Cancer stem cells (CSC) are a subpopulation of cells residing within a tumor that are hypothesized to be responsible for tumor initiation, metastasis, and recurrence. These cells have stem-cell-like characteristics including the capability to self-renew, be in a quiescent state, and be capable of long-term clonal repopulation. Increased stress, hypoxia and inflammation have been demonstrated to induce a plastic phenotype for CSCs, allowing for either tumor growth or tumor escape. Increasing data has suggested that inflammation induces a pluripotent and aggressive CSC population, yet the mechanism of how inflammation can direct plasticity is not fully understood. In addition, obesity within the United States has reached epidemic proportions and is associated with more than nine types of cancers. The obese environment is characterized as participating in a chronic, low-level, pro-inflammatory state that is self-perpetuating, yet how the obese microenvironment affects CSC plasticity and tumor progression is unknown. Therefore, the purpose of this study is to investigate the mechanism of how obesity induced inflammation can impact the CSC population, and the association between increased adiposity and aggressive cancer phenotypes. This study will allow for an enhanced mechanistic understanding of the CSC phenotype within obesity and may lead towards the development of novel anti-cancer immunotherapies.