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Genomes and Genes | Adelaide M CarothersSummaryAffiliation: Massachusetts General Hospital Country: USA Publications
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Publications
Deficient E-cadherin adhesion in C57BL/6J-Min/+ mice is associated with increased tyrosine kinase activity and RhoA-dependent actomyosin contractilityAdelaide M Carothers
Department of Surgery, Carrie Hall, Room 116, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
Exp Cell Res 312:387-400. 2006..Thus, the positive regulation of E-cadherin adhesion provided by Apc+ in vivo allows proper negative regulation of Egfr, Src, Pyk2, and MAPK, as well as RhoA activities...
Apc deficiency is associated with increased Egfr activity in the intestinal enterocytes and adenomas of C57BL/6J-Min/+ miceAmy E Moran
Department of Surgery, Weill College of Medicine of Cornell University, and Strang Cancer Prevention Center, New York, New York 10021, USA
J Biol Chem 279:43261-72. 2004....
Carnosol inhibits beta-catenin tyrosine phosphorylation and prevents adenoma formation in the C57BL/6J/Min/+ (Min/+) mouseAmy E Moran
Department of Surgery, New York Presbyterian Hospital and Weill Medical College of Cornell University, New York, NY, USA
Cancer Res 65:1097-104. 2005..Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress beta-catenin tyrosine phosphorylation...
Persistent cyclooxygenase-2 inhibition downregulates NF-{kappa}B, resulting in chronic intestinal inflammation in the min/+ mouse model of colon tumorigenesisAdelaide M Carothers
Department of Surgery, Brigham and Women s Hospital, Boston, MA 02115, USA
Cancer Res 70:4433-42. 2010..Our findings argue that celecoxib resistance is an acquired adaptation to changes in the crypt microenvironment that is associated with chronic intestinal inflammation and impaired acute wound-healing responsiveness...
Estrogen receptors alpha and beta are inhibitory modifiers of Apc-dependent tumorigenesis in the proximal colon of Min/+ miceNancy L Cho
Departments of Surgery and Pathology, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
Cancer Res 67:2366-72. 2007..Our results indicate that ERalpha and ERbeta are inhibitory modifiers of Apc-dependent colon tumorigenesis. As a result, loss of E(2) and ER signaling in postmenopausal women may contribute to colorectal cancer development...
Modulation of tumor formation and intestinal cell migration by estrogens in the Apc(Min/+) mouse model of colorectal cancerSara H Javid
Department of Surgery, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
Carcinogenesis 26:587-95. 2005..In conclusion, both coumestrol and E(2) prevent intestinal tumorigenesis and ameliorate enterocyte migration and intercellular adhesion in the Apc(Min/+) mouse model of CRC...
Chronic cyclooxygenase-2 inhibition promotes myofibroblast-associated intestinal fibrosisJennifer S Davids
Department of Surgery, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
Cancer Prev Res (Phila) 3:348-58. 2010..We conclude that chronic COX-2 inhibition alters TGFbeta signaling in the intestinal mucosa, producing conditions consistent with chronic inflammation...
Changes in antitumor response in C57BL/6J-Min/+ mice during long-term administration of a selective cyclooxygenase-2 inhibitorAdelaide M Carothers
Department of Surgery, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
Cancer Res 66:6432-8. 2006..Chronic uninterrupted celecoxib treatment, however, induces untoward effects that enhance early progression events in intestinal tumorigenesis and may contribute to treatment toxicity...
Aberrant crypt foci in the adenoma prevention with celecoxib trialNancy L Cho
Department of Surgery, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
Cancer Prev Res (Phila) 1:21-31. 2008..Our overall results indicated that nondysplastic ACF were not accurate surrogate endpoint biomarkers of recurrent colorectal adenomas in the APC trial...
Immunohistochemical and molecular analysis of tyrosine kinase activity in desmoid tumorsNancy L Cho
Department of Surgery, Brigham and Women s Hospital, Boston, Massachusetts, USA
J Surg Res 173:320-6. 2012..Partial response to tyrosine kinase inhibitors (TKI) has previously been described. Here, we examined the role of the tyrosine kinases c-Src and c-Kit in driving desmoid tumorigenesis...
Adenomatous polyposis coli truncation alters cytoskeletal structure and microtubule stability in early intestinal tumorigenesisSara A Hughes
Department of Surgery, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
J Gastrointest Surg 6:868-74; discussion 875. 2002..These changes are consistent with the defects in enterocyte migration and junctional complex formation observed in the Min/+ model of early APC-associated colorectal tumorigenesis...
Mesenchymal stromal cell mutations and wound healing contribute to the etiology of desmoid tumorsAdelaide M Carothers
Department of Surgery, Brigham and Women s Hospital, Boston, Massachusetts MA 02115, USA
Cancer Res 72:346-55. 2012..The differentiation potential of these MSCs combined with expression of BMI-1, a transcriptional repressor downstream of Hedgehog and Notch signaling, suggests that desmoid tumors may respond to therapies targeting these pathways...
Sulindac reverses aberrant expression and localization of beta-catenin in papillary thyroid cancer cells with the BRAFV600E mutationNancy L Cho
Department of Surgery, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
Thyroid 20:615-22. 2010..In this study, we tested the hypothesis that the nonsteroidal antiinflammatory drug sulindac would reverse aberrant beta-catenin activity in thyroid cancer cells...
Inhibition of intestinal tumorigenesis in Apcmin/+ mice by (-)-epigallocatechin-3-gallate, the major catechin in green teaJihyeung Ju
Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ 08854 8020, USA
Cancer Res 65:10623-31. 2005....
