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La inmunoedición del cáncer es un proceso dinámico compuesto de tres fases: eliminación (EL), equilibrio (EQ) y escape (ES) que abarca las posibles funciones protectoras del huésped y de esculpir el tumor del sistema inmunitario durante el desarrollo del tumor. Los modelos animales son herramientas útiles para estudiar enfermedades como el cáncer. El presente estudio fue diseñado para caracterizar la interacción entre el adenocarcinoma mamario M-406 y CBi, CBi - y CBi / L líneas de ratones endogámic Cancer immunoediting is a dynamic process composed of three phases: elimination (EL), equilibrium (EQ) and escape (ES) that encompasses the potential host-protective and tumor-sculpting functions of the immune system throughout tumor development. Animal models are useful tools for studying diseases such as cancer. The present study was designed to characterize the interaction between mammary adenocarcinoma M-406 and CBi, CBi− and CBi/L inbred mice lines. Fil: Pagura, Lucas. Facultad de Ciencias Bioquímicas y Farmacéuticas. Universidad Nacional de Rosario; Rosario; Argentina Fil: Cáceres, Juan Manuel. Facultad de Ciencias Médicas. Universidad Nacional de Rosario; Rosario; Argentina Fil: Cardinali, Albertina. Facultad de Ciencias Médicas. Universidad Nacional de Rosario; Rosario; Argentina Fil: Scharovsky, Graciela Olga. Institute of Experimental Genetics. School of Medical Sciences. National University of Rosario; Rosario; Argentina Fil: Di Masso, Ricardo José. Facultad de Ciencias Médicas. Universidad Nacional de Rosario; Rosario; Argentina Fil: Zacarias-Fluck, Mariano. Preclinical Research. Vall d’Hebron Institute of Oncology (VHIO); Barcelona; Spain Fil: Rico, María José. Institute of Experimental Genetics. School of Medical Sciences. National University of Rosario; Rosario; Argentina Fil: Rozados, Viviana R. Institute of Experimental Genetics. School of Medical Sciences. National University of Rosario; Rosario; Argentina

Cancer immunoediting is a dynamic process composed of three phases: elimination (EL), equilibrium (EQ), and escape (ES), that encompasses the potential host-protective and tumor-sculpting functions of the immune system throughout tumor development. Inbred mice models provide an interesting tool for identifying genes that control susceptibility to breast cancer. Inbred CBi/L FS mice were artificially selected by body conformation from CBi mice. The M-406 mammary adenocarcinoma appeared spontaneously in CBi female mouse and it is maintained in vivo in mice of the same line. When CBi/L FS mice are s.c. challenged with M-406 they show the three phases: 51.6% in ES, 18.5% in EQ en 29.8% in EL. The aim of this study was to evaluate in CBi/L FS mice in the three phases of M-406 tumor growth: 1) the profile of cytokines Th1(IL-2; INF-γ); Th2(IL-4; IL-10) in serum and 2) the effect of conditioned media (CM) from CBi/L FS mononuclear cells on tumor cells proliferation. The serum and CM cytokines were evaluated by ELISA. CMs were obtained after 24h incubation of mononuclear cells from CBi/L FS seeded at 4x105 cells/well, in RPMI + 10% BFS. Tumor cells (5x104 cells/well) were incubated 24h with different CMs and proliferation evaluated (WST-1). In serum we observed the presence of high levels of INF-γ in the ES condition, compared with EQ and EL (p Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3552. doi:1538-7445.AM2012-3552

Breast cancer is a complex, multifactor disease that affects about 10% of women in industrialized countries. Inbred mice models provide an interesting tool for identifying genes that control susceptibility to breast cancer. CBi- mice was artificially selected for body conformation from CBi. The mammary adenocarcinoma M-406 developed spontaneously in CBi female mouse and is maintained in vivo in mice of the same line. When CBi- mice are s.c. challenged with M-406 they show 100% take and 100% regression (resistance). In contrast, the tumor grows exponentially (susceptibility) in CBi mice. The aim of this study was to characterize the tumor behavior in both F1 reciprocal hybrids [(CBi × CBi-) and (CBi- × CBi) n=48], and in the four F2 combinations between them: F2A [(CBi- × CBi) × (CBi- × CBi)]; F2B [(CBi- × CBi) × (CBi × CBi-)]; F2C [(CBi × CBi-) X (CBi- × CBi)] and F2D [(CBi × CBi-) X (CBi × CBi-)] n=185. Adult female and male mice where challenged s.c. with M-406 by trocar, three tumor fragments (∼8 × 105cells). Tumors were measured three times/week and tumor volumes were calculated as follows: V = 0.4 (ab2), where V = volume (mm3), a = largest diameter (mm) and b = smallest diameter (mm). Tumor volume vs time data were fit to an exponential growth model Vt: S*e[k*t]. M-406 grew exponentially in 45/48 F1 mice. Non statistical differences were found in tumor growth rates between sexes on the reciprocal F1s. Significant differences in tumor volume doubling time (TvDT = 0.69/k) were observed between sexes in two of the four F2 combinations: F2A [females: 5.34 ± 0.44; males: 4.27 ± 0.26; t=2.154, P=0.038] and F2D [females: 4.04 ± 0.14; males: 4.85 ± 0.38; t=1.804, P=0.041]. When comparing females TvDT, F2D had a faster growth rate than F2A (P=0.0097), while non statistical differences were evident in males (P = 0.102). It is concluded that susceptibility to M-406 in CBi mice is inherited as a dominant trait. Genes involved in susceptibility inheritance would be autosomic, as the tumor behaviour in both F1 reciprocal hybrids is similar. The analysis of F2 alternative combinations allowed the identification of maternal effect as well as sexual dimorphism influencing tumor growth. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2390. doi:10.1158/1538-7445.AM2011-2390