Welcome to the Faubert Lab
Metabolism is at the core of nearly every biological function. Alterations of metabolic flux are a defining characteristic of cancer, as it supports cancer cell growth and survival.
Our lab seeks to understand how metabolic rewiring in cancer contributes to disease progression.
The lab utilizes mass spectrometry-based platforms, isotope tracers, and flux analysis to dissect the metabolic programs that underlie key malignant features.
Ultimately, we aim to use our findings for clinical benefit, including new therapeutic strategies, imaging techniques, and biomarkers.
Research Focus
Interrogating the metabolism of metastatic cancer
- Investigating Non-Small Cell Lung Cancer
- Studying Metabolism with Isotope Tracing
- Metabolic Alterations Support Metastasis
Non-small cell lung cancer (NSCLC) causes the most cancer-related deaths worldwide. One reason for this lethality is the ability of these tumors to metastasize, as almost half of all patients with NSCLC will develop metastatic disease. By investigating the underlying biology that drives, supports, or prevents metastasis, we aim to identify new treatment opportunities.
Our knowledge of lung cancer metabolism has progressed in recent years. We now understand how heterogeneous and dynamic lung cancer metabolism can be, and our laboratory is interested in how altered metabolism supports lung cancer metastasis.
Cancer cells are remarkably adaptable. While some metabolic processes are maintained in any environment, other pathways are significantly changed based on the media, neighboring cells, or organ environment.
Understanding how cancer cells adapt to these different environments, particularly in the context of metastasis, is a central focus of the lab.
We use stable isotope tracers to study the metabolic activity in cells, animal models, and patients. Stable isotope tracers are safe, non-radioactive, and can be used at physiological concentrations. By following these tracers through metabolic pathways, we gain important insights into the metabolic activity of cancer.
If we target these differences therapeutically, can we limit metastasis?
Not all tumors metastasize. So, what makes aggressive tumors different?
One contributing factor is the underlying metabolic differences between aggressive and non-aggressive tumors. To study this, the lab utilizes unique, patient-derived lung cancer xenografts to study metastasis. These PDXs match the metabolic phenotype of the primary tumor and spontaneously metastasize in mice, providing a tractable model to evaluate the role of metabolism in promoting and driving metastatic features.
If we target these metabolic differences therapeutically, can we limit metastasis?