = 1.363, p = 0.030). Patients with PCa were further divided into the low risk group and the high risk group according to the Gleason score. Univariate analysis (p = 0.047) and logistic regression analysis (OR = 2.249, p = 0.036) revealed that LDL-C was a significant factor influencing the Gleason score. Patients with PCa were categorised into four groups based on TNM staging. One-way analysis of variance (ANOVA) analysis (p = 0.015) and ordinal logistic regression analysis (OR = 2.414, p = 0.007) demonstrated that LDL-C was a significant factor influencing TNM staging. CONCLUSIONS: This study revealed the important role of LDL-C in the development of PCa, highlighting its influence as an independent risk factor. Thus, LDL-C may promote the proliferation and invasion of PCa cells.


Subject(s)
Cholesterol, LDL , Prostatic Neoplasms , Humans , Male , Retrospective Studies , Prostatic Neoplasms/blood , Prostatic Neoplasms/pathology , Aged , Cholesterol, LDL/blood , Middle Aged , Risk Factors , Neoplasm Grading , Neoplasm Staging
2.
Onco Targets Ther ; 14: 3051-3062, 2021.
Article in English | MEDLINE | ID: mdl-33994797

ABSTRACT

INTRODUCTION: Programmed cell death 1 ligand 1 (PD-L1) can be upregulated in cancer cells via interferon gamma (IFNγ) in the tumor microenvironment. IFNγ/PD-L1 signaling is associated with the response to immune checkpoint blockade in melanoma patients. Our previous investigation indicated that the microsatellite instability-high (MSI-H) cell line might exhibit selective hyperresponsiveness to IFNγ treatment, which contributes to increased PD-L1 expression and may be a mechanism of response to anti-PD-1 therapy in colorectal cancer. METHODS: The present study evaluated the expression of PD-L1 in a set of MSI and microsatellite stability (MSS) cell lines with IFNγ treatment. The differential signaling molecules associated with signal transducer and activator of transcription (STAT) contributing to hyperresponsiveness to IFNγ exposure were also investigated. Furthermore, we established a coculture assay containing CT26 cells with higher expression of PD-L1 and peripheral blood mononuclear cells (PBMCs) in vitro. Changes in cancer cell viability as well as apoptosis status in response to anti-PD-1 therapy were demonstrated. We further observed changes in the percentage of CD4+ and CD8+ lymphocytes after PD-1 immunotherapy in the coculture assay. Finally, the average extent of inflammation and adaptive immunity factors in the assay was also investigated. RESULTS: This in vitro study revealed that the MSI cell line might exhibit hyperresponsiveness to IFNγ exposure, and IFNγ induced upregulation of PD-L1 mainly through increased STAT1 and decreased STAT3 signaling. IFNγ/PD-L1 signaling participated in the response to anti-PD-1 therapy mainly through the CTL profile. DISCUSSION: Our findings reinforce previous knowledge of the fact that the response to immune checkpoint blockade occurs mainly in patients with a preexisting intratumoral IFNγ/PD-L1 signal, thus suggesting potential therapeutic strategies to enhance responsiveness to PD-1 blockade immunotherapy in most patients with colorectal cancer.

3.
ACS Appl Mater Interfaces ; 12(31): 35259-35265, 2020 Aug 05.
Article in English | MEDLINE | ID: mdl-32640154

ABSTRACT

A new discovery of highly hierarchical fibrillar biogenic silica with mesoporous structure derived from the perennial plant Equisetum fluviatile was made. By removing the organic compounds through chemical and heat treatment, the biogenic silica skeleton can largely retained the original highly hierarchical structure of the plant stems. Infrared spectra, X-ray diffraction, and small-angle X-ray scattering, as well as nitrogen sorption analysis, were employed to characterize the crystalline phases, nanostructure, and porosity of the resulting material. Scanning electron microscopy and transmission electron microscopy investigation reveal that the biogenic silica are fibers with diameters of about 120-150 µm and lengths of more than a few centimeters. These fibers consist of smaller fasciculus with diameters of about 5-15 µm that are composed of three levels of particles with mass and surface fractal characteristics: primary particles on the order of 3-5 nm, secondary particles on the order of 9-12 nm, and tertiary particles on the order of 90-120 nm in size. It is also shown that the biogenic silica have mesoporous structure with an average pore size of 4-6 nm and a specific surface of 100-300 m2/g. Heat treatment at high temperature and residual K+ significantly affects the characteristics of the mesoporous structure of the biogenic silica, although it has little effect on the surface fractal structure of the secondary particles.


Subject(s)
Equisetum/chemistry , Silicon Dioxide/chemistry , Particle Size , Porosity , Surface Properties
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