C C Maley
Affiliation: Massachusetts Institute of Technology
- Selective instability: maternal effort and the evolution of gene activation and deactivation ratesCarlo C Maley
Fred Hutchinson Cancer Research Center, PO Box 19024, Seattle, WA 98109 1024, USA
Artif Life 9:317-26. 2003....
- NSAIDs modulate clonal evolution in Barrett's esophagusRumen L Kostadinov
Genomics and Computational Biology Graduate Program, University of Pennsylvania, Philadelphia, Pennsylvania, USA
PLoS Genet 9:e1003553. 2013..Barrett's cells maintained relative equilibrium level of SGAs over time with occasional punctuations by expansion of clones having massive amount of SGAs...
- Solving the puzzle of metastasis: the evolution of cell migration in neoplasmsJun Chen
Genomics and Computational Biology Program, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America
PLoS ONE 6:e17933. 2011..We suggest that resource heterogeneity within primary tumors selects for cell migration, and that cell emigration is a by-product of that selection...
- Sequence space coverage, entropy of genomes and the potential to detect non-human DNA in human samplesZhandong Liu
Genomics and Computational Biology Graduate Group, School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
BMC Genomics 9:509. 2008..Genomes store information for building and maintaining organisms. Complete sequencing of many genomes provides the opportunity to study and compare global information properties of those genomes...
- An in vitro co-culture model of esophageal cells identifies ascorbic acid as a modulator of cell competitionLauren M F Merlo
The Wistar Institute, 3601 Spruce St, Philadelphia, PA 19104, USA
BMC Cancer 11:461. 2011..We have examined competition between normal and Barrett's esophagus cell lines, in the hopes of identifying a system that could screen for potential chemopreventive agents...
- Multistage carcinogenesis in Barrett's esophagusCarlo C Maley
The Wistar Institute, Cellular and Molecular Oncogenesis, 3601 Spruce Street, Philadelphia, PA 19104, USA
Cancer Lett 245:22-32. 2007..The final events that lead to invasion and metastasis are unknown. Evolutionary biology provides important tools to understand clonal evolution in progression and cancer prevention...
- Genetic clonal diversity predicts progression to esophageal adenocarcinomaCarlo C Maley
The Wistar Institute, 3601 Spruce St, Philadelphia, Pennsylvania 19104, USA
Nat Genet 38:468-73. 2006..6) and ploidy abnormalities. Progression to cancer through accumulation of clonal diversity, on which natural selection acts, may be a fundamental principle of neoplasia with important clinical implications...
- Natural selection in neoplastic progression of Barrett's esophagusCarlo C Maley
Molecular and Cellular Oncogenesis Program, The Wistar Institute, 3601 Spruce St, Philadelphia, PA 19104, USA
Semin Cancer Biol 15:474-83. 2005..Evolutionary analyses provide insights for clinical management, including rates of progression to cancer and emergence of resistance to interventions...
- Cancer prevention strategies that address the evolutionary dynamics of neoplastic cells: simulating benign cell boosters and selection for chemosensitivityCarlo C Maley
Division of Human Biology, Fred Hutchinson Cancer Research Center, P O Box 19024, Mailstop C1 157, Seattle, WA 98109, USA
Cancer Epidemiol Biomarkers Prev 13:1375-84. 2004..Effective therapeutic and prevention strategies will have to alter the competitive dynamics of a neoplasm to counter progression toward invasion, metastasis, and death...
- Selectively advantageous mutations and hitchhikers in neoplasms: p16 lesions are selected in Barrett's esophagusCarlo C Maley
Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA
Cancer Res 64:3414-27. 2004..Virtually all of the other lesion expansions, including microsatellite shifts, could be explained as hitchhikers on p16 lesion clonal expansions. These techniques can be applied to any neoplasm...
- Exploring the relationship between neutral and selective mutations in cancerC C Maley
Fred Hutchinson Cancer Research Center, 1100 Fairview Ave, N Seattle, WA 98109, USA
Artif Life 6:325-45. 2000..The model also suggests that selective mutations facilitate the development of cancer, so that the more selective mutations necessary for the development of cancer, the greater the chance of developing it...
- Genetic mechanisms of TP53 loss of heterozygosity in Barrett's esophagus: implications for biomarker validationV Jon Wongsurawat
Divisions of Human Biology and Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
Cancer Epidemiol Biomarkers Prev 15:509-16. 2006..If an alternative biomarker assay, such as fluorescence in situ hybridization (FISH), provided equivalent results, then translation to the clinic might be accelerated, because LOH genotyping is presently limited to research centers...
- Barrett's esophagus and its progression to adenocarcinomaCarlo C Maley
The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
J Natl Compr Canc Netw 4:367-74. 2006..However, most of these results should be confirmed in additional cohorts before they are used to change clinical practice...
- Mutagen sensitivity and neoplastic progression in patients with Barrett's esophagus: a prospective analysisDennis L Chao
Division of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, C1 157, Seattle, WA 98109, USA
Cancer Epidemiol Biomarkers Prev 15:1935-40. 2006....
- Cancer as an evolutionary and ecological processLauren M F Merlo
Cellular and Molecular Oncology Program, The Wistar Institute, 3601 Spruce Street, Philadelphia, Pennsylvania 19104, USA
Nat Rev Cancer 6:924-35. 2006..The tools of evolutionary biology and ecology are providing new insights into neoplastic progression and the clinical control of cancer...
- NSAIDs modulate CDKN2A, TP53, and DNA content risk for progression to esophageal adenocarcinomaPatricia C Galipeau
Human Biology Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America
PLoS Med 4:e67. 2007..We aimed to evaluate somatic genetic abnormalities with NSAIDs as predictors of EA in a prospective cohort study of patients with BE...
- Extent of low-grade dysplasia is a risk factor for the development of esophageal adenocarcinoma in Barrett's esophagusAmitabh Srivastava
Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Am J Gastroenterol 102:483-93; quiz 694. 2007..The aim of this discovery study was to evaluate the hypothesis that extent of LGD and HGD are risk factors for progression to EA...
- Open questions in oesophageal adenocarcinogenesisCarlo C Maley
Molecular and Cellular Oncogenesis Program, The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA
Gut 56:897-8. 2007
- The combination of genetic instability and clonal expansion predicts progression to esophageal adenocarcinomaCarlo C Maley
Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA
Cancer Res 64:7629-33. 2004..This implies that interventions that limit expansion of genetically unstable clones may reduce risk of progression to cancer...
- Biologic properties of columnar epithelium underneath reepithelialized squamous mucosa in Barrett's esophagusJason L Hornick
Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Am J Surg Pathol 29:372-80. 2005..Prospective studies of large numbers of patients with BUSI will be required to determine the magnitude of its risk of progression to cancer...
- Progress in chemoprevention drug development: the promise of molecular biomarkers for prevention of intraepithelial neoplasia and cancer--a plan to move forwardGary J Kelloff
National Cancer Institute, Bethesda, Maryland 20852, USA
Clin Cancer Res 12:3661-97. 2006....
- Animal cell differentiation patterns suppress somatic evolutionJohn W Pepper
Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, Arizona, United States of America
PLoS Comput Biol 3:e250. 2007..These results are relevant not only to understanding the evolutionary origins of multicellularity, but also the causes of pathologies such as cancer and senescence in extant metazoans, including humans...