Research Topics
Genomes and Genes | Daniel W RosenbergSummaryAffiliation: University of Connecticut Health Center Country: USA Publications
Research Grants
| Collaborators
|
Detail Information
Publications
Mutations in BRAF and KRAS differentially distinguish serrated versus non-serrated hyperplastic aberrant crypt foci in humansDaniel W Rosenberg
Colon Cancer Prevention Program, Neag Comprehensive Cancer Center, and Center for Molecular Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA
Cancer Res 67:3551-4. 2007....- Genetic signatures of high- and low-risk aberrant crypt foci in a mouse model of sporadic colon cancerPrashant R Nambiar
Center for Molecular Medicine and Program in Colorectal Cancer, University of Connecticut Health Center, Farmington, Connecticut 06030-3101, USA
Cancer Res 64:6394-401. 2004..In addition to providing insight into colon cancer promotion, our data identify potential biomarkers for determining colon cancer risk in humans... 
Genetic deletion of mPGES-1 suppresses intestinal tumorigenesisMasako Nakanishi
Center for Molecular Medicine, Department of Cell Biology, University of Connecticut Health Center, Farmington, CT 06030 3101, USA
Cancer Res 68:3251-9. 2008..Our data show the feasibility of targeting mPGES-1 for cancer chemoprevention with the potential for improved tolerability over traditional nonsteroidal anti-inflammatory drugs and selective COX-2 inhibitors...- Microsatellite instability in aberrant crypt foci from patients without concurrent colon cancerEmily J Greenspan
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, CT, USA
Carcinogenesis 28:769-76. 2007..These lesions may be precursors to MSI-low CRC, providing a potential early biomarker to assess the effects of cancer prevention strategies... - Strain-specific homeostatic responses during early stages of Azoxymethane-induced colon tumorigenesis in miceKishore Guda
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, CT 06030, USA
Int J Oncol 31:837-42. 2007.... - Cytoplasmic phospholipase A2 levels correlate with apoptosis in human colon tumorigenesisMei Dong
Center for Molecular Medicine, Program in Colorectal Cancer, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030 3101, USA
Clin Cancer Res 11:2265-71. 2005..Our data further support the model in which colon cancer growth is favored when intracellular arachidonic acid levels are suppressed by inhibition of cPLA(2) or by a high-COX-2/low-cPLA(2) phenotype... - Cytoplasmic phospholipase A2 deletion enhances colon tumorigenesisJillian N M Ilsley
Program in Colorectal Cancer, Center for Molecular Medicine, University of Connecticut Health Center, Farmington, Connecticut 06030, USA
Cancer Res 65:2636-43. 2005..Our findings indicate that the proapoptotic role of cPLA(2) in the colon may supercede its contribution to eicosanoid production in tumor development... - Azoxymethane-induced pre-adipocyte factor 1 (Pref-1) functions as a differentiation inhibitor in colonic epithelial cellsMei Dong
The University of Connecticut Health Center, Center for Molecular Medicine, Farmington, Connecticut, USA
Carcinogenesis 25:2239-46. 2004..In addition, detection of Pref-1 in a human colon tumor cell line suggests that it may also participate in human colon tumorigenesis... - Deoxycholic acid promotes the growth of colonic aberrant crypt fociChristopher Flynn
The Carole and Ray Neag Comprehensive Cancer Center, The University of Connecticut Health Center, Farmington, Connecticut, USA
Mol Carcinog 46:60-70. 2007.... 
Selective PGE(2) suppression inhibits colon carcinogenesis and modifies local mucosal immunityMasako Nakanishi
Center for Molecular Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA
Cancer Prev Res (Phila) 4:1198-208. 2011..These results provide new insights into how PGE(2) controls antitumor immunity...- Molecular alterations associated with sulindac-resistant colon tumors in ApcMin/+ miceEmily J Greenspan
Center for Molecular Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030 3101, USA
Cancer Prev Res (Phila) 3:1187-97. 2010..Together, these observations may be translatable to designing novel clinical therapies using combinations of agents that target multiple molecular pathways to overcome sulindac resistance... - Aberrant crypt foci as predictors of colorectal neoplasia on repeat colonoscopyJoseph C Anderson
Carole and Ray Neag Comprehensive Cancer Center, University of Connecticut Health Center, Farmington, CT 06030 1845, USA
Cancer Causes Control 23:355-61. 2012..To estimate the risk for colorectal neoplasia detected on repeat colonoscopy in relation to aberrant crypt foci (ACF) frequency reported during the previous baseline examination... - Expression of secretory phospholipase A2 in colon tumor cells potentiates tumor growthGlenn S Belinsky
Center for Molecular Medicine, The Neag Comprehensive Cancer Center, University of Connecticut Health Center, Farmington, Connecticut 06030 3101, USA
Mol Carcinog 46:106-16. 2007..Mechanisms that may account for differences between the tumor explant model versus the Apc(Min) model of intestinal cancer are discussed... - Dietary iron promotes azoxymethane-induced colon tumors in miceJillian N M Ilsley
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, CT 06030, USA
Nutr Cancer 49:162-9. 2004..Our results suggest that, following carcinogen exposure, elevated dietary iron promotes the growth of tumors with altered cellular homeostasis through a mechanism that is independent of oxidative stress... - Aberrant crypt foci in patients with a positive family history of sporadic colorectal cancerRichard G Stevens
Colon Cancer Prevention Program, Neag Comprehensive Cancer Center, University of Connecticut Health Center, CT, USA
Cancer Lett 248:262-8. 2007..4; the mean was significantly higher in the patients with a positive family history of CRC (9.0, p<0.01; n=43) or a personal history of advanced adenoma (7.5, p<0.05; n=34)... - Epigenetic alterations in RASSF1A in human aberrant crypt fociEmily J Greenspan
Center for Molecular Medicine, UCHC School of Medicine, University of Connecticut Health Center, Farmington, CT 06030-3101, USA
Carcinogenesis 27:1316-22. 2006..Importantly, CIM of RASSF1A is an early epigenetic aberration, occurring in the absence of synchronous colon tumors and is not accompanied by field effects into the surrounding epithelium... - Anti-inflammatory effects of freeze-dried black raspberry powder in ulcerative colitisDavid C Montrose
Center for Molecular Medicine and Colon Cancer Prevention Program, University of Connecticut Health Center, Farmington, CT 06030, USA
Carcinogenesis 32:343-50. 2011..These findings demonstrate a potent anti-inflammatory effect of BRB during DSS-induced colonic injury, supporting its possible therapeutic or preventive role in the pathogenesis of UC and related neoplastic events... - Multistage gene expression profiling in a differentially susceptible mouse colon cancer modelKishore Guda
Center for Molecular Medicine, University of Connecticut Health Center, 263, Farmington Avenue, Farmington, CT 06030-3101, USA
Cancer Lett 191:17-25. 2003..Overall, our data indicate time- and strain-specific genetic alterations during different stages of colon tumorigenesis following AOM treatment... - Increased frequency of serrated aberrant crypt foci among smokersJoseph C Anderson
Colon Cancer Prevention Program, Neag Comprehensive Cancer Center, University of Connecticut Health Center, Farmington, CT 06030 1845, USA
Am J Gastroenterol 105:1648-54. 2010..Our goal was to examine whether smoking at least 20 pack years was associated with an increased frequency of ACF... - Dietary methyl donor depletion protects against intestinal tumorigenesis in Apc(Min/+) miceKrishna Kadaveru
Molecular Medicine, University of Connecticut Health Center, Farmington, CT 06030, USA
Cancer Prev Res (Phila) 5:911-20. 2012..Further studies are warranted to investigate the complex interplay of methyl donor status and cancer protection in high-risk populations... - Vascular endothelial growth factor and enhanced angiogenesis do not promote metastatic conversion of a newly established azoxymethane-induced colon cancer cell lineGlenn S Belinsky
Center for Molecular Medicine, School of Medicine, University of Connecticut Health Center, Farmington, Connecticut 06030 3101, USA
Mol Carcinog 43:65-74. 2005..The established murine colon epithelial cell line provides a useful experimental model to further elaborate genetic and epigenetic factors that may promote or inhibit colon tumorigenesis and metastasis... - Defective processing of the transforming growth factor-beta1 in azoxymethane-induced mouse colon tumorsKishore Guda
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, Connecticut 06030, USA
Mol Carcinog 37:51-9. 2003.... - Roles of cPLA2alpha and arachidonic acid in cancerMasako Nakanishi
Center for Molecular Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 0603, USA
Biochim Biophys Acta 1761:1335-43. 2006..We also discuss the potential contribution of cPLA(2)alpha and AA to apoptosis, and the regulatory mechanisms leading to aberrant expression of cPLA(2)alpha... - Mouse models for the study of colon carcinogenesisDaniel W Rosenberg
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, CT 06030 3101, USA
Carcinogenesis 30:183-96. 2009..We will also describe the general features of lesions formed in response to carcinogen treatment, including the underlying molecular aberrations and how these changes may relate to the pathogenesis of human colorectal cancer... - Role of Notch signaling in colon homeostasis and carcinogenesisShingo Miyamoto
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, Connecticut, USA
Cancer Sci 102:1938-42. 2011..Moreover, we discuss novel therapeutic strategies that are under development for targeting Notch signaling in cancer stem cells... - Ibuprofen inhibits activation of nuclear {beta}-catenin in human colon adenomas and induces the phosphorylation of GSK-3{beta}Emily J Greenspan
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, Connecticut 06030, USA
Cancer Prev Res (Phila) 4:161-71. 2011..These data suggest that ibuprofen can effectively target both the Wnt/β-catenin and NF-κB pathways, and potentially uncovers a novel mechanism through which NSAIDS may exert their chemopreventive efficacy... - Planar spindle orientation and asymmetric cytokinesis in the mouse small intestineElizabeth S Fleming
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, CT 06030 3101, USA
J Histochem Cytochem 55:1173-80. 2007..This type of image analysis may be useful for studying the regulation of spindle position during tissue remodeling and tumor formation... - cPLA2 is protective against COX inhibitor-induced intestinal damageDavid C Montrose
Center for Molecular Medicine and Colon Cancer Prevention Program, Department of Cell Biology, University of Connecticut Health Center, Farmington, Connecticut 06030, USA
Toxicol Sci 117:122-32. 2010..Our data demonstrate that cPLA(2) appears to be an important component in conferring protection against COX inhibitor-induced enteropathy, which may be mediated through affects on enterocytic mitochondria... - The contribution of methotrexate exposure and host factors on transcriptional variance in human liverGlenn S Belinsky
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, CT 06030 3101, USA
Toxicol Sci 97:582-94. 2007..Differences in complement expression provide the rationale for future correlative studies between MTX-induced liver fibrosis and C5 alleles in order to identify patients with increased risk for fibrosis... - Epidemiology of colonic aberrant crypt foci: review and analysis of existing studiesRichard G Stevens
Colon Cancer Prevention Program CCPP, Neag Comprehensive Cancer Center, University of Connecticut Health Center UCHC, 263 Farmington Avenue, Farmington, CT 06030 6325, United States
Cancer Lett 252:171-83. 2007..This information can then be used to improve the design of prospective studies, and of clinical intervention trials that use ACF as an intermediate endpoint... - Carcinogen-induced colon tumors in mice are chromosomally stable and are characterized by low-level microsatellite instabilityKishore Guda
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, CT 06030-3101, USA
Oncogene 23:3813-21. 2004..Based on our molecular and cytogenetic findings, we propose that carcinogen-induced tumors may develop via mechanisms independent of the 'classical' CIN or MSI pathways... - mPGES-1 as a target for cancer suppression: A comprehensive invited review "Phospholipase A2 and lipid mediators"Masako Nakanishi
Center for Molecular Medicine, University of Connecticut Health Center, 263 Farmington Ave, Farmington, CT 06030 3101, USA
Biochimie 92:660-4. 2010..The role of mPGES-1 in the pathogenesis of various cancers is discussed. In addition, an overview of recent efforts to develop small molecule inhibitors that target the protein with high selectivity is also be reviewed... - Inverse association between phospholipase A2 and COX-2 expression during mouse colon tumorigenesisMei Dong
Center for Molecular Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030 3101, USA
Carcinogenesis 24:307-15. 2003.... - Utilizing endoscopic technology to reveal real-time proteomic alterations in response to chemopreventionMasako Nakanishi
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, CT, USA
Proteomics Clin Appl 1:1660-6. 2007..This approach should be broadly applicable for assessing lesion responsiveness in a wide range of translational and human clinical studies... - Number of aberrant crypt foci associated with adiposity and IGF1 bioavailabilityHelen Swede
Colon Cancer Prevention Program, Neag Comprehensive Cancer Center, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030 6325, USA
Cancer Causes Control 20:653-61. 2009..Evidence has been derived from studies of cancer and polyps. Supporting data about aberrant crypt foci (ACF), putative pre-polyp changes, have been generated only from animal studies to date... - CD13 is dispensable for normal hematopoiesis and myeloid cell functions in the mouseBeata Winnicka
Center for Vascular Biology, Department of Immunology, University of Connecticut Health Center, 263 Farmington Ave, Farmington, CT 06030 3501, USA
J Leukoc Biol 88:347-59. 2010.... - Role of the alternating reading frame (P19)-p53 pathway in an in vivo murine colon tumor modelPrashant R Nambiar
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, Connecticut 06030-3101, USA
Cancer Res 62:3667-74. 2002..The AOM colon cancer model may be well suited for studying tumor promotion events that precede p53 disruption... - Oxidative damage in colon and mammary tissue of the HFE-knockout mouseRichard G Stevens
Department of Community Medicine, University of Connecticut Health Center, Farmington 06030, USA
Free Radic Biol Med 34:1212-6. 2003..226, p =.02) tissue among those mice on the standard iron diet compared to those on the low iron diet. These results suggest that dietary modification may affect the course of iron overload from HFE mutations... - Murine models of ulcerative colitisChristopher Flynn
Center for Molecular Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-3101, USA
Arch Pharm Res 26:433-40. 2003..This review examines and distills what has been leamed from these models and how this information is related back to human UC... - Preliminary analysis of azoxymethane induced colon tumors in inbred mice commonly used as transgenic/knockout progenitorsPrashant R Nambiar
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, CT 06030-3101, USA
Int J Oncol 22:145-50. 2003..Lack of invasiveness and metastasis in even the most sensitive strains provides a model system for studying the potential role of 'metastasis genes' in imparting a malignant phenotype... - Suppression of kinesin expression disrupts adenomatous polyposis coli (APC) localization and affects beta-catenin turnover in young adult mouse colon (YAMC) epithelial cellsHongyi Cui
Center for Molecular Medicine, University of Conneticut Health Center, Farmington 06030, USA
Exp Cell Res 280:12-23. 2002..These data indicate that KHC-mediated APC translocation is tightly coordinated with beta-catenin turnover in the cell... - The induction of aberrant crypt foci (ACF) in the colons of rats by trihalomethanes administered in the drinking waterAnthony B DeAngelo
National Health and Environmental Effects Research Laboratory, Office of Research and Development, U S Environmental Protection Agency MD 68, Research Triangle Park, NC 27711, USA
Cancer Lett 187:25-31. 2002..These studies demonstrate that brominated THMs administered in the drinking water significantly induced preneoplastic ACF in the colon of rats... - APC-dependent suppression of colon carcinogenesis by PPARgammaGeoffrey D Girnun
Dana Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, One Jimmy Fund Way, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 99:13771-6. 2002..This finding suggests a potentially important use for PPARgamma ligands as chemopreventative agents in colon cancer... - Cyclooxygenase-2 regulation in colon cancer cells: modulation of RNA polymerase II elongation by histone deacetylase inhibitorsXin Tong
Department of Molecular and Cell Biology, University of Connecticut, Storrs, Connecticut 06269 3125, USA
J Biol Chem 280:15503-9. 2005..We propose that histone deacetylases regulate a transcriptional block on the Cox-2 and c-myc genes and that this block may be a potential target for pharmacological intervention... - Repression of prostaglandin dehydrogenase by epidermal growth factor and snail increases prostaglandin E2 and promotes cancer progressionJason R Mann
Departments of Cell and Developmental Biology, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, 2300 Pierce Avenue, Nashville, TN 37232, USA
Cancer Res 66:6649-56. 2006..These data indicate that PGDH may serve a tumor suppressor function in colorectal cancer and provide a possible COX-2-independent way to target PGE(2) to inhibit cancer progression... - Circumvention and reactivation of the p53 oncogene checkpoint in mouse colon tumorsWataru Aizu
Department of Molecular and Cell Biology, 91 North Eagleville Road, University of Connecticut, Storrs, CT 06269-3125, USA
Biochem Pharmacol 72:981-91. 2006.... - The p50-p50 NF-kappaB complex as a stimulus-specific repressor of gene activationXin Tong
Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269, USA
Mol Cell Biochem 265:171-83. 2004..Our findings demonstrate a novel gene regulatory mechanism for the NF-kappaB p50-p50 complex: a signal-specific transcriptional repression that appears to selectively inhibit stimuli that transiently activate p65-p50 complexes... - p53 and its co-activator p300 are inversely regulated in the mouse colon in response to carcinogenWataru Aizu
Department of Molecular and Cell Biology, University of Connecticut, 75 North Eagleville Road, U-3125, Storrs, CT 06269, USA
Toxicol Lett 144:213-24. 2003..We propose that inefficient gene activation by p53 in the colon contributes to the organotrophic effects of AOM... - HDAC3 overexpression and colon cancer cell proliferation and differentiationColleen C Spurling
Department of Molecular and Cell Biology, University of Connecticut, Storrs, Connecticut, USA
Mol Carcinog 47:137-47. 2008..Our data support a central role for HDAC3 in regulating the cell proliferation and differentiation of colon cancer cells and suggest a potential mechanism by which colon cancers may become resistant to luminal butyrate...
Research Grants
- Altered Arachidonic Acid Balance and Colon CancerDaniel Rosenberg; Fiscal Year: 2006..Our goal would be to improve targeting of individuals most likely to respond to chemopreventive agents that impact the AA metabolic pathway. ..