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001-es BibID:BIBFORM033096
035-os BibID:PMID:16239965 WOS:000233022100026
Első szerző:Bálint Klára
Cím:Activation of Notch1 signaling is required for beta-catenin-mediated human primary melanoma progression / Klara Balint, Min Xiao, Chelsea C. Pinnix, Akinobu Soma, Imre Veres, Istvan Juhasz, Eric J. Brown, Anthony J. Capobianco, Meenhard Herlyn, Zhao-Jun Liu
Dátum:2005
Megjegyzések:Notch is a highly conserved transmembrane receptor that determines cell fate. Notch signaling denotes cleavageof the Notch intracellular domain, its translocation to the nucleus, and subsequent activation of targetgene transcription. Involvement of Notch signaling in several cancers is well known, but its role in melanomaremains poorly characterized. Here we show that the Notch1 pathway is activated in human melanoma.Blocking Notch signaling suppressed whereas constitutive activation of the Notch1 pathway enhanced primarymelanoma cell growth both in vitro and in vivo yet had little effect on metastatic melanoma cells. Activation ofNotch1 signaling enabled primary melanoma cells to gain metastatic capability. Furthermore, the oncogeniceffect of Notch1 on primary melanoma cells was mediated by ?-catenin, which was upregulated followingNotch1 activation. Inhibiting ?-catenin expression reversed Notch1-enhanced tumor growth and metastasis.Our data therefore suggest a ?-catenin?dependent, stage-specific role for Notch1 signaling in promoting the
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
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Megjelenés:The Journal of Clinical Investigation. - 115 : 11 (2005), p. 3166-3176. -
További szerzők:Xiao, Min Pinnix, Chelsea C. Soma, Akinobu Veres Imre (1963-) (bőrgyógyász) Brown, Eric J. Capobianco, Anthony J. Herlyn, Meenhard Liu, Zhao-Jun Juhász István (1956-) (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:bibEB00010211
035-os BibID:PMCID:PMC288423
Első szerző:Juhász István (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus)
Cím:Development of pemphigus vulgaris-like lesions in severe combined immunodeficiency disease mice reconstituted with lymphocytes from patients / Istvan Juhasz, Gerald S. Lazarus, George F. Murphy, Ie-Ming Shih, Meenhard Herlyn
Dátum:1993
Megjegyzések:Pemphigus vulgaris is an autoimmune blistering disease that is induced by binding of antibodies to a 130/85-kD protein complex on epidermal keratinocytes. An in vivo experimental model of this disease was developed by reconstituting severe combined immunodeficiency (SCID) mice with 1-10 x 10(7) PBL from patients with naturally occurring pemphigus vulgaris. Of 49 reconstituted mice, 34 (69%) produced human IgG levels of > 0.1 mg/ml. Circulating anti-pemphigus antibodies were found in 20 of the 34 successfully reconstituted mice; 44% of these animals had deposits of human IgG in their own skin after it was traumatized by either heat or cold. Spontaneous pemphigus vulgaris-like blisters associated with human IgG deposits were rarely found in mouse skin. By contrast, allogeneic human skin grafted to 10 to 12 mice before reconstitution with patients' PBL developed pemphigus vulgaris-like lesions containing human IgG deposits. These results demonstrate that SCID mice can serve as a model of an antibody-mediated human autoimmune skin disease.
Tárgyszavak:idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Journal of Clinical Investigation. - 92 : 5 (1993), p. 2401-2407. -
További szerzők:Lazarus, Gerald S. Murphy, George F. Herlyn, Meenhard Shih, Ie-Ming
Internet cím:DOI
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3.

001-es BibID:bibEBI12849
Első szerző:Yan, Homg-Chin
Cím:Human/severe combined immunodeficient mouse chimeras : an experimental in vivo model system to study the regulation of human endothelial cell-leukocyte adhesion molecules / Homg-Chin Yan, Istvan Juhasz, Joseph Pilewski, George F. Murphy, Meenhard Herlyn, Steven M. Albelda
Dátum:1993
ISSN:0021-9738 1558-8238
Megjegyzések:The ability of circulating white blood cells to enter inflamed tissues is mediated by specific cell adhesion molecules thought to be expressed in a programmed and sequential manner to form an "adhesion cascade." Because of the complexity of this process, it is becoming increasingly important to develop in vivo models. Two major problems have limited the utility of current animal models. The first is the inability of many of the antibodies developed against cell adhesion molecules in human cell culture models to cross-react in animals. The second is the uncertainty in extrapolating animal (particularly rodent) findings to humans. To circumvent these problems, full thickness human skin grafts were transplanted onto immunodeficient (severe combined immunodeficient) mice. After 4-6 wk, the transplanted skin grafts closely resembled normal skin histologically and maintained their human vasculature as determined by immunohistochemical staining with human-specific endothelial cell markers. Intradermal injection of tumor necrosis factor-alpha resulted in the reversible upregulation of the leukocyte-endothelial adhesion molecules E-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1, and in an active inflammatory reaction with migration of murine leukocytes into cytokine-injected areas. These results indicate that the severe combined immunodeficient mouse/human skin transplant model provides a useful in vivo system in which to study human endothelium during the process of inflammation.
Tárgyszavak:idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Journal of Clinical Investigation. - 91 : 3 (1993), p. 986-996. -
További szerzők:Juhász István (1956-) (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus) Pilewski, Joseph Murphy, George F. Herlyn, Meenhard Albelda, Steven M.
Internet cím:DOI
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