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Different drug sensitivity in two neuroblastoma cell lines established from the same patient before and after chemotherapy
Author(s) -
Kuroda Hiroshi,
Sugimoto Tohru,
Ueda Kazumitsu,
Tsuchida Shigeki,
Horii Yoshihiro,
Inazawa Johji,
Sato Kiyomi,
Sawada Tadashi
Publication year - 1991
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910470518
Subject(s) - chemotherapy , neuroblastoma , drug , medicine , sensitivity (control systems) , oncology , cancer research , cell culture , pharmacology , biology , genetics , electronic engineering , engineering
Abstract Drug resistance is one of the major impediments to the treatment of advanced neuroblastoma. Two neuroblastoma cell lines established from the same patient before (KP‐N‐AY) and after (KP‐N‐AYR) chemotherapy are described. Both cell lines were established from bone‐marrow metastases of a 2½‐year‐old patient with stage IV neuroblastoma. Chromosomal analysis, catecholamine assessment and the surface membrane phenotype of these cell lines confirmed that the tumors were of neuroblastoma origin. Compared with the KP‐N‐AY cell line, the KP‐N‐AYR line had decreased N‐ myc amplification but increased N‐ myc expression. An in vitro sensitivity test using a clonogenic assay showed the KP‐N‐AYR cell line to be 3.0‐fold resistant to adriamycin and 2.7‐fold resistant to cis ‐platinum as compared with the KP‐N‐AY cell line. The expression of the multi‐drug‐resistance gene ( MDR I) was not observed in either cell line by the ribonuclease protection assay. The KP‐N‐AY cell line revealed only faint MDR I RNA by the polymerase chain reaction, whereas the KP‐N‐AYR cell line had no expression of the MDR I gene. The level of glutathione‐S‐transferase‐π was significantly higher in the KP‐N‐AYR cell line than in the KP‐N‐AY cell line. These findings suggest that the development of clinical drug resistance may be associated with the enhanced glutathione‐S‐transferase‐π activity but not with MDR I gene expression.