Peter D. Canoll, MD, PhD
- Professor of Pathology & Cell Biology at CUMC
- Director of Neuropathology
My research has focused on understanding the molecular and cellular mechanisms of gliomagenesis and, on interactions between glioma cells and the brain microenvironment. By targeting glial progenitor cells in the adult brain, my laboratory has developed genetically engineered mouse models that recapitulate the histological and molecular features of human glioma. We are applying a variety of cutting edge techniques to characterize cellular alterations that accumulate in these mouse models and in human glioma tissue. I serve as the director of neuropathology and as the primary neuropathologist on all clinical trials run by the Columbia Brain Tumor Program. Over the last 14 years I have analyzed and diagnosed hundreds of brain tumors. My over-arching goal is to apply my clinical and research experience to help bridge the analysis of laboratory experiments and human disease, and to advance the development of more informative diagnosis and more effective treatments for brain tumors.
Departments and Divisions
- Department of Pathology & Cell Biology
Division of Anatomic Pathology
- Anatomic Pathology
Areas of Expertise
Education & Training
- New York University School of Medicine
- Residency: NewYork-Presbyterian Hospital/Weill Cornell Medical Center
- Herbert Irving Comprehensive Cancer Center
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10/2016-present Professor of Pathology and Cell Biology, CUMC, New York, NY
07/2014-present Director of Neuropathology, CUMC, New York, NY
07/2011-09/2016 Associate Professor of Pathology and Cell Biology, CUMC, New York, NY
07/2006-06/2011 Assistant Professor of Pathology and Cell Biology, CUMC, New York, NY
07/2002-06/2006 Assistant Professor in Clinical Pathology, CUMC, New York, NY
07/2000-06/2002 Fellow in Neuropathology, Department of Pathology, New York Presbyterian Hospital/Columbia University, New York, NY
07/1998- 06/2000 Resident in Anatomic Pathology, Department of Pathology, New York Presbyterian Hospital/ Cornell Medical Center, New York, NY
Honors & Awards
1996 Merck Scholar
1998 Distinguished Performance in Research, Associated Medical Schools of New York
2000 Inspiration Award for Pediatric Brain Tumor Research, Children’s Brain Tumor Foundation
2001 Sontag Foundation Award, American Brain Tumor Association
2008 Teacher of the year award for outstanding small group preceptor
2009 Adult Translational Award, Society for Neuro-oncology
2015 Fundamentals outstanding teacher award
- Mechanisms of glioma growth and invasion
TARGETING MUTANT IDH1 FOR A NOVEL SYNTHETIC LETHAL INTERACTION IN MALIGNANT GLIOMAS (Federal Gov)
May 15 2018 - Feb 28 2023
SINGLE CELL ANALYSIS OF THE INFILTRATIVE MARGINS OF GLIOBLASTOMA AND POST-TREATMENT RECURRENCE (Federal Gov)
Jul 1 2017 - Jun 30 2022
MECHANISMS OF REGULATION OF PROGENITOR PROLIFERATION AND TRANSFORMATION (Federal Gov)
Sep 1 2017 - Aug 31 2021
DUAL INHIBITION OF MITOCHONDRIAL MATRIX CHAPERONES AND ANTI-APOPTOTIC BCL-2 FAMILY MEMBERS FOR GLIOBLASTOMA THERAPY. (Federal Gov)
Aug 1 2016 - Jul 31 2021
IDENTIFICATION AND MOLECULAR CHARACTERIZATION OF SOMATIC MUTATIONS IN MCD (Federal Gov)
Sep 30 2016 - Jun 30 2021
PLEXINB2 FUNCTION IN GLIOMA INVASION AND GLIOMA STEM CELL MAINTENANCE (Federal Gov)
Apr 1 2016 - Mar 31 2021
TARGETING TREATMENT-RESISTANT GLIOBLASTOMA CELLS WITH FERROPTOSIS INDUCING DRUGS (Private)
Jan 3 2019 - Dec 31 2020
CHRONIC CONVECTION ENHANCED DELIVERY (CED) OF TOPOTECAN FOR GLIOBLASTOMA (Federal Gov)
Jul 1 2012 - Nov 30 2019
DO SEIZURES STIMULATE GLIOMA PROGRESSION? (Federal Gov)
Aug 1 2017 - Jul 31 2019
DISCOVERY OF NOVEL MOLECULAR ABNORMALITIES UNDERLYING NON-LESIONAL FOCAL EPILEPSY (Federal Gov)
Sep 30 2014 - Jul 31 2019
CANCER CENTER SUPPORT GRANT (Federal Gov)
Jul 1 2014 - Jun 30 2019
FINE-SCALE MAPPING OF ELECTROPHYSIOLOGICAL AND CELLULAR ALTERATIONS IN A MOUSE MODEL OF TUMOR ASSOCIATED EPILEPSY (Private)
Jun 1 2018 - May 30 2019
EFFECTS OF CANNABIS ON NEURONAL TRANSLATION (Federal Gov)
Apr 1 2016 - Mar 31 2019
TARGETING KIF11 TO TREAT GLIOBLASTOMA INVASION AND PROLIFERATION (Federal Gov)
Jul 1 2017 - Jun 30 2018
MECHANISM OF REGULATION OF PROGENITOR PROLIFERATION AND TRANSFORMATION (Federal Gov)
Sep 15 2016 - Aug 31 2017
TARGETING THE MTOR PATHWAY IN GILOMA-ASSOCIATED EPILEPSY IN MICE AND HUMANS (Private)
Sep 1 2015 - Aug 31 2017
TARGETING KIF11 TO TREAT GLIOBLASTOMA INVASION AND PROLIFERATION (Federal Gov)
Sep 30 2016 - Jun 30 2017
GLIOMA INDUCED ALTERATIONS IN NEURONAL TRANSCRIPTION AND TRANSLATION (Federal Gov)
Sep 15 2014 - Aug 31 2016
MOLECULAR MOTORS AND GLIOMA DISPERSION (Federal Gov)
Sep 15 2012 - Aug 31 2016
THE ENDURES STUDY: ENVIRONMENTAL DYNAMICS UNDERLYING RESPONSIVE EXTREME SURVIVORS OF GLIOBLASTOMA (Private)
Jul 1 2015 - Jun 30 2016
BRAIN TUMOR ECOLOGY COLLABORATIVE (BTEC) (Private)
Jan 1 2013 - Dec 31 2015
PHASE II CLINICAL TRIAL OF PERIFOSINE + TEMSIROLIMUS FOR RECURRENT GLIOBLASTOMA WITH TISSUE AND IMAGING CORRELATES OF RESPONSE (Private)
Jan 1 2013 - Dec 31 2015
ENDURES: ENVIRONMENTAL DYNAMICS UNDERLYING RESPONSIVE EXTREME SURVIVORS OF GLIOBLASTOMA (Private)
Sep 1 2014 - Jun 11 2015
THE ROLE OF WHITE MATTER PROGENITORS IN GLIOMA FORMATION AND PROGRESSION (Federal Gov)
Sep 1 2009 - Jan 31 2015
PREDICTING AND CONTROLLING GLIOMA RECURRENCE: THE ROLE OF HETEROGENEITY AND MICROENVIRONMENT (Private)
Oct 22 2012 - May 31 2014
IDH1 AND IDH2 MUTATIONS AND ASSOCIATION WITH FORMATION OF GLIOMAS (Private)
Jul 1 2011 - Jun 30 2013
PREDICTING AND CONTROLLING GLIOMA RECURRENCE:THE ROLE OF HETEROGENEITY AND MICROENVIRONMENT (Private)
Jun 1 2011 - Oct 19 2012
MYOSIN II AND GLIOMA DISPERSION (Federal Gov)
Sep 1 2010 - Aug 31 2012
ABTA 2011 MEDICAL STUDENT SUMMER FELLOWSHIP PROGRAM (Private)
Jun 1 2011 - Jul 30 2012
DISCOVERY AND DEVELOPMENT OF A NOVEL GLIOBLASTOMA TREATMENT THAT SELECTIVELY REDUCES BMI-1 EXPRESSION IN TUMOUR STEM CEL (Private)
May 26 2010 - May 25 2012
1. Receptor Tyrosine Kinases And Phosphatases In Glial Proliferation And Differentiation: During my graduate studies at NYU, I worked with Jose Musacchio and Joesph Schlessinger to identify a new family of receptor tyrosine phosphatases that are selectively expressed in the brain. I used in situ hybridization to determine the cell-specific expression patterns of several of these genes and discovered that PTPRZ (aka RPTP-beta) is expressed in glial progenitors and undergoes alternative splicing during glial differentiation. I also worked with Jim Salzer (NYU) to characterize the role of receptor tyrosine kinases (ErbB 2, 3, and 4) in glial development, and showed that neuregulins (neuron derived ligands for ErbB receptors) can control the proliferation and differentiation of oligodendrocyte progenitor cells (OPCs).
a. Canoll, P.D., Barnea, G., Levy, J.B., Sap, J., Ehrlich, M., Silvennoinen, O., Schlessinger, J. and Musacchio, J.M. The expression of a novel receptor-type tyrosine phosphatase suggests a role in morphogenesis and plasticity of the nervous system. Brain Research Developmental Brain Research, 1993, 75:293-298.
b. Canoll, P.D., Petanceska, S., Schlessinger, J. and Musacchio, J.M. Three forms of RPTP-b are differentially expressed during gliogenesis in the developing rat brain and during glial cell differentiation in culture. Journal of Neuroscience Research, 1996, 44:199-215.
c. Canoll, P.D., Musacchio, J.M., Hardy, R., Reynolds, R., Marchionni, M.A. and Salzer, J.L. GGF/Neuregulin promotes the proliferation and survival and inhibits the differentiation of cells in the oligodendrocyte lineage. Neuron, 1996, 17: 229-243.
d. Canoll, P.D., Kraemer, R., Teng, K.K., Marchionni, M.A., Salzer, J.L. GGF/Neuregulin induces a phenotypic reversion of differentiated oligodendrocytes. Molecular Cellular Neuroscience, 1999, 13: 79-94.
2. Adult Glial Progenitors As The Cell Of Origin For Proneural Glioma: My research over the last 10 years has focused on understanding the cellular and molecular mechanisms of glial transformation and gliomagenesis. Using stereotaxic delivery of transforming retroviruses, my laboratory was the first to show that OPCs in the adult what matter that can give rise to malignant gliomas. We have also developed several genetically engineered mouse models to determine the effects of specific genetic alterations on adult glial progenitors and to characterize how these alterations lead to tumor formation. Using cross-species comparison of genomic and transcriptomic analyses we discovered that these mouse models resemble a specific subtype of human glioma (Proneural GBM). We also identified the master regulator transcription factors that control the Proneural phenotype and characterized how this transcriptional network changes during glial transformation and glioma progression. In collaboration with Patrizia Casaccia (Mount Sinai Medical School) we have shown how the regulation of OPC proliferation and differentiation is altered during glial transformation. This work has revealed several potential therapeutic targets, such as Topoisomerase IIA, which appear to be particularly important for the treatment of proneural GBM.
a. Assanah M, Lockhead R, Ogden A, Bruce J, Goldman J, Canoll P. Glial progenitors in adult white matter are driven to form malignant gliomas by PDGF expressing retroviruses The Journal of Neuroscience, 2006, 26 (25) 6781-6790.
b. Lei L, Sonabend AM, Guarnieri P, Soderquist C, Ludwig T, Rosenfeld, S, Bruce J, Canoll P, Glioblastoma models reveal the connection between adult glial progenitors and the Proneural phenotype. PLOS ONE, 2011.
c. Sonabend AM, Bansal M, Guarnieri P, Lei L, Amendolara B, Soderquist C, Leung R, Yun J, Sisti J, Kennedy B, Bruce S, Bruce, R, Shakya R, Ludwig T, Rosenfeld SS, Sims PA, S, Bruce JN, Califano A, Canoll P, The Transcriptional Regulatory Network of Proneural Glioma Determines the Genetic Alterations Selected During Tumor Progression. Cancer Research, 2014, 74(5), 1440-1451. doi: 10.1158/0008-5472.CAN-13-2150
d. Magri, L, Swiss, VA, Jablonska, B, Lei, L, Pedre, X, Walsh, M, Zhang, W, Gallo, V, Canoll, P, Casaccia, P E2F1 Coregulates Cell Cycle Genes and Chromatin Components during the Transition of Oligodendrocyte Progenitors from Proliferation to Differentiation, The Journal of Neuroscience, 2014, 22 January 34(4): 1481-1493
3. Preclinical Models To Test The Effects Of Targeted Therapy In Glioma: During the course our mechanistic studies on gliomagenesis, my lab has developed several new rodent glioma models, including a variety of mouse models that harbor different genetic alterations and fluorescent/bioluminescent reporter systems. These models have proven to be powerful systems for preclinical studies, because tumors that recapitulate the histopathological and molecular features of human glioma form with 100% penetrance in the context of an intact immune system, and response to treatment can be monitored by bioluminescence imaging. In collaboration with Jeffrey Bruce’s lab at Columbia University, we have used these animal models to test the effects of novel targeted therapies and drug delivery systems, including intracerebral convection enhanced delivery (CED) of chemotherapeutics directly into brain tumors. Most notably, these studies have shown that drugs that target topoisomerases (Topotecan and Etoposide) are highly effective against proneural glioma.
a. Lopez KA, Tannenbaum AM, Assanah MC, Linskey KR, Yun JP, Kangarlu A, Gil O, Canoll P, Bruce JN, Convection-enhanced delivery of topotecan into a PDGF-driven model of glioblastoma prolongs survival and ablates both tumor initiating cells and recruited glial progenitors. Cancer Reseach, 71, 3963-3971, 2011.
b.Sonabend AM, Yun J, Lei L, Leung R, Soderquist C, Crisman C, Gill BJ, Carminucci A, Sisti J, Castelli M, Sims PA, Bruce JN, Canoll P, Murine cell line model of Proneural glioma for evaluation of anti-tumor therapies. J Neurooncol. 2013 May;112(3):375-82. doi: 10.1007/s11060-013-1082-x. Epub 2013 Mar 16
c. Sonabend AM, Carminucci AS, Amendolara B, Bansal M, Leung R, Lei L, Realubit R, Li H, O J, Karan C, Yun J, Showers C, Rothcock R, Califano A, Canoll P, Bruce JN, Convection-Enhanced Delivery Of Etoposide Is Effective Against Murine Proneural Glioblastoma, Neuro-oncology, 2014
d. Lu F, Chen Y, Zhao C, Wang H, He D, Xu L, Wang J, He X, Deng Y, Lu EE, Liu X, Verma R, Bu H, Drissi R, Fouladi M, Stemmer-Rachamimov AO, Burns D, Xin M, Rubin JB, Bahassi el M, Canoll P, Holland EC, Lu RQ. "Olig2-Dependent Reciprocal Shift in PDGF and EGF Receptor Signaling Regulates Tumor Phenotype and Mitotic Growth in Malignant Glioma." Cancer Cell, 2016, 29(5): 669-683.
4. Mechanisms Of Glioma Invasion: My lab has developed methods to monitor glioma cell migration in living slices of brain tissue. Using this system we have characterized the dynamics of glioma motility and have identified the paths of glioma infiltration along white matter tracks and blood vessels. In collaboration with Steven Rosenfeld (now at the Cleveland Clinic), we identified nonmuscule myosin II (NMMII) as an essential motor for in glioma invasion, and showed that blocking NMMII or its upstream regulator Rho Kinase (ROCK), can inhibit glioma invasion. We are currently testing the therapeutic potential of targeting ROCK and NMMII in glioma.
a. Farin A, Suzuki SO, Weiker M, Goldman JE, Bruce JN, Canoll P. Transplanted glioma cells migrate and proliferate on host brain vasculature: a dynamic analysis. Glia, 2006, 53(8) 799-808.
b. Beadle, C., Assanah, M.C., Monzo, P., Vallee, R., Rosenfeld, S.S., and Canoll, P. The Role of Myosin II in Glioma Invasion of the Brain. Molecular biology of the cell, 2008, 19(8), 3357-3368.
c. Assanah, M.C., Bruce, J.N., Suzuki, S.O., Chen, A., Goldman, J.E., Canoll, P. “PDGF stimulates the massive expansion of glial progenitors in the neonatal forebrain” Glia, 2009, 57, 1835-47.
d. Ivkovic S, Beadle, C, Swanson K, Massey S, Noticewala, S, Bresnik A, Canoll P, and Steven Rosenfeld, Direct Inhibition Of Myosin II Effectively Blocks Glioma Invasion In The Presence Of Multiple Motogens. Molecular Biology of the Cell, 2012, 23: 533-542.
5. Cell-Type Specific Alterations At The Infiltrative Margins Of Glioma: Regions of non-enhancing tumor at the infiltrative margin are virtually always left behind after surgery for glioma, and it is this residual tissue that gives rise to recurrence, and which neuro-oncologists and radiation oncologist must treat. To address this important problem, Jeff Bruce, Peter Sims and I have initiated a large-scale, multi-investigator effort at Columbia University to collect and analyze radiographically localized biopsies from the contrast-enhancing core and non-enhancing margins of GBM. One major challenge to analyzing tissue at the margins of GBM is that it contains a complex mixture of infiltrating glioma cells and non-neoplastic brain cell. To address this issue, we have used a computational approach to deconvolve the homogenate expression data into cell type-specific expression profiles and identified subtype-specific patterns in cellular composition, and showed how these patterns are altered in post-treatment recurrent tumor.
In collaboration with Steven Rosenfeld, we have performed computational deconvolution of RNA-seq data from radiographically localized biopsies to determine the cell type-specific expression patterns of molecular motors in the contrast enhancing center and non-enhancing margins of human GBM. These studies have revealed that the mitotic kinesin KIF11 is significantly upregulated in GBM, with the highest expression in OPC-like/Proneural glioma cells—a pattern that was most pronounced when examining the samples from the non-enhancing margins of GBM.
In collaboration with Peter Sims’ lab, we engineered a new mouse model of glioma in which the retrovirus-transformed cells harbor the RiboTag allele. This model allows cell type-specific expression of HA-tagged polysomes, so that actively translated mRNA can be purified from brain tissue homogenate by immunoprecipitation and analyzed by RNA-seq and Ribosome profiling. Using this approach, we showed that translation efficiency (the number of ribosomes per transcript) varies across cell types and is significantly lower in proneural glioma cells compared to normal brain. These findings suggest that proneural glioma cells are under translational stress, and this may represent a targetable vulnerability in the treatment of these tumors. More recently, we have used ribosome profiling to characterize neuron-specific translation in the cerebral cortex of CamK-cre/RiboTag mice.
a. Gill B, Pisapia D, Malone H, Goldstein H, Lei L, Sonabend A, Yun J, Samanamud J, Sims J, Teich AF, Sheth S, McKhann G, Sisti M, Bruce JN, Sims PA, Canoll P, MRI-localized biopsies reveal subtype-specific differences in molecular and cellular composition at the margins of Glioblastoma. 2014, PNAS, 111, 12550-12555.
b. Gonzalez C, Sims JS, Hornstein N, Mela A, Garcia F, Lei L, Gass DA, Amendolara B, Bruce JN, Canoll P, Sims PA, Ribosome Profiling Reveals a Cell-Type Specific Translational Landscape in Glioma. 2014, J. Neuroscience, 34, 10924-10936.
c. Venere M, Horbinski CM, Crish JF, Vasanji A, Major J, Burrows A, Chang C, Prokop J, Wu Q, Sims PA, Canoll P, Summer MK, Rosenfeld SS, Rich JN, The Mitotic Kinesin KIF11 is a Central Driver of Invasion, Proliferation, and Self Renewal in Glioblastoma.2015, Science Translational Medicine 7, 304ra143.
d. Hornstein N, Torres D, Das Sharma S, Tang G, Canoll P, Sims PA. Ligation-free ribosome profiling of cell type-specific translation in the brain. 2016 Genome Biol 17, 149.
For a complete list of publications, please visit PubMed.gov