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001-es BibID:	BIBFORM005174
035-os BibID:	(scopus)38349044364 (wos)000253278400023
Első szerző:	Barok Márk (biofizikus)
Cím:	Trastuzumab decreases the number of circulating and disseminated tumor cells despite trastuzumab resistance of the primary tumor / Márk Barok, Margit Balázs, Péter Nagy, Zsuzsa Rákosy, Andrea Treszl, Enikő Tóth, István Juhász, John W. Park, Jorma Isola, György Vereb, János Szöllősi
Dátum:	2008
ISSN:	304-3835 (Print)
Megjegyzések:	We have recently shown that despite of the fact that the ErbB2-positive JIMT-1 human breast cancer cells intrinsically resistant to trastuzumab in vitro, trastuzumab inhibited the outgrowth of early phase JIMT-1 xenografts in SCID mice via antibody-dependent cellular cytotoxicity (ADCC). Here we show that trastuzumab significantly reduces the number of circulating and disseminated tumor cells (CTCs and DTCs) in this xenograft model system at a time when the primary tumor is already unresponsive to trastuzumab. This observation suggests that ErbB2 positive CTCs and DTCs might be sensitive to trastuzumab-mediated ADCC even if when the primary tumor is already non-responsive. Thus, trastuzumab treatment might also be beneficial in the case of patients with breast cancer that is already trastuzumab resistant.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk analysis Animals antagonists and inhibitors Antibodies Antibodies, Monoclonal Antigens Antigens, CD45 Antineoplastic Agents article Biophysics blood Bone Marrow Breast Neoplasms Cell Line, Tumor Cells Chromosomes, Human,X drug effects Drug Resistance, Neoplasm drug therapy EGFR Epidermal Growth Factor ErbB2 Female genetics Histocompatibility Antigens Histocompatibility Antigens Class I Human Humans Hungary Immunohistochemistry immunology In Situ Hybridization,Fluorescence In Vitro metabolism Mice Mice, Scid mouse Neoplasm Circulating Cells Neoplasm Metastasis pathology pharmacology Receptor, Epidermal Growth Factor Research Research Support Support therapeutic use Time Factors Trastuzumab resistance Xenograft Model Antitumor Assays egyetemen (Magyarországon) készült közlemény
Megjelenés:	Cancer Letters. - 260 : 1-2 (2008), p. 198-208. -
További szerzők:	Balázs Margit (1952-) (sejtbiológus, molekuláris genetikus) Nagy Péter (1971-) (biofizikus) Rákosy Zsuzsa (1978-) (sejtbiológus, molekuláris biológus, genetikus) Treszl Andrea (1974-) (molekuláris biológus) Tóth Enikő Juhász István (1956-) (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus) Park, John W. Isola, Jorma Vereb György (1965-) (biofizikus, orvos) Szöllősi János (1953-) (biofizikus)
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001-es BibID:	BIBFORM042484
035-os BibID:	(scopus)23844475901 (wos)000231845600013
Első szerző:	Mocanu, Maria-Magdalena
Cím:	Associations of ErbB2, beta1-integrin and lipid rafts on Herceptin (Trastuzumab) resistant and sensitive tumor cell lines / Maria-Magdalena Mocanu, Zsolt Fazekas, Miklós Petrás, Péter Nagy, Zsolt Sebestyén, Jorma Isola, József Tímár, John W. Park, György Vereb, János Szöllősi
Dátum:	2005
ISSN:	0304-3835
Megjegyzések:	ErbB2-mediated transmembrane signaling is a key target of novel anticancer agents such as Herceptin. Our comparison of Herceptin resistant (JIMT-1, MKN-7) and sensitive (SKBR-3, N-87) cell lines demonstrates the importance of ErbB2 association patterns involving integrins and lipid rafts. Flow cytometric FRET and confocal microscopic measurements revealed colocalization and molecular proximity between b1-integrins and ErbB2, as well as their association with lipid rafts. A weak functional interaction between ErbB2 and b1-integrin and the fact that ErbB2 did not co-patch with b1-integrins uponcrosslinking imply that ErbB2 and b1-integrin define two distinct molecular association clusters from a functional point of view. Although Herceptin-sensitive cell lines expressed more ErbB2 and fewer b1-integrin molecules on their surface than their resistant counterparts, this finding probably does not explain the Herceptin resistant phenotype due to the weak interaction between b1-integrins and ErbB2. Our results imply that the true significance of the expression profile of proteins involved inoncogenesis can only be understood after characterizing their molecular interactions.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Antibodies Antibodies,Monoclonal Antigens,CD29 Biophysics Breast Neoplasms Cell Line Cell Membrane Drug Resistance,Neoplasm Humans Hungary Membrane Microdomains metabolism pathology pharmacology Phenotype physiology Proteins Receptor,erbB-2 Research Support Tumor Cells,Cultured egyetemen (Magyarországon) készült közlemény
Megjelenés:	Cancer Letters. - 227 : 2 (2005), p. 201-212. -
További szerzők:	Fazekas Zsolt (1971-) (biofizikus) Petrás Miklós (1977-) (orvos) Nagy Péter (1971-) (biofizikus) Sebestyén Zsolt Isola, Jorma Timár József Park, John W. Vereb György (1965-) (biofizikus, orvos) Szöllősi János (1953-) (biofizikus)
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001-es BibID:	BIBFORM005188
Első szerző:	Pályiné Krekk Zsuzsanna (molekuláris biológus)
Cím:	EGFR and ErbB2 are functionally coupled to CD44 and regulate shedding, internalization and motogenic effect of CD44 / Palyi-Krekk, Z., Barok, M., Kovacs, T., Saya, H., Nagano, O., Szollosi, J., Nagy, P.
Dátum:	2008
ISSN:	304-3835 (Print)
Megjegyzések:	Activation of the ErbB family of receptor tyrosine kinases is involved in a range of human cancers. Transmembrane signaling mediated by ErbB proteins is stimulated by peptide growth factors and is blocked by monoclonal antibodies such as trastuzumab and pertuzumab. ErbB receptors exert their function in conjunction with non-ErbB proteins, e.g. CD44. Here we show that epidermal growth factor (EGF) and heregulin induce CD44 shedding in JIMT-1, an ErbB2-overexpressing cell line resistant to trastuzumab, accompanied by internalization and intramembrane proteolysis of CD44 and enhanced cellular motility. These effects of EGF and heregulin are blocked by pertuzumab. Trastuzumab inhibits the heregulin- and hyaluronan oligosaccharide-induced shedding and internalization of CD44 and their motogenic effect. Trastuzumab also blocks CD44 shedding from JIMT-1 xenograft tumors in vivo. At the same time the internalization rate of trastuzumab is increased by hyaluronan oligosaccharide treatment in vitro. Our experiments point to an unexpected, but potentially important mechanism of action of ErbB receptor-targeted monoclonal antibodies used in the treatment of cancer.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Antibodies article Biophysics CD44 Cell Line EGFR Epidermal Growth Factor ErbB2 Human Hungary In Vitro Proteins Receptor tyrosine kinase transmembrane signaling Tyrosine
Megjelenés:	Cancer Letters 263 : 2 (2008), p. 231-242. -
További szerzők:	Barok Márk (1976-) (biofizikus) Kovács Tamás (1985-) (általános orvos) Saya, Hideyuki Nagano, Osamu Szöllősi János (1953-) (biofizikus) Nagy Péter (1971-) (biofizikus)
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