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A cell-intrinsic role for TLR2-MYD88 in intestinal and breast epithelia and oncogenesis.
Scheeren, Ferenc A; Kuo, Angera H; van Weele, Linda J; Cai, Shang; Glykofridis, Iris; Sikandar, Shaheen S; Zabala, Maider; Qian, Dalong; Lam, Jessica S; Johnston, Darius; Volkmer, Jens P; Sahoo, Debashis; van de Rijn, Matt; Dirbas, Frederick M; Somlo, George; Kalisky, Tomer; Rothenberg, Michael E; Quake, Stephen R; Clarke, Michael F.
Afiliação
  • Scheeren FA; 1] Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA [2] The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.
  • Kuo AH; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA.
  • van Weele LJ; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA.
  • Cai S; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA.
  • Glykofridis I; The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.
  • Sikandar SS; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA.
  • Zabala M; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA.
  • Qian D; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA.
  • Lam JS; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA.
  • Johnston D; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA.
  • Volkmer JP; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA.
  • Sahoo D; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA.
  • van de Rijn M; Department of Pathology, Stanford University, Stanford, California 94305, USA.
  • Dirbas FM; Department of Surgery, Stanford University, Stanford, California 94305, USA.
  • Somlo G; Department of Medical Oncology, Beckman Research Institute and City of Hope Comprehensive Cancer Center, Duarte, California 91010, USA.
  • Kalisky T; Department of Bioengineering and Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA.
  • Rothenberg ME; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA.
  • Quake SR; Department of Bioengineering and Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA.
  • Clarke MF; 1] Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive Stanford, California 94305, USA [2] Department of medicine, Division of Oncology, Stanford University, Stanford, California 94305, USA.
Nat Cell Biol ; 16(12): 1238-48, 2014 Dec.
Article em En | MEDLINE | ID: mdl-25362351
It has been postulated that there is a link between inflammation and cancer. Here we describe a role for cell-intrinsic toll-like receptor-2 (TLR2; which is involved in inflammatory response) signalling in normal intestinal and mammary epithelial cells and oncogenesis. The downstream effectors of TLR2 are expressed by normal intestinal and mammary epithelia, including the stem/progenitor cells. Deletion of MYD88 or TLR2 in the intestinal epithelium markedly reduces DSS-induced colitis regeneration and spontaneous tumour development in mice. Limiting dilution transplantations of breast epithelial cells devoid of TLR2 or MYD88 revealed a significant decrease in mammary repopulating unit frequency compared with the control. Inhibition of TLR2, its co-receptor CD14, or its downstream targets MYD88 and IRAK1 inhibits growth of human breast cancers in vitro and in vivo. These results suggest that inhibitors of the TLR2 pathway merit investigation as possible therapeutic and chemoprevention agents.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Mama / Neoplasias da Mama / Neoplasias do Colo / Receptor 2 Toll-Like / Fator 88 de Diferenciação Mieloide / Carcinogênese / Mucosa Intestinal Idioma: En Revista: Nat Cell Biol Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Holanda País de publicação: Reino Unido
Texto completo
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Mama / Neoplasias da Mama / Neoplasias do Colo / Receptor 2 Toll-Like / Fator 88 de Diferenciação Mieloide / Carcinogênese / Mucosa Intestinal Idioma: En Revista: Nat Cell Biol Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Holanda País de publicação: Reino Unido