TY - JOUR
T1 - Oxaliplatin
T2 - Preclinical perspectives on the mechanisms of action, response and resistance
AU - Seetharam, R. N.
AU - Sood, A.
AU - Goel, S.
N1 - Copyright:
Copyright 2010 Elsevier B.V., All rights reserved.
PY - 2009/9/24
Y1 - 2009/9/24
N2 - Oxaliplatin is a third-generation platinum compound that has shown a wide range of antitumour activity in metastatic cancer and in multiple cell lines. It contains a diaminocyclohexane carrier ligand and is one of the least toxic platinum agents. In the past decade, the use of oxaliplatin for the treatment of colorectal cancer has become increasingly popular because neither cisplatin nor carboplatin demonstrate significant activity. Similar to cisplatin, oxaliplatin binds to DNA leading to GG intrastrand cross-links. Oxaliplatin differs from its parent compounds in its mechanisms of action, cellular response and development of resistance, which are not fully understood. Like most chemotherapeutic agents, efficacy of oxaliplatin is limited by the development of cellular resistance. ERCC1 (Excision Repair Cross-Complementation group 1) mediated nucleotide excision repair pathway appears to be the major pathway involved in processing oxaliplatin because loss of mismatch repair does not lead to oxaliplatin resistance. Recent findings support the involvement of many genes and different pathways in developing oxaliplatin resistance. This mini-review focuses on the effects of oxaliplatin treatment on cell lines with special emphasis to colorectal cell lines.
AB - Oxaliplatin is a third-generation platinum compound that has shown a wide range of antitumour activity in metastatic cancer and in multiple cell lines. It contains a diaminocyclohexane carrier ligand and is one of the least toxic platinum agents. In the past decade, the use of oxaliplatin for the treatment of colorectal cancer has become increasingly popular because neither cisplatin nor carboplatin demonstrate significant activity. Similar to cisplatin, oxaliplatin binds to DNA leading to GG intrastrand cross-links. Oxaliplatin differs from its parent compounds in its mechanisms of action, cellular response and development of resistance, which are not fully understood. Like most chemotherapeutic agents, efficacy of oxaliplatin is limited by the development of cellular resistance. ERCC1 (Excision Repair Cross-Complementation group 1) mediated nucleotide excision repair pathway appears to be the major pathway involved in processing oxaliplatin because loss of mismatch repair does not lead to oxaliplatin resistance. Recent findings support the involvement of many genes and different pathways in developing oxaliplatin resistance. This mini-review focuses on the effects of oxaliplatin treatment on cell lines with special emphasis to colorectal cell lines.
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U2 - 10.3332/ecancer.2009.153
DO - 10.3332/ecancer.2009.153
M3 - Short survey
AN - SCOPUS:77956050458
SN - 1754-6605
VL - 3
JO - ecancermedicalscience
JF - ecancermedicalscience
IS - 1
M1 - 153
ER -