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001-es BibID:	BIBFORM076959
035-os BibID:	(WoS)000465167600015 (Scopus)85058854414
Első szerző:	Abdelwahab, E. M. M.
Cím:	Mitochondrial dysfunction is a key determinant of the rare disease lymphangioleiomyomatosis and provides a novel therapeutic target / E. M. M. Abdelwahab, S. Pal, K. Kvell, V. Sarosi, P. Bai, R. Rue, V. Krymskaya, D. McPhail, A. Porter, J. E. Pongracz
Dátum:	2019
ISSN:	0950-9232
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Oncogene. - 38 (2019), p. 3093-3101. -
További szerzők:	Pal, Sunita Kvell Krisztián Sárosi Veronika Bai Péter (1976-) (biokémikus) Rue, R. Krymskaya, V. McPhail, D. Porter, A. Pongrácz Judit
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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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
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001-es BibID:	BIBFORM045966
Első szerző:	Remenyik Éva (bőrgyógyász)
Cím:	Antigen-specific immunity does not mediate acute regression of UVB-induced p53-mutant clones / Éva Remenyik, Norbert M. Wikonkál, Wengeng Zhang, Vipin Paliwal, Douglas E. Brash
Dátum:	2003
ISSN:	0950-9232
Megjegyzések:	Chronic irradiation of human or murine epidermis with ultraviolet B (UVB) induces clones of p53-mutant keratinocytes. Clones precede and parallel the induction of carcinomas, suggesting that they are an early stage of UVB carcinogenesis. In the absence of UVB, these clones rapidly regress. For UVB-induced murine skin tumors and papillomas, regression is known to involve antigen-specific immunity. To determine whether antigen-specific immunity influences the creation, expansion, or regression of p53-mutant clones, we studied Rag1 knockout mice deficient in the recombination activating gene 1 required for development of B, alphabetaT, gammadeltaT, and natural killer T cells. Since tissue homeostasis could affect proliferation or persistence of clones, we also examined the effect of Rag1 on UVB-induced hyperplasia and apoptosis. Mice were irradiated with UVB daily for 7-11 weeks to create p53-mutant clones, and then retained in the absence of UV. After UV ended, epidermal thickness decreased and p53-mutant clones observed in the epidermal sheets regressed, with no significant differences between Rag1(-/-) and wild type. During the initial chronic UVB irradiation, increasing irradiation time increased both the number and size of p53-mutant clones, with no significant difference between genotypes. We conclude that antigen-specific immunity is not involved in the initiation, expansion, or acute regression of p53-mutant clones.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Oncogene. - 22 : 41 (2003), p. 6369-6376. -
További szerzők:	Wikonkál Norbert, M. Zhang, Wengeng Paliwal, Vipin Brash, Douglas E.
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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