Research

Despite aggressive clinical treatments which include surgical resection, radiation, and chemotherapy, tumor recurrence is essentially universal in cancer patients, which is due, at least in part, to tumor cell heterogeneity. One of the currently prevailing models explaining intratumoral heterogeneity is the Cancer Stem Cell (CSC) hypothesis (Figure 1). According to this model, cancer stem cells (CSCs) represent a subset of a heterogeneous cancer population that possess characteristics associated with normal stem cells, specifically the ability to give rise to all cancer cell types found in a particular cancer sample. CSCs may generate tumors through the stem cell processes of self-renewal and differentiation into multiple non-tumorigenic cell types. Convincing evidence indicates that CSCs are inefficiently eliminated by current therapeutic treatments and suggests that CSC persistence could be responsible for disease maintenance and/or recurrence. Developing therapeutic interventions that specifically target CSCs, an appealing strategy for improving cancer treatment, requires an understanding of how CSCs escape normal regulatory mechanisms and become malignant. Our laboratory is utilizing combined molecular, biochemical, genomic and proteomic approaches to dissect signaling pathways in breast cancer stem cells. Interdisciplinary collaborations are established to leverage other expertise in nanotechnology and mathematical modeling to assist understanding the behaviors of CSCs both in vitro and in vivo and develop novel CSC-targeted therapies.

Publications

Hexin Chen - Bibliography