| Grant number: | 18/10529-2 |
| Support type: | Regular Research Grants |
| Duration: | December 01, 2018 - February 28, 2021 |
| Field of knowledge: | Biological Sciences - Immunology - Cellular Immunology |
| Principal Investigator: | Ana Paula Campanelli |
| Grantee: | Ana Paula Campanelli |
| Home Institution: | Faculdade de Odontologia de Bauru (FOB). Universidade de São Paulo (USP). Bauru , SP, Brazil |
| Assoc. researchers: | Karen Angélica Cavassani |
Abstract
Inflammation is a component of the tumor microenvironment and represents the 7th hallmark of cancer. Although the evidence suggests that inflammation causes cancer, formal proof is still required. It will be important to define which cellular and molecular components are common to all cancer-promoting inflammatory responses, and which are specific to particular tissues and tumor types. The interplay between these pathways, their hierarchy, and whether they can be targeted for therapy remain largely to be determined. Inflammatory cells and molecules influence every characteristic of cancer development including the tumour cells' ability to metastasize. Tumor-associate Macrophages (TAMs) have been described as "obligate partners" for tumor-cell migration, invasion and metastasis. Several investigations have demonstrated that that macrophage depletion or absence of CFS-1 results in reduction of tumor progression and lower rates of metastasis. TAMs comprise most of the infiltrating cells associated with solid tumors, and their recruitment to and activation at tumor sites is largely regulated by tumor-derived signals including chemokines, cytokines, and endogenous signals. Since monocytes and macrophages and their phenotypic variants play crucial roles in the immune response against tumors, therefore, we aimed to evaluate the genome wide gene expression profile in monocytes from metastatic versus non-metastatic patients. (AU)