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Carlo
Maley, Ph.D.
Assistant Professor, Dept. of Molecular and Cellular Oncogenesis, The Wistar Institute
Cancer Biology Program
Address
The Wistar Institute, Room 352B
3601 Spruce St.
Philadelphia, PA 19104
Office tel.: 215 495-6838
Lab tel.: 215 495-6839
Fax: 215 495-6829
E-mail: cmaley@wistar.org
Education
Oberlin
College: BA (Computer Science and Psychology), 1991.
University of Oxford: M.Sc. (Zoology), 1993.
MIT: Ph.D. (Computer Science;Computational Biology), 1998.
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Research
Interests
- Evolution in cancer, neoplastic progression and therapeutic resistance.
Key words: evolution, meoplastic progression, therapeutic resistance, cancer,
Barrett's esophagus, ecology, computational modeling, cancer stem cells, population genetics, diversity.
Search PubMed for articles
Description
of Research
The
Maley laboratory is applying evolutionary and ecological theory
to neoplastic progression and therapeutic resistance in order
to modulate the evolution of neoplastic cells and thereby
prevent cancer and its relapse. We take three, mutually reinforcing
approaches to these problems: computational simulations to
explore hypotheses, data mining of (application of evolutionary
theory to) genetic data from neoplasms, and evolutionary experiments
in tissue culture.
Current projects in the lab include:
Measuring
genetic diversity in neoplasms and testing if it predicts
both progression and therapeutic resistance.
Applying
phylogenetic methods to measure the parameters of evolution
in neoplasms.
Developing
in vitro competition assays to find cancer prevention drugs.
Developing
experimental models of Barrett’s Esophagus.
Harnessing
clonal evolution to prevent cancer.
Computational
modeling of the mechanisms of clonal expansion.
Computational
modeling of neoplastic progression.
Recent
Publications
Maley, C.C. (2007) Multistage carcinogenesis
in Barrett’s esophagus. Cancer Letters, 245:22–32,
2007.
Galipeau, P.C., Li X, Blount, P.L., Maley,
C.C. Sanchez, C.A. Odze, R.D., Ayub, K. Rabinovitch,
P.S., Vaughan, T.V. Reid, B.J.(2007) NSAIDs modulate CDKN2A,
TP53, and DNA vontent tisk for progression to rsophageal sdenocarcinoma.
PLoS Medicine. 4(2):e67.
Merlo, L., Pepper, J., Reid, B.J., Maley,
C.C.(2006) Cancer as an evolutionary and ecological
process. Nature Reviews Cancer, 6:924–35.
Maley, C.C., Galipeau, P.C.,
Finley, J.C., Wongsurawat, V.J., Li, X., Sanchez, C.A., Paulson,
T.G., Blount, P.L., Risques, R., Rabinovitch, P.S. and Reid,
B.J. (2006) Genetic clonal diversity predicts progression
to esophageal adenocarcinoma. Nature Genetics, 38:468–473.
Maley, C. C., Reid, B. J.,
Forrest, S. (2004) Cancer prevention strategies that address
the evolution of neoplastic cells: Simulating benign cell
boosters and selection for chemosensitivity. Cancer Epidemiology,
Biomarkers and Prevention, 13:1375-84.
Lab
Rotation Projects
3D organotypic reconstruct tissue culture models of Barrett's esophagus
Modulating clonal competition in neoplastic progression
The effects of NSAIDs and vitamin C on neoplastic progression
Measuring genetic diversity
Selecting for chemosensitivity
Neoplastic progression in cervical cancer
Tumor suppressor genes in humpback whales
Slowing somatic evolution
The evolution of metastasis
The evolution of anti-angiogenic factors
- Lab personnel:
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Dr. Lauren Merlo - Postdoctoral Researcher
Dr. Marcin Imielinski - Postdoctoral Researcher
Rumen Kostadinov - Graduate Student
Kathleen Sprouffske - Graduate Student
Rachelle Kosoff - Research Assistant
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