Mus musculus
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ABSTRACT:
PROVIDER: PRJNA297042 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Tumor-Host Signaling Interaction Reveals a Systemic, Age-Dependent Splenic Immune Influence on Tumor Development
| PRJNA297040 | ENA
Project description:Tumor-Host Signaling Interaction Reveals a Systemic, Age-Dependent Splenic Immune Influence on Tumor Development [control mice]
| PRJNA297041 | ENA
Project description:The concept of age-dependent host control of cancer development raises the natural question of how these effects manifest across the host tissue/organ types with which a tumor interacts, one important component of which is the aging immune system. To investigate this, changes in the spleen, an immune nexus in the mouse, was examined for its age-dependent interactive influence on the carcinogenesis process. The model is the C57BL/6 male mice (adolescent, young adult, middle-aged, and old or 68, 143, 551 and 736 days old respectively) with and without a syngeneic murine tumor implant. Through global transcriptome analysis, immune-related functions were found to be key regulators in the spleen associated with tumor progression as a function of age with CD2, CD3, CCL19, and CCL5 being the key molecules involved. Surprisingly, other than CCL5, all key factors and immune-related functions were not active in spleens from non-tumor bearing old mice. Our findings of age-dependent tumor-spleen signaling interaction suggest the existence of a global role of the aging host in carcinogenesis. Suggested is a new avenue for therapeutic improvement that capitalizes on the pervasive role of host aging in dictating the course of this disease.
2015-10-12 | GSE73450 | GEO
Project description:The concept of age-dependent host control of cancer development raises the natural question of how these effects manifest across the host tissue/organ types with which a tumor interacts, one important component of which is the aging immune system. To investigate this, changes in the spleen, an immune nexus in the mouse, was examined for its age-dependent interactive influence on the carcinogenesis process. The model is the C57BL/6 male mice (adolescent, young adult, middle-aged, and old or 68, 143, 551 and 736 days old respectively) with and without a syngeneic murine tumor implant. Through global transcriptome analysis, immune-related functions were found to be key regulators in the spleen associated with tumor progression as a function of age with CD2, CD3, CCL19, and CCL5 being the key molecules involved. Surprisingly, other than CCL5, all key factors and immune-related functions were not active in spleens from non-tumor bearing old mice. Our findings of age-dependent tumor-spleen signaling interaction suggest the existence of a global role of the aging host in carcinogenesis. Suggested is a new avenue for therapeutic improvement that capitalizes on the pervasive role of host aging in dictating the course of this disease.
2015-10-12 | GSE73449 | GEO
Project description:Cachexia is a highly debilitating multifactorial syndrome affecting more than 50% of patients with advanced cancer. RAGE (receptor for advanced glycation end-products) signaling in mice sustains hallmarks of cancer cachexia (CC), including inflammation, the release of tumor-derived CC factors, and skeletal muscle catabolism. Indeed, mice lacking RAGE (Ager−/− mice) showed delayed loss of muscle mass and strength and dramatically increased survival. Here, we investigated the specific contribution to CC of RAGE expressed at tumor and muscle level by using: i) WT and Ager−/− mice subcutaneously injected with LLC (Lewis lung carcinoma) cell clones stably transfected with full-length (fl) RAGE, RAGEΔcyto (a non-transducing form of RAGE) or empty vector; and, ii) a newly generated tamoxifen-inducible conditional AgermKO mouse model, in which the RAGE gene is selectively deleted in skeletal muscles, injected with LLC cells. We found that: i) modulation of RAGE expression in LLC clones did not alter their cachectic potential; ii) Ager−/− mice did not activate muscle catabolism irrespective of the injected LLC clone, suggesting that RAGE overexpression in the tumor is not sufficient per se to induce muscle atrophy; and, iii) LLC-injected AgermKO mice showed increased survival, maintenance of muscle performance, resistance to the loss of body, muscle mass and performance, and reduced circulating CC factors compared with LLC-bearing control (Agerflox) mice. An increase in hybrid myofibers expressing both slow and fast MyHC isoforms characterized muscles of LLC-AgermKO . Different and unexpected proteomic signatures were found in muscles of tumor-bearing mice in dependence on RAGE expression and thirty-five proteins emerged as modulated in common in LLC/AgermKO and LLC/Ager–/– vs LLC/Agerflox mice suggesting novel mechanisms involved in the resistance against CC. Thus, RAGE engagement at myofiber rather than tumor level is a determinant in sustaining CC. Nevertheless, total ablation of the receptor maximally protects against cancer-induced muscle wasting, indicating that systemic targeting of RAGE might represent a promising strategy to counteract the cachexia syndrome in cancer patients.
2026-05-04 | PXD060768 | Pride
Project description:To determine the influence of primary tumors on pre-metastatic lungs, we have employed whole genome microarray expression profiling as a discovery platform to identify gene signatures of alveolar type II epithelial cells (AT-II) in TLR3 deficient mice (Tlr3-/-) and wide-type (WT) littermates with tumor bearing. We subcutaneously inoculated Tlr3-/- and WT mice with Lewis lung carcinoma (LLC). Two weeks later, lung tissues from Tlr3-/- and WT mice were dissociated and AT-II cells were sorted. AT-II cells from mice without tumor bearing were set as controls. Primary tumor induced gene expression in AT-II cells from Tlr3-/- and WT mice was measured at 2 weeks after tumor inoculation subcutaneously. AT-II cells from mice without tumor bearing were set as controls.
2016-08-10 | E-GEOD-76397 | biostudies-arrayexpress
Project description:Age plays a crucial role in the interplay between tumor and host; with further perturbations induced by irradiation. Proton irradiation on tumors induces biological modulations including inhibition of angiogenic and immune factors critical to “hallmark” processes impacting tumor development, in addition to physical targeting advantages. These advantages have provided promising results for proton therapy in cancer. Additionally, protons have implications for carcinogenesis risk of space travel (due to the high proportion of high energy protons in space radiation). Through a systems biology approach, we investigated how host tissue (i.e. splenic tissue) of tumor-bearing mice is altered with age, with or without whole-body proton exposure. Transcriptome analysis was performed on splenic tissue from adolescent (68 day) versus old (736 day) C57BL/6 male mice injected with Lewis lung carcinoma cells with or without three fractionations of 0.5Gy (1GeV) proton irradiation. Global transcriptome analysis indicated that proton irradiation of adolescent hosts caused significant signaling changes within splenic tissues that support carcinogenesis within the mice, as compared to old subjects. Increases in cell cycling and immunosuppression in irradiated adolescent hosts with CDK2, MCM7, CD74, and RUVBL2 as the key players were involved in the regulatory changes in host environment response (i.e. spleen). These results suggest a significant biological component to proton irradiation, operative through host age, that would indicate a modulation of host’s ability to support carcinogenesis in adolescence and the bestowal of resistance to immunosuppression, carcinogenesis, and genetic perturbation by old age.
2015-06-22 | GSE67243 | GEO
Project description:To determine the influence of primary tumors on pre-metastatic lungs, we have employed whole genome microarray expression profiling as a discovery platform to identify gene signatures of alveolar type II epithelial cells (AT-II) in TLR3 deficient mice (Tlr3-/-) and wide-type (WT) littermates with tumor bearing. We subcutaneously inoculated Tlr3-/- and WT mice with Lewis lung carcinoma (LLC). Two weeks later, lung tissues from Tlr3-/- and WT mice were dissociated and AT-II cells were sorted. AT-II cells from mice without tumor bearing were set as controls.
2016-08-10 | GSE76397 | GEO
Project description:To investigate the interaction between lung alveolar macrophages and lung cancer cells in vivo, gene expression analysis was performed using orthotopic tumor bearing animal model with C57BL/6 mice and Lewis Lung Carcinoma (LLC) cells. CD45+, F4/80+, Siglec-F+ population was sorted as alveolar macrophage population with fluorescence-activated cell sorting (FACS) technique.
2022-11-23 | GSE193913 | GEO
Project description:The objective of this study is to compare transcriptional features in tumor-infiltrating (TI) regulatory T (Treg) cells with TI CD4+ conventional T (Tconv) cells, splenic Treg cells of tumor-bearing mice, splenic Tconv cells of tumor-bearing mice, splenic Treg cells of normal mice, or splenic Tconv cells of normal mice.
2019-09-30 | GSE120280 | GEO