Teresa Davoli, Ph.D.
Assistant Professor
Institute for Systems Genetics
NYU Langone Health
Seminar Information
The maintenance of a normal complement of the genome is a requirement for the success of multicellular organisms. Aneuploidy refers to the presence of an abnormal (lower or higher than euploid) number of chromosomes or chromosome arms. Although detrimental at the organismal level, aneuploidy is extremely frequent (~90%) in human tumors (Beroukhim et al., 2010). Despite the fact that aneuploidy is so frequent in cancer, little is known about whether and how aneuploidy contributes to tumorigenesis and how aneuploidy could be targeted for cancer therapy. What are the causes and consequences of aneuploidy in cancer? How does aneuploidy affect patients’ response to therapy, especially immunotherapy? How does aneuploidy impact the transcriptome, proteome and metabolism of cancer cells? These are among the main questions the Davoli Lab is interested in. For example, we conducted a combined analysis of point mutation and copy number data in primary human tumor samples and demonstrated that the distribution of cancer driver genes can predict the frequency of whole chromosome or chromosome arm aneuploidy across cancers (Davoli et al., 2013; Sack, Davoli et al. 2018). This suggests that the recurrent patterns of aneuploidy in cancer act as driver events during tumorigenesis. Furthermore, through an analysis of genomics and transcriptomic data from primary human tumors, we recently identified a negative association between the level of cancer aneuploidy and the extent of tumor immune infiltrate, especially of cytotoxic T cells (Davoli et al., 2017). Our ongoing research interest is to determine whether and how cancer aneuploidy regulates different aspects of cancer development and therapy response utilizing a combination of experimental and computational approaches. Lab website: www.davolilab.com.
Dr. Davoli obtained her Ph.D. in 2013 from The Rockefeller University working with Dr. Titia de Lange on studying how telomere dysfunction promotes aneuploidy during tumorigenesis. During her postdoctoral training, she worked with Dr. Stephen Elledge using genomics approaches to understand the consequences of cancer aneuploidy for tumor formation and for therapy response in cancer patients. In May 2018, Dr. Davoli started her lab at the Institute for Systems Genetics at NYU School of Medicine in New York. Her lab uses functional genetics and computational approaches to study the causes and consequences of genomic instability in cancer. Dr. Davoli has received the Weintraub Graduate Student award in 2013 and she was a Helen Hay Whitney Postdoctoral Scholar. Dr. Davoli was a V Foundation Scholar and was also awarded the Melanoma Research Alliance Young Investigator Award, the Breast Cancer Alliance Young Investigator Award.
Her lab focuses on dissecting the causes and consequences of chromosome gains and losses in solid tumors, including colorectal cancer, breast cancer and melanoma. Dr. Davoli recently found that tumors with a high level of aneuploidy tend to be immune cold and to be refractory to immunotherapy. Her long-term goals are to decipher how aneuploidy can be utilized as a biomarker for therapy response and as a potential target for novel cancer treatments that take advantage of synthetic lethalities associated with the aneuploid state.