Haigis looks to understand the role of mitochondria in human health. In particular, Haigis has studied how the enzymatic networks in the mitochondrion modulate a cell's metabolism. She joined the
Harvard Medical School in 2006. One of her first graduate students,
Lydia W. S. Finley, demonstrated that expression of genes critical to
glycolysis was boosted when SIRT3 decreased. The SIRT3 gene is the most depleted in tumor cells – it drives cancel cell proliferation, and mice lacking in SIRT3 result in mice spontaneously developing breast tumors. Haigis has demonstrated the role of mitochondrial
sirtuins (a protein family involved in the regulation of biological processes) in metabolism and disease. She revealed that ammonia, a metabolic waste product that is lethal to most biological tissue, was used to boost the growth of cancer cells. She has shown that damage to DNA (which can accelerate cancer) activates the SIRT4 gene, and mice lacking SIRT4 developed spontaneous lung tumors. Her lab also demonstrated that
prolyl-hydroxylase 3 (PHD3), a signaling enzyme, breaks down fats inside the mitochondrion, and is suppressed in a subset of cancers (including
acute myeloid leukemia). == Awards and honors ==