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1.
001-es BibID:
BIBFORM001053
035-os BibID:
(scopus)34447298092 (wos)000248154300017
Első szerző:
Barok Márk (biofizikus)
Cím:
Trastuzumab causes antibody-dependent cellular cytotoxicity-mediated growth inhibition of submacroscopic JIMT-1 breast cancer xenografts despite intrinsic drug resistance / Barok M., Isola J., Pályi-Krekk Zs., Nagy P., Juhász I., Vereb Gy., Kauraniemi P., Kapanen A., Tanner M., Vereb Gy., Szöllősi J.
Dátum:
2007
Megjegyzések:
Trastuzumab is a recombinant antibody drug that is widely used for the treatment of breast cancer. Despite encouraging clinical results, some cancers are primarily resistant to trastuzumab, and a majority of those initially responding become resistant during prolonged treatment. The mechanisms of trastuzumab resistance have not been fully understood. We examined the role of antibody-dependent cellular cytotoxicity (ADCC) using JIMT-1 cells that are ErbB2 positive but intrinsically resistant to trastuzumab in vitro. Unexpectedly, in experiments mimicking adjuvant therapy of submacroscopic disease in vivo (JIMT-1 cells inoculated s.c. in severe combined immunodeficiency mice), trastuzumab was able to inhibit the outgrowth of macroscopically detectable xenograft tumors for up to 5-7 weeks. The effect is likely to be mediated via ADCC because trastuzumab-F(ab')(2) was ineffective in this model. Moreover, in vitro ADCC reaction of human leukocytes was equally strong against breast cancer cells intrinsically sensitive (SKBR-3) or resistant (JIMT-1) to trastuzumab or even against a subline of JIMT-1 that was established from xenograft tumors growing despite trastuzumab treatment. These results suggest that ADCC may be the predominant mechanism of trastuzumab action on submacroscopic tumor spread. Thus, measuring the ADCC activity of patient's leukocytes against the tumor cells may be a relevant predictor of clinical trastuzumab responsiveness in vivo.
Tárgyszavak:
Orvostudományok
Természettudományok
Elméleti orvostudományok
Biológiai tudományok
idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
ErbB2 receptor
trastuzumab
breast cancer
antibody therapy
Megjelenés:
Molecular Cancer Therapeutics. - 6 : 7 (2007), p. 2065-2072. -
További szerzők:
Isola, Jorma
Pályiné Krekk Zsuzsanna (1974-) (molekuláris biológus)
Nagy Péter (1971-) (biofizikus)
Juhász István (1956-) (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus)
Vereb György (1938-) (biokémikus, sejtbiológus)
Kauraniemi, Päivikki
Kapanen, Anita I.
Tanner, Minna
Vereb György (1965-) (biofizikus, orvos)
Szöllősi János (1953-) (biofizikus)
Internet cím:
elektronikus változat
DOI
Borító:
Saját polcon:
2.
001-es BibID:
BIBFORM004879
Első szerző:
Nagy Péter (biofizikus)
Cím:
Decreased accessibility and lack of activation of ErbB2 in JIMT-1, a herceptin-resistant, MUC4-expressing breast cancer cell line / Nagy, P., Friedlander, E., Tanner, M., Kapanen, A. I., Carraway, K. L., Isola, J., Jovin, T. M.
Dátum:
2005
ISSN:
0008-5472
Megjegyzések:
Overexpression of erbB2 in breast tumors is associated with poor prognosis and is a target of receptor-oriented cancer therapy. Trastuzumab (Herceptin), a monoclonal antibody against a membrane-proximal epitope in the extracellular region of erbB2, shows a therapeutic effect against a fraction of erbB2-amplified breast tumors. Unfortunately, resistance to Herceptin is common, and its cause is as yet unclear. Here we investigated the properties of erbB2 in a Herceptin-resistant cell line, JIMT-1, established from a breast cancer patient showing erbB2 gene amplification and primary resistance to Herceptin. The expression profile of erbB proteins, Herceptin-induced erbB2 internalization, and down-regulation in JIMT-1 were similar to those in Herceptin-sensitive lines. However, the mean number of Herceptin Mab binding sites in JIMT-1 was 1/5 that of the expressed erbB2 molecules, although 5% to 10% of the cells showed a approximately 10-fold higher Herceptin binding than the main population. Herceptin Fab and Mab 2C4, an antibody binding to an epitope in the ectodomain further removed from the membrane, bound more efficiently to JIMT-1 cells than Herceptin Mab, implying that erbB2 was partly masked. The expression of MUC4, a membrane-associated mucin that according to reports contributes to the masking of membrane proteins, was higher in JIMT-1 than in Herceptin-sensitive lines, and its level was inversely correlated with the Herceptin binding capacity of single cells. Knockdown of MUC4 expression by RNA interference increased the binding of Herceptin. Western blotting showed a low level of proteolytic processing, shedding, and tyrosine phosphorylation of erbB2 in JIMT-1. The latter finding may explain its Herceptin-resistant phenotype characterizing both the low and high Herceptin binding subpopulations. We conclude that masking of erbB2 in JIMT-1 leads to diminished Herceptin binding and isolation of erbB2 from its normal interaction and activation partners.
Tárgyszavak:
Orvostudományok
Elméleti orvostudományok
idegen nyelvű folyóiratközlemény külföldi lapban
Antibodies
Antibodies,Monoclonal
Antineoplastic Agents
Binding Sites
biosynthesis
Breast Neoplasms
Cell Line
Cell Line,Tumor
Cells
chemistry
Down-Regulation
Drug Resistance,Neoplasm
drug therapy
Enzyme Activation
enzymology
Epitopes
Gene Amplification
Humans
immunology
Membrane Proteins
metabolism
Metalloproteases
Mucins
pharmacology
Phenotype
Phosphorylation
Proteins
Receptor,erbB-2
Research
Support
therapy
Tyrosine
Megjelenés:
Cancer Research. - 65 : 2 (2005), p. 473-482. -
További szerzők:
Friedländer Elza (1980-) (biofizikus)
Tanner, Minna
Kapanen, Anita I.
Carraway, Kermit L.
Isola, Jorma
Jovin, Thomas M.
Internet cím:
elektronikus változat
Borító:
Saját polcon:
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