"I attended a retreat held for patients, survivors and families affected by brain cancer and attended several open sessions for physicians and patients. More often than not, the answer to questions about causes, cures, diagnoses, and prognoses for brain cancer sufferers was, 'I don't know.' At the conclusion of the retreat, I left with a firm resolve to apply myself at the bench to address those questions and provide the answers to the people so supportive of my post-doctoral research."

- Dr. Anna M. Kenney

View CV

Academic Appointment

  • Associate Professor in the Department of Pediatrics (Oncology) at Emory School of Medicine, since 1/2013

Administrative Appointment

  • Director, Pediatric Neuro-Oncology Basic Research Program at Children's Healthcare of Atlanta, Egleston

About DSA-Funded Research

Cell Cycle Regulation in Central Nervous System Progenitor Cells by Sonic Hedgehog Signaling and N-myc

Future effective brain cancer treatments will be those that target molecules specifically affecting tumor growth, thereby avoiding all the devastating side effects of current treatments such as surgery, radiation and chemotherapy. To identify growth regulators that could be attacked by anti-tumor strategies, we must understand how cell division occurs in cells that give rise to brain tumors. In adults, neural stem cells have been identified as a source of brain tumors. The childhood brain tumor medulloblastoma develops from immature cells in the cerebellum, the part of the brain coordinating movement. A protein called "Sonic hedgehog" (Shh) is involved in proliferation of neural stem cells and developing cerebellar neurons. Shh turns on a gene called N-myc, which regulates other genes further downstream in the process of cell growth and division. N-myc is implicated in many human cancers, including gliomas, neuroblastomas, and medulloblastomas. My research will address the causes and consequences of N-myc activity in neural stem cells and immature cerebellar neurons. First, I will determine how growth-regulating molecules control the amount of N-myc protein in these cells. Next, I will produce mice with mutations affecting the amount of N-myc protein, to test the idea that increased N-myc protein contributes to abnormal development and consequently, brain tumors. Finally, I will investigate the way chromosomal structure itself determines which genes N-myc activates in dividing immature brain cells. My goal is to identify proteins that may be targets for anti-tumor drug design, and to develop mice to use for modeling childhood and adult brain cancers.


"Anna is outstanding...Her work has yielded important insights...She possesses the qualities of dedication and innovative thinking we look for in an academic, and I anticipate that she will be a leader in [this] new field."

David H. Rowitch, M.D., Ph.D.
Dana-Farber Cancer Research Institute, Boston

"As a scientist, Anna displays a range of often mutually exclusive qualities that suggest a splendid future as an independent investigator. She is solid, yet creative and productive, yet careful...Within five years she will become a nationally known figure in brain cancer research."

C.D. Stiles, Ph.D.
Dana-Farber Cancer Research Institute, Boston

DSA Collaborations 

  • Although not directly related to the Sontag-funded project, several projects were completed with Michael Taylor.


Taylor Collaborations

  • Northcott PA*, Fernandez-L A*. Hagan JP*, Ellison DW, Grajkowska W, Gillespie Y, Grundy R, Van Meter T, Rutka JT, Croce CM#, Kenney AM#, Taylor MD#. (2009) The miR-17/92 polycistron is up-regulated in Sonic hedgehog-driven medulloblastomas and induced by N-myc in Sonic hedgehog-treated cerebellar neural precursors. Cancer Research 69: 3249-3255 PMC2836891

*co-first authors; #co-corresponding authors

  • Bhatia B, Northcott PA, Hambardzumyan D, Govindarajan B, Brat DJ, Arbiser JA, Holland EC, Taylor MD, Kenney AM. (2009) Tuberous sclerosis complex suppression in cerebellar development and medulloblastoma: separate regulation of mTOR activity and p27kip1 localization. Cancer Research 69: 7224-7234 PMC2745891
  • Fernandez-L A, Northcott PA, Dalton J, Fraga C, Ellison D, Taylor MD, Kenney AM. (2009) YAP1 is amplified and up-regulated in hedgehog-associated medulloblastomas and mediates Sonic hedgehog-driven neural precursor proliferation. Genes and Development, 23: 2675-2692. PMC2788333

*Nature Reviews Cancer Research Highlight: Nature Reviews Cancer 10, 6 (January 2010)

  • Fernandez-L A, Squatrito M, Northcott PA, Awan A, Holland EC, Taylor MD, Nahle Z, Kenney AM. (2011) Oncogenic YAP promotes radioresistance and genomic instability in medulloblastoma through IGF2-mediated Akt activation. Oncogene, 31: 1923-37. PMC3583298

Publications from original Sontag project

  • Kenney, AM*, Browd SR*, Gottfried, ON, Pedone, CA, Fults, DW. (2006) N-myc substitutes for IGF signaling in a mouse model of Sonic hedgehog-induced medulloblastoma formation. Cancer Research 66: 2666-2672. * equal contribution
  • Hatton BA, Knoepfler PS, Kenney AM, Rowitch DH, de Alboran IM, Olson JM, Eisenman RN. (2006) N-myc is an essential downstream effector of Sonic hedgehog signaling during both normal and neoplastic cerebellar growth. Cancer Research 66: 8655-61
  • CheslerL, Schlieve C, Goldenberg DD, Kenney A, Kim G, McMillan A, Matthay KK, Rowitch D, Weiss WA. (2006) Inhibition of phosphoinositol 3-kinase destabilizes MYCN protein and blocks malignant progression in neuroblastoma. Cancer Research 66: 8139-8146
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