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PMID: 8381186 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S. Review

The current status of camptothecin analogues as antitumor agents.

Journal of the National Cancer Institute ·Vol. 85 ·No. 4 ·1993-02-17 ·Pages 271-91

Slichenmyer WJ, Rowinsky EK, Donehower RC, Kaufmann SH

Abstract

The nuclear enzyme topoisomerase I (topo I) has been recently recognized as the target for the anticancer drug camptothecin (CPT) and its derivatives. Two of the agents that target this enzyme--topotecan (TPT) and CPT-11--appear to be active against a broad range of human tumors. In the following presentation, we review 1) the role of topo I in normal cells, 2) the chemistry and proposed mechanism of action of CPT and its analogues, 3) the results of preclinical and clinical testing of TPT and CPT-11, and 4) mechanisms of resistance to these agents. In normal cells, topo I is thought to be involved in gene transcription and DNA replication. During the course of its normal catalytic cycle, topo I transiently forms a covalent bond with DNA. CPT and its derivatives slow the religation step of the enzyme and stabilize the covalent adduct between topo I and DNA. In S-phase cells, advancing replication forks convert these topo I-DNA adducts into double-strand breaks that appear to be responsible for the cytotoxicity of these agents. Preclinical studies demonstrate antineoplastic activity for TPT and CPT-11 in a variety of tumor models. Phase I studies have identified neutropenia as the dose-limiting toxicity for both drugs. Gastrointestinal effects might also be dose-limiting for CPT-11 administered on some schedules. CPT-11 has shown antitumor activity in phase II trials for patients with carcinomas of lung, cervix, ovary, colon, and rectum and for patients with non-Hodgkin's lymphoma. Phase II studies of TPT are in progress. Resistance to the cytotoxic effects of these agents might result from decreased production of topo I or from production of a mutated form of topo I. In addition, decreased metabolic activation of CPT-11 (which is a pro-drug) and active efflux of TPT by P-glycoprotein-mediated transport might contribute to resistance. As agents with a novel mechanism of action, tolerable toxicity, and encouraging antitumor activity in early clinical trials, TPT and CPT-11 are undergoing further clinical development. If these agents can be successfully combined with other active chemotherapy agents, the topo I-directed agents offer the potential for significant advances in the treatment of patients with a variety of malignancies.

MeSH Terms
Animals Antineoplastic Agents, Phytogenic Camptothecin/analogs & derivatives,pharmacology,therapeutic use Clinical Trials as Topic Combined Modality Therapy DNA Topoisomerases, Type I/physiology Forecasting Humans Irinotecan Topotecan
Chemicals
Antineoplastic Agents, Phytogenic Irinotecan Topotecan DNA Topoisomerases, Type I Camptothecin
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Slichenmyer W J
Johns Hopkins Oncology Center, Baltimore, MD 21287.
Rowinsky E K
Donehower R C
Kaufmann S H
Article Info
Journal
Journal of the National Cancer Institute
Abbr.
J Natl Cancer Inst
ISSN
0027-8874
Published
1993-02-17
Pages
271-91
Language
English
Region
United States
NLM ID
7503089
Subset
IM
Grants
NCI NIH HHS · CA-50435 · United States
NCI NIH HHS · K12CA-01709 · United States
NCI NIH HHS · N01CM-07302 · United States
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