Protagonismo del sistema inmune en el microambiente de los tumores malignos de la mama / Role of the immune system in the microenvironment of malignant tumors of breast

Los avances recientes en la comprensión de los mecanismos génicos y moleculares del cáncer de mama han revelado que el sistema inmune protagoniza los eventos responsables del desarrollo y la progresión del tumor. Las células de la respuesta inmune innata y adaptativa, así como diversos mediadores solubles liberados por ellas, pueden establecer una respuesta antitumoral protectora o, por el contrario, inducir eventos de inflamación crónica que favorezcan la promoción y progresión de esta enfermedad. Esta dualidad, se protagoniza en el microambiente del tumor, el cual puede regular la carcinogénesis en dependencia del infiltrado de células inmunes que predominen. Esta revisión, pretende resumir los conocimientos actuales de la relación sistema inmune-cáncer de mama, enfatizando en las células inmunes del microambiente del tumor y su importancia como biomarcadores de evolución clínica de la enfermedad(AU)

The recent advances in the understanding of the genetic and molecular mechanisms of breast cancer have demonstrated that immune system plays important events responsible for the development and progression of the tumor. The cells of the innate and adaptive immune system, as well as diverse soluble mediators, may establish a protective anti-tumor response or, on the contrary, to induce events of chronic inflammation that favor promotion and progression of disease. This duality occurs in the tumor microenvironment, which can regulate the carcinogenesis depending on the predominant immune cells. This revision summarizes the current knowledge of the relationship between immune system - breast cancer, emphasizing in the immune cells of the tumor microenvironment and its importance as biological markers of the clinical evolution of the disease(AU)

In Vivo Antitumor Activity of Metal Silver and Silver Nanoparticles in the L5178Y-R Murine Lymphoma Model.

Aims: To evaluate the antitumor potential of metal silver and polyvinilpyrrolidone nanoparticle-encapsulated silver on L5178Y-R murine lymphoma cell growth and survival of tumor-bearing mice. Study Design: In vitro and in vivo (pre-clinical) study. Place and Duration of Study: Universidad Autónoma de Nuevo León, Facultad de Ciencias Biológicas, Departamento de Microbiología e Inmunología, San Nicolás de los Garza, N.L., México, from January 2009 to December 2011. Methodology: Concentration-response cell viability assay was performed in vitro and mice survival studies were done using a L5178Y-R tumor-bearing mouse model. The PROBIT regression analysis was performed to determine the in vitro LC50. In vivo survival distributions were calculated by Kaplan-Meier and Cutler-Ederer analysis, and survival curves comparisons and hypothesis testing was done using the log-rank method. Results: Metal silver induced up to 100% L5178Y-R cells cytotoxicity, with an LC50 of 1.8 X 10-8 M, whereas silver nanoparticles caused up to 78% cytotoxicity, with an LC50 of 14.4 X 10-8 M. In addition, Intramuscular administration of metal silver and silver nanoparticles administered at the time of tumor injection significantly (P = .05) increased mice survival, where 70% and 60% of mice survived at day 35 respectively, as compared with such treatments administered 7 days after tumor induction (55% and 25% survival respectively); vincristine treatment caused 50% mice survival and tumor-bearing control mice had 20% survival. These results open further approaches on treating several types of cancer using free and nanoparticle-encapsulated silver-based therapies

Detection of a factor released by L5178Y lymphoblasts that inhibits mouse Macrophage-Activation induced by lipopolysaccharides

Background. Several factors inhibit cellular immune response by deactivating macrophages, but very few, such as those described here, prevent macrophage activation. Methods. Ascites liquid from 12-day-old BALB/c mice bearing 5178Y lymphoma tumors was collected, and cell-free ascites liquid (CFAL) was separated from lymphoblasts. The supernatant (SI) was obtained from the homogenized and centrifuged lymphoblasts Then, macrophage cultures contaning 0.2 X 10 a the sixth cells from lymphoma-bearing or hearthly mice were added to 10 µL of CFAL or S1, plus 5 µg of lipopolysaccharides (LPS)/mL, 40 U interferon-ç or a blend of both. Macrophages were incubated with CFAL or S1 prior to or after adding the activators to investigate whether any of the previously mentioned lymphoma fraction inhibited macrophage activation or whether they deactivated them. The effect of CFAL or S1 was estimated as the diminution of the amount of nitric ixide released by the experimental macrophage cultures with respect to controls (activated macrophages treated with none of the lymphoma fractions). Results. LPS, IFN-ç, and the LPS/ç blend activated macrophages from both lymphomabearing and healthy mice. None of the lymphoma fractions deactivated macrophages. CFAL, but not S1, inhibited the macrophage activation, i.e., the percentage of inhibition of nitric oxide releasing 76.7 percent in macrophages from healthy and lymphomabearing mice, respectively. In addition, CFAL was unable to inhibit macrophage-activation effect of IFN-ç or the LPS/IFN-ç blend. Conclusions. Mouse L5178Y Lymphoma releases a factor that in vitro inhibits the macrophage activation induced by LPS, but not by IFN-ç controls