- Assistant Professor, Department of Pathology
The University of Chicago
Depts. Of Pathology and Pediatrics
Section of Heme/Onc.
900 East 57th Street
Chicago, IL 60637
Room KCBD 5128, 5th Fl.
Megan McNerney received her BA at Northwestern University and MD and PhD at the University of Chicago. As an Immunology PhD student in Vinay Kumar’s lab, she studied how natural killer cells eliminate tumor cells, and discovered a novel system of natural killer cell inhibition. She completed her postdoctoral work in Kevin White’s laboratory within the Institute of Genomics and Systems Biology at the University of Chicago, where she characterized the genetic abnormalities in high-risk myeloid neoplasm. Dr. McNerney is a Leukemia and Lymphoma Society Fellow and was named the 2013 Leukemia and Lymphoma Society, Illinois Chapter, Researcher of the Year. She is a recent recipient of the Cancer Research Foundation Young Investigator Award and Riviera Country Club United-4 A Cure Award. Other honors include the Robert W. Wissler Fellowship Award, the Leon O. Jacobson Basic Science Prize, the Robert E. Priest Pathology Merit Award, the Elaine Frank Family Fellowship for Medical Research, and the College of American Pathologists Resident Research Grant. Dr. McNerney’s lab focuses on the genomics and transcriptional regulation of high-risk myeloid neoplasms. Major efforts in the lab are to determine somatic changes in myeloid malignancies, understanding the cis-regulatory logic of haploinsufficient transcriptional regulation in hematopoiesis and leukemia, and leveraging this information to identify new therapies.
Myeloid Malignancy Genomics
Transcriptional Regulation in Hematopoiesis and Leukemogenesis
Dr. McNerney’s research focuses on the genomics of therapy-related and de novo acute myeloid leukemias (AML). A high-risk subset of patients is unresponsive to treatment and their survival is less than a year. Understanding the underlying genetic changes in these neoplasms is essential to identifying new therapeutic strategies for patients. Using next-generation sequencing and other genomic approaches, Dr. McNerney determined the genetic changes that occur in high-risk myeloid leukemias. She demonstrated that these leukemias have a distinct mutational profile. Half of high-risk myeloid neoplasms exhibit haploinsufficiency of the CUX1 transcription factor, a tumor suppressor gene on chromosome 7 (McNerney et al. 2013, Blood 121:869 link= http://www.ncbi.nlm.nih.gov/pubmed/23212519). In addition, mutations that activate the RAS signaling pathway occur at significantly higher frequency than other AMLs (McNerney et al. 2014, British Journal of Haematology, in press). Both of these somatic changes likely cooperate to drive leukemogenesis. Her laboratory is now leveraging this information to find new treatments for this disease, with the ultimate goal of improving patient survival. Current approaches include identifying the aberrant transcriptional networks downstream of CUX1 loss, using genome-wide approaches such as RNA-seq and ChIP-seq. Of particular interest is understanding the cis-regulatory logic that defines dose-sensitive CUX1 gene targets. In addition, her lab is developing a mouse model of high-risk myeloid leukemia for pre-clinical drug testing.
Genomic and Molecular Pathology
Hematopoietic Malignancy Genomics
Dr. McNerney is board-certified in Clinical Pathology and is an Attending in the Genomic and Molecular Pathology clinical diagnostic lab. Her clinical role is identifying cancer mutations to guide patient diagnosis and treatment decisions.
Positions for graduate students and postdocs are currently available. Please contact Megan McNerney (firstname.lastname@example.org).
Please take a moment to check out Megan McNerney's featured article: http://www.nature.com/nature/journal/v509/n7502_supp/full/509S66a.html
- Widespread genetic epistasis among cancer genes
- The CD2 family of NK cell receptors
- Targeted disruption of the 2B4 gene in mice reveals an in vivo role of 2B4 (CD244)
- Role of natural killer cell subsets in cardiac allograft rejection
- Requirement of homotypic NK cell interactions through 2B4(CD244)/CD48 in the generation of NK
- Regulatory defects in Cbl and Mitogen-Activated Protein Kinase (Extracellular Signal-Related Kinase)
- Oral cavity tumors in younger patients show a poor prognosis and do not contain viral RNA
- Nfkb1 is a haploinsufficient DNA damage-specific tumor suppressor
- NK cell subsets in allograft rejection and tolerance
- Genetic pathways leading to therapy-related myeloid neoplasms
- Dominant Role of Oncogene Dosage and Absence of Tumor Suppressor Activity in Nras-Driven Hematopoiet
- Development of warm auto- and alloantibodies in a three year-old boy
- Bionimbus: a cloud for managing, analyzing and sharing large genomics datasets
- An integrated genomic approach to the assessment and treatment of acute myeloid leukemia
- A new self: MHC class I independent NK cell self-tolerance
- 2B4 acts as a non-MHC binding inhibitory receptor on mouse NK cells
- 2B4 (CD244) – CD48 interactions provide a novel MHC class I-independent system
- 2B4 (CD244) is a non-MHC binding receptor with multiple functions on natural killer cells and CD8+ T