CCL

Összesen 11 találat.
#/oldal:
Részletezés:
Rendezés:

1.

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
külföldön készült közlemény
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
DOI
Borító:

2.

001-es BibID:BIBFORM033116
Első szerző:Fukunaga-Kalabis, Mizuho
Cím:Downregulation of CCN3 expression as a potential mechanism for melanoma progressionCCN3 inhibits growth and invasion of melanoma / M. Fukunaga-Kalabis, G. Martinez, S. M. Telson, Z-J. Liu, K. Balint, I. Juhász, D. E. Elder, B. Perbal, M. Herlyn
Dátum:2008
ISSN:0950-9232
Megjegyzések:Coculture of human melanocytes with keratinocytes upregulates CCN3, a matricellular protein critical to maintenance of normal homeostasis of melanocytes in the skin. CCN3 affects two fundamental features of melanocyte physiology: it inhibits melanocyte proliferation and stimulates their adhesion to the basement membrane. Here we report that expression of CCN3 is downregulated in advanced melanomas. Aggressive melanoma cell lines did not respond to treatment with CCN3 inducers, such as interleukin-1beta (IL-1beta), while less aggressive melanoma cell lines responded similarly to melanocytes. Immunostaining analyses revealed that CCN3 was present in melanoma cells close to the epidermal-dermal interface, but not in melanoma cells that had invaded deep into the dermis or had metastasized to lymph nodes. Contrary to our expectations, overexpression of CCN3 in 1205Lu metastatic melanoma cells did not affect their adhesion to collagen IV. However, CCN3 decreased the transcription and activation of matrix metalloproteinases and suppressed the invasion of 1205Lu melanoma cells. These results suggest that the lack of CCN3 in advanced melanoma cells contributes to their invasive phenotype. Whereas major matricellular proteins, such as osteopontin, tenascin or secreted protein acidic and rich in cysteine (SPARC), are strongly upregulated in melanoma cells; CCN3 is the first member of this family that is downregulated.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
melanoma
CCN3
matricellular protein
matrix metalloproteinase
külföldön készült közlemény
Megjelenés:Oncogene. - 27 (2008), p. 2552-2560. -
További szerzők:Martinez, G. Telson, S. M. Liu, Zhao-Jun Bálint Katalin Elder, David E. Perbal, Bernard Herlyn, Meenhard Juhász István (1956-) (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

3.

001-es BibID:BIBFORM039093
Első szerző:Juhász István (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus)
Cím:Repopulation of Langerhans cells during wound healing in an experimental human skin/SCID mouse model / Juhász István, Simon Miklós, Herlyn Meenhard, Hunyadi János
Dátum:1996
ISSN:0165-2478
Megjegyzések:The epidermal repopulation of Langerhans cells (LCs) during wound healing was examined using a human skin severe combined immunodeficient (SCID) mouse model. The experiments, were carried out after proving the human origin of keratinocytes repopulating the wound beds using the W6/32 monoclonal antibody. It was shown that CD1a- and HLA-DR-positive dendritic cells (mostly LCs) are already detectable 2 days after injury within the newly formed epithelium. In the excisional wounds investigated, neither HLA-DR nor ICAM-1 expression of human keratinocytes was observed. Our present data suggest that LC repopulation is an early event in the process of re-epithelization.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Immunology Letters. - 52 : 2-3 (1996), p. 125-128. -
További szerzők:Simon Miklós Herlyn, Meenhard Hunyadi János (1943-) (bőrgyógyász, kozmetológus, allergológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM033149
Első szerző:Juhász István (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus)
Cím:Stage-related structures on melanoma cells / Istvan Juhasz, Meenhard Herlyn
Dátum:1990
Tárgyszavak:Orvostudományok Klinikai orvostudományok előadáskivonat
Megjelenés:Proceedings of the International Conference held in Newcastle, 4-7th September, 1990 / ed. P. Hersey. - p. 256-267.
További szerzők:Herlyn, Meenhard
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

001-es BibID:bibEB00010212
035-os BibID:PMID:7694470
Első szerző:Juhász István (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus)
Cím:Regulation of extracellular matrix proteins and integrin cell substratum adhesion receptors on epithelium during cutaneous human wound healing in vivo / Istvan Juhasz, George F. Murphy, Horng-Chin Yan, Meenhard Herlyn, Steven M. Albelda
Dátum:1993
Megjegyzések:Although changes in extracellular matrix proteins during wound healing have been well documented, little is known about the regulation of corresponding extracellular matrix adhesion receptors (integrins). To study this process in a human in vivo model, full thickness human skin grafts were transplanted onto severe combined immunodeficient mice and deep excisional wounds involving both the epidermal and dermal layers were then made. The changes in the expression of cell matrix proteins and epithelial integrins over time were analyzed with specific antibodies using immunohistochemistry. Wounding was associated with alterations in extracellular matrix proteins, namely, loss of laminin and type IV collagen in the region of the wound and expression of tenascin and fibronectin. Changes were also noted in the integrins on the migrating keratinocytes. There was marked up-regulation of the alpha v subunit and de novo expression of the fibronectin receptor (alpha 5 beta 1) during the stage of active migration (days 1 to 3 after wounding). In the later stages of wound healing, after epithelial integrity had been established, redistribution of the alpha 2, alpha 3, alpha 6, and beta 4 collagen/laminin-binding integrin subunits to suprabasal epidermal layers was noted. Thus, during cutaneous wound healing, keratinocytes up-regulate fibronectin/fibrinogen-binding integrins and redistribute collagen/laminin-binding integrins. This study demonstrates that the human skin/severe combined immunodeficient chimera provides a useful model to study events during human wound repair.
Tárgyszavak:idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:American Journal of Pathology. - 143 : 5 (1993), p. 1458-1469. -
További szerzők:Murphy, George F. Yan, Horng-Chin Herlyn, Meenhard Albelda, Steven M.
Internet cím:elektronikus változat
Borító:

6.

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
elektronikus változat
Borító:

7.

001-es BibID:bibEB00010210
035-os BibID:PMID:8342600
Első szerző:Juhász István (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus)
Cím:Growth and invasion of human melanomas in human skin grafted to immunodeficient mice / Istvan Juhasz, Steven M. Albelda, David E. Elder, George F. Murphy, Koji Adachi, Dorothee Herlyn, Istvan T. Valyi-Nagy, Meenhard Herlyn
Dátum:1993
Megjegyzések:An orthotopic model of human melanoma was developed in which malignant cells were injected into human skin grafted to nude and SCID mice. Melanoma cells proliferated and invaded the human skin grafts with characteristic patterns. Three of six melanomas grew as multiple nodules and infiltered the grafts without major architectural changes in the dermis, whereas the others invaded the dermis along collagen fibers with prominent endothelial vessels. By contrast, melanoma cells inoculated into mouse skin grew as diffusely expanding nodules that did not invade the murine dermis. In human skin grafts, human melanoma cells were angiogenic for human blood vessels, and murine vessels were only found at the periphery of grafts. Tumor cells invaded the human vessels, and four out of seven cell lines metastasized to lungs, suggesting that this model is useful to determine in vivo the interactions between normal and malignant human cells.
Tárgyszavak:idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:American Journal of Pathology. - 143 : 2 (1993), p. 528-537. -
További szerzők:Albelda, Steven M. Elder, David E. Murphy, George F. Adachi, Koji Herlyn, Dorothee Vályi-Nagy István Herlyn, Meenhard
Internet cím:elektronikus változat
Borító:

8.

001-es BibID:bibEBI14268
Első szerző:Simon Miklós Jr.
Cím:Thrombospondin receptor (CD36) expression of human keratinocytes during wound healing in a human skin-SCID mouse skin repair model / Simon, M. Jr., Juhász, I., Herlyn, M., Hunyadi, J.
Dátum:1996
Megjegyzések:Using a human skin/severe combined immunodeficient (SCID) chimeric mouse model, we examined the keratinocyte expression of the thrombospondin receptor (CD36) and its ligand thrombospondin-1 (TSP1) in acute uninflamed wounds. Positive suprabasal keratinocyte expression of CD36 was observed as early as 30 minutes after wounding in the adjacent, intact epidermis; it disappeared 4 days later. Keratinocytes of the freshly re-epithelised wounds and those of the surrounding epidermis remained TSP1-negative throughout the whole observation period of 7 days. Our results indicate that CD36-positive keratinocytes, probably in connection with activated, TSP1-positive thrombocytes, may play an important role in the early phase of wound healing.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Dermatology. - 23 : 5 (1996), p. 305-309. -
További szerzők:Juhász István (1956-) (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus) Herlyn, Meenhard Hunyadi János (1943-) (bőrgyógyász, kozmetológus, allergológus)
Borító:

9.

001-es BibID:bibEBI12846
035-os BibID:PMID:8478142
Első szerző:Vályi-Nagy István
Cím:Spontaneous and induced differentiation of human melanoma cells / Istvan Valyi-Nagy, Ie-Ming Shih, Tibor Gyorfi, David Greenstein, Istvan Juhasz, David E. Elder, Meenhard Herlyn
Dátum:1993
Megjegyzések:Malignant melanoma cells can differentiate spontaneously in vivo and in vitro into cells with a finite lifespan. Analysis of differentiating cells from primary melanomas in culture revealed a flat, fibroblast-like morphology and expression of the fibroblast-associated marker leucine aminopeptidase (LAP). Differentiation was also observed in a minor sub-population of permanent cell lines derived from metastatic lesions. An experimental model of melanoma cell differentiation was then developed, using the pyrimidine analog bromodeoxyuridine (BUdR). BUdR-treated cells had a flat morphology, were contact-inhibited, had up to 20-fold increased surface area, expressed LAP, no longer proliferated anchorage-independently in soft agar, and 3 out of 4 cell lines were non-tumorigenic in athymic nude mice. Our results show that models of differentiation of melanoma cells can be established that help to define pathways of differentiation.
Tárgyszavak:idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:International Journal of Cancer. - 54 : 1 (1993), p. 159-165. -
További szerzők:Shih, Ie-Ming Győrfi Tibor Greenstein, David Juhász István (1956-) (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus) Elder, David E. Herlyn, Meenhard
Internet cím:elektronikus változat
DOI
Borító:

10.

001-es BibID:bibEBI12844
Első szerző:Vályi-Nagy István
Cím:Undifferentiated keratinocytes control growth, morphology, and antigen expression of normal melanocytes through cell-cell contact / Vályi-Nagy, I. T. , Hirka, G., Jensen, P. J., Shih, I. M., Juhász, I., Herlyn, M.
Dátum:1993
ISSN:0023-6837 1530-0307
Megjegyzések:BACKGROUND: Melanocytes in the normal human epidermis are generally dendritic and neither proliferate nor express melanoma-associated antigens. In culture, on the other hand, melanocytes are bi- to tripolar, proliferate with 2 to 4 day doubling times, and express melanoma-associated antigens. This observation prompted us to investigate the regulatory role of keratinocytes for growth, morphology, and antigen expression of melanocytes. EXPERIMENTAL DESIGN: Melanocytes and keratinocytes were cultured under three different co-culture conditions: (a) separated by a semiporous membrane, (b) in monolayer cultures allowing direct contact between cells, and (c) in three-dimensional epidermal reconstructs. RESULTS: Melanocytes separated from keratinocytes by semiporous membranes remained di- and tripolar and could not proliferate in medium optimal for keratinocytes. When cell-cell contact was established between melanocytes and undifferentiated, but not differentiated, keratinocytes, melanocytes proliferated at a rate similar to keratinocytes and they developed multiple dendrites. In co-cultures allowing the multi-layered growth of keratinocytes, melanocytes were nonproliferative when juxtaposed to undifferentiated keratinocytes in the basal layer, but proliferated when surrounded by differentiated keratinocytes in the intermediate and upper layers. Expression of melanoma-associated antigens on melanocytes decreased to similar levels as in normal skin when melanocytes were in direct contact with undifferentiated, but not differentiated, keratinocytes. CONCLUSIONS: Undifferentiated, but not differentiated, keratinocytes control growth, morphology, and antigen expression of melanocytes through direct cell-cell contact. These results suggest that the phenotypic characteristics of nevus and melanoma cells in the dermis, i.e., proliferation and expression of tumor-associated antigens, may be due to their loss of contact with undifferentiation keratinocytes.
Tárgyszavak:idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Laboratory Investigation. - 69 : 2 (1993), p. 152-159. -
További szerzők:Hirka G. Jensen, P. J. Shih, Ie-Ming Juhász István (1956-) (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus) Herlyn, Meenhard
Borító:

11.

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
elektronikus változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.