GSE211223
CD45+ and CD45- cells of benign v/s metastatic mouse breast tumors
Metastasis remains a leading cause of all cancer related mortalities and therapeutic challenges.   To successfully establish tumors and metastasiz, cancer cells must escape recognition and elimination by modulating immune cells during surveillance. Therapies that  mount anti-tumor response of the adaptive immune system and target the immune evasion mechanisms have entered the clinic. However, the number of patients that respond to these therapies remains humble. This is likely due to the pro-tumor and immunosuppressive mechanisms of innate immune system that remain elusive. Tumor immune cells demonstrate tremendous intra- and inter-tumoral heterogeneity. Presence of high neutrophil to lymphocyte ratio is typically associated with high risk of metastasis and poor patient outcome, which suggests that immune cells, specifically myeloid cells of metastatic tumors have distinct biological functions. We aim to identify these distinct biological functions and the candidates that may have prognostic and therapeutic potential using a non-metastatic and metastatic tumor from the 4T1 mouse breast cancer model. Overall design: 67NR (non-metastatic) and 66cl4 (metastatic) tumors of the immunocpmpetent 4T1 mouse breast cancer model were indiced in mice by orthotopic injections. After development of tumors, they were resected and dissociated to form single cell suspension. The cells were sorted  based on CD45 expression into immune (CD45+) and non-immune (CD45-) cells. RNA was extracted from the sorted cell populations and transcriptome sequencing of immune and non-immune cells from both the tumors was done to understand the distinct biological functions associated with each subset. contributor: Genomic Core Facility