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1.
Int J Oncol ; 62(6)2023 06.
Artículo en Inglés | MEDLINE | ID: mdl-37114561

RESUMEN

Malignant tumors seriously endanger human health and life, and restrict economic development. Human leukocyte antigen (HLA) is the expression product of the human major histocompatibility complex, which, at present, is the most complex known polymorphic system. The polymorphism and expression of HLA molecules have been demonstrated to be associated with the occurrence and development of tumors. HLA molecules can regulate the proliferation of tumor cells and inhibit antitumor immunity. In the present review, the structure and function of HLA molecules, the polymorphism and expression of HLA in tumor tissue, the roles of HLA in tumor cells and tumor immunity, and the potential clinical application of HLA in tumor immunotherapy are summarized. The overall aim of the present review is to provide relevant information for the development of antitumor immunotherapies involving HLA in the clinic.


Asunto(s)
Antígenos de Histocompatibilidad Clase I , Neoplasias , Humanos , Antígenos de Histocompatibilidad Clase I/genética , Antígenos HLA/genética , Neoplasias/genética , Neoplasias/terapia , Antígenos de Histocompatibilidad Clase II , Inmunoterapia
2.
Stem Cell Rev Rep ; 15(1): 23-34, 2019 02.
Artículo en Inglés | MEDLINE | ID: mdl-30430389

RESUMEN

CD133 is a wildly used cancer stem cell marker. The purpose of this study was to explore the significance of CD133 mRNA in human cancers mainly based on The Cancer Genome Atlas (TCGA) database. Bioinformatic analyses were done by using public repositories, including BioGPS, SAGE Genie tools, Oncomine analysis, Regulome Explorer, COSMIC analysis, and Kaplan-Meier Plotter. The main findings in this study were: 1) High CD133 mRNA was correlated with a benign survival rate of gastric cancer and lung cancer; 2) Transmembrane protein 125 (TMEM125) in bladder urothelial carcinoma and intercellular adhesion molecule 2 (ICAM2) in ovarian serous cystadenocarcinoma were closely related to CD133 expression; 3) The location and the topological structure of CD133 protein were not determined by its transcript variant in cancer cells; 4) CD38 and CD200 may be used as novel surface markers for solid cancers. However, the mechanism of these findings is not completely clear, further studies have to be performed in the future.


Asunto(s)
Antígeno AC133/genética , Minería de Datos , Neoplasias/genética , Antígeno AC133/metabolismo , Regulación Neoplásica de la Expresión Génica , Estudio de Asociación del Genoma Completo , Humanos , Mutación/genética , Pronóstico , ARN Mensajero/metabolismo , Análisis de Supervivencia
4.
Asian Pac J Cancer Prev ; 13(7): 3119-21, 2012.
Artículo en Inglés | MEDLINE | ID: mdl-22994720

RESUMEN

Non-small-cell lung cancer (NSCLC) is a leading cause of cancer deaths worldwide. Crizotinib has been approved by the U.S. Food and Drug Administration for the treatment of patients with advanced NSCLC. However, understanding of mechanisms of action is still limited. In our studies, we confirmed crizotinib-induced apoptosis in A549 lung cancer cells. In order to assess mechanisms, small molecular docking technology was used as a preliminary simulation of signaling pathways. Interesting, our results of experiments were consistent with the results of computer simulation. This indicates that small molecular docking technology should find wide use for its reliability and convenience.


Asunto(s)
Carcinoma de Pulmón de Células no Pequeñas/tratamiento farmacológico , Neoplasias Pulmonares/tratamiento farmacológico , Modelos Biológicos , Pirazoles/administración & dosificación , Piridinas/administración & dosificación , Transducción de Señal/efectos de los fármacos , Antineoplásicos/farmacología , Apoptosis/efectos de los fármacos , Sitios de Unión/efectos de los fármacos , Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Carcinoma de Pulmón de Células no Pequeñas/patología , Línea Celular Tumoral , Simulación por Computador , Crizotinib , Humanos , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patología , Modelos Moleculares , Fosforilación/efectos de los fármacos , Inhibidores de Proteínas Quinasas/farmacología , Reproducibilidad de los Resultados , Proteína smad3/metabolismo
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