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epipodophyllotoxin/hypersensitivity
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Diagnosis and management of hypersensitivity reactions related to common cancer chemotherapy agents.
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OBJECTIVE
To review clinical hypersensitivity reactions related to common cancer chemotherapy agents and to discuss potential management strategies.
METHODS
PubMed searches were performed for articles published from 1970 to 2008 regarding hypersensitivity to cancer chemotherapy and related agents
Prevention and management of antineoplastic-induced hypersensitivity reactions.
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Acute hypersensitivity reactions (HSRs) are an unpredictable and potentially catastrophic complication of treatment with chemotherapeutic agents. Reactions may affect any organ system in the body and range widely in severity from mild pruritus to systemic anaphylaxis. Certain classes of
Nuclear topoisomerase II levels correlate with the sensitivity of mammalian cells to intercalating agents and epipodophyllotoxins.
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We have investigated the biochemical basis for the hypersensitivity to intercalating agents and epipodophyllotoxins of a Chinese hamster cell mutant, ADR-1. More topoisomerase II-induced DNA strand breaks are accumulated by ADR-1 than by parental CHO-K1 cells following exposure to the intercalating
Review of hypersensitivity reactions to antineoplastic agents.
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OBJECTIVE
To review the characteristics and management of hypersensitivity reactions caused by antineoplastic agents.
METHODS
We conducted a search in the Pubmed and EMBASE databases for the last 10 years.
RESULTS
Almost all chemotherapeutic agents have the potential to cause hypersensitivity
The complex clinical picture of presumably allergic side effects to cytostatic drugs: symptoms, pathomechanism, reexposure, and desensitization.
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The number of drugs used for the treatment of different types of cancers is constantly increasing and actually exceeds 100 distinct chemical formulations. The use of most cytotoxic agents is associated with potential hypersensitivity reactions, and the constant increase of their administration has
Chemotherapy and biotherapy-induced hypersensitivity reactions.
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Nearly all chemotherapy and biotherapy drugs used in cancer treatment today can cause hypersensitivity reactions. Certain groups of drugs frequently associated with these reactions include the asparaginases, taxanes, platinum compounds, epipodophyllotoxins, and the monoclonal antibodies. Recognizing
Prevention and handling of acute allergic and infusion reactions in oncology.
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Drug hypersensitivity reactions (HSR) are adverse events resembling allergy which occur at therapeutic doses. Both anticancer chemotherapeutics and monoclonal antibodies have the potential for acute HSR. all infusion reactions involve the immune system; however, some (anaphylactic) are allergic in
Cyclic AMP-dependent protein kinase type I is involved in hypersensitivity of human breast cells to topoisomerase II inhibitors.
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Topoisomerase II (Topo II) is an essential enzyme that catalyzes the breakage of double-strand DNA and is the target of several effective anticancer drugs, including the epipodophyllotoxins. The regulatory subunits of the cyclic AMP-dependent protein kinase are differentially expressed in normal and
Hypersensitivity reactions to chemotherapeutic drugs.
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There is an ever-increasing number of therapeutics used to treat cancer. A recent publication listed 86 currently available antineoplastic medications. Despite this large number, hypersensitivity reactions are not common except with platinum compounds (cisplatin, carboplatin), epipodophyllotoxins
Adverse events to nontargeted and targeted chemotherapeutic agents: emphasis on hypersensitivity responses.
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Use of cytotoxic agents is associated with potential hypersensitivity reactions which are common with platinum compounds, L-asparaginase, taxanes, procarbazine and epipodophyllotoxins. Mechanisms underlying the reactions may involve IgE, non-allergic or a number of pathogenetically unclear events.
Hypersensitivity of lymphoblastoid lines derived from ataxia telangiectasia patients to the induction of chromosomal aberrations by etoposide (VP-16).
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Mammalian DNA topoisomerase II represents the cellular target of many antitumor drugs, such as epipodophyllotoxin VP-16 (etoposide). The mechanism by which VP-16 exerts its cytotoxic and antineoplastic actions has not yet been firmly established, although the unique correlation between sensitivity
Systemic therapy emergencies.
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Systemic oncologic therapies can cause multiple emergency situations. There are, however, two unique emergencies directly related to chemotherapy administration: drug extravasation and hypersensitivity reactions (HSRs). Most drugs can cause varying degrees of local tissue injury when extravasated.
Isolation of two Chinese hamster ovary cell mutants hypersensitive to topoisomerase II inhibitors and cross-resistant to peroxides.
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We have isolated two Chinese hamster ovary cell lines, designated ADR-4 and ADR-5, which exhibit hypersensitivity to intercalating agents and epipodophyllotoxins. These drugs are thought to exert their cytotoxicity via an interaction with the enzyme topoisomerase II. However, there is no apparent
Cross-sensitivity to topoisomerase II inhibitors in cytotoxic drug-hypersensitive Chinese hamster ovary cell lines.
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We have isolated a Chinese hamster ovary cell line, designated ADR-1, which exhibits hypersensitivity to a range of drugs which are thought to inhibit the action of the enzyme topoisomerase II. These include anthracyclines, other classes of intercalating agents, and the epipodophyllotoxin,
Long-term effects of intravenous hyperalimentation administered during intensive chemotherapy for small cell bronchogenic carcinoma.
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Sixty-five patients with small cell bronchogenic carcinoma received their first two of three courses of intensive induction chemotherapy with (30 patients) or without (35 patients) intravenous hyperalimentation (IVH). Patients predominantly had extensive disease (55%), Zubrod's performance status 0
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