Secondary Malignancies Following Cancer Chemotherapy

Boffetta, Paolo; Kaldor, John

doi:10.3109/02841869409121767

Cited by 105 publications

(73 citation statements)

References 35 publications

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“…However, few secondary malignancies have been definitely linked to chemotherapy, since studies on this problem are complicated by methodological problems. 44 A causal relationship has been established between alkylating agents and leukaemia and between cyclophosphamide and bladder cancer. 44 In the orbito-ocular region, pleomorphic adenoma of the lacrimal gland has been reported in a child after treatment of acute lymphoblastic leukaemia.…”

Section: Second Orbito-ocular Malignancymentioning

confidence: 99%

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Toxicidad ocular de la quimioterapia sistémica anticancerosa

Omoti

2006

Pharmacy pract. (Granada Ed. impr.)

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*The increased use of chemotherapeutic agents has resulted in longer cancer patient survival. Consequently the ophthalmologist is seeing more patients with adverse ocular side effects secondary to these antineoplastic agents. Ocular toxicity induced by cancer chemotherapy includes a broad spectrum of disorders, reflecting the unique anatomical, physiological and biochemical features of the eye. Understanding the ocular side effects will assist the ophthalmologist and oncologist to recognize them early and intervene before blindness occurs. Anticipation of various treatmentrelated toxicities may also provide the opportunity for pharmacists to develop intervention strategies that could minimize or eliminate an expected side effect. The ophthalmologist should examine patients on anticancer therapy at baseline and three monthly thereafter. The various ocular side effects of anticancer chemotherapeutic agents, tamoxifen, and interferon on the adnexia, anterior segment, posterior segment and neuro-ophthalmic structures were reviewed.

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Section: Second Orbito-ocular Malignancymentioning

confidence: 99%

“…44 A causal relationship has been established between alkylating agents and leukaemia and between cyclophosphamide and bladder cancer. 44 In the orbito-ocular region, pleomorphic adenoma of the lacrimal gland has been reported in a child after treatment of acute lymphoblastic leukaemia. 45 …”

Section: Second Orbito-ocular Malignancymentioning

confidence: 99%

Toxicidad ocular de la quimioterapia sistémica anticancerosa

Omoti

2006

Pharmacy pract. (Granada Ed. impr.)

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“…5 The drug resistance gene O 6 -methylguanine-DNA-methyltransferase (MGMT) codes for a DNA repair enzyme that when overexpressed renders normal mammalian cells resistant to O 6 -alkylating agents, such as the nitrosoureas and related methylating compounds. 8,9,43 However, since these antineoplastic drugs produce DNA damage which may have toxic or mutagenic repercussions, 11 their use for dominant selection of gene-modified cells may be hazardous. Alternative dominant selectable markers that are well-defined and widely utilized comprise the mutant variants of the human dihydrofolate reductase (DHFR) gene which maintain a role in folate metabolism when introduced into cells, but confer drug resistance against the cytotoxicity of antifolates, such as methotrexate and trimetrexate.…”

Section: Figure 5 Dose-dependent Selection and Enrichment Of Cd-ires-mentioning

confidence: 99%

“…For instance, cells modified with the prokaryotic Neo R gene may elicit an immune reaction in vivo, 10 MDR-transduced hemato- poietic stem cells, when transplanted in mice, can lead to a myeloproliferative syndrome, 5 and MGMT gene-modified cells require selection with the DNA damaging alkylating agents. 11 Desirable features for a drug selectable marker would include low or absent immunogenicity, little or no collateral biochemical perturbation of engineered cells and lastly, chemical selection with drugs having low mutagenic activity.…”

Section: Introductionmentioning

confidence: 99%

Human cytidine deaminase as an ex vivo drug selectable marker in gene-modified primary bone marrow stromal cells

et al. 2002

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Naturally occurring drug resistance genes of human origin can be exploited for selection of genetically engineered cells co-expressing a desired therapeutic transgene. Their nonimmunogenicity in clinical applications would be a major asset. Human cytidine deaminase (hCD) is a chemoresistance gene that inactivates cytotoxic cytosine nucleoside analogs, such as cytosine arabinoside (Ara-C). The aim of this study was to establish if the hCD gene can serve as an ex vivo dominant selectable marker in engineered bone marrow stromal cells (MSCs). A bicistronic retrovector comprising the hCD cDNA and the green fluorescent protein (GFP) reporter gene was generated and used for transduc

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“…In the bone marrow acute toxicity frequently manifests as myelosuppression whilst chronic injury is more insidious and may result in the development of a secondary malignancy such as leukaemia. 1 Such myelotoxicity constrains the dose and frequency of drug exposure. A possible solution to this problem is to enhance the resistance of sensitive tissues to these effects.…”

Section: Introductionmentioning

confidence: 99%

Protection of committed murine haemopoietic progenitors against BCNU toxicity does not predict protection of primitive, multipotent spleen colony-forming cells – implications for chemoprotective gene therapy

et al. 1999

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The effect of expression of an O 6 -benzylguanine (O 6 -beG)-resistant mutant (hATPA/GA) of human O 6 -alkylguanine-DNA alkyltransferase (ATase) on the in vivo toxicity and clastogenicity of the anti-tumour agent N,NЈ-bis(2-chloroethyl)-Nnitrosourea (BCNU) to murine bone marrow has been investigated. When compared with control animals, the bipotent granulocyte-macrophage colony-forming (GM-CFC) progenitor population of the hATPA/GA transduced mice were somewhat more resistant to BCNU (1.4-fold, P = 0.047) and this effect was more significant in the presence of the ATase inactivator O 6 -beG (3.5-fold, P = 0.001). The polychromatic erythrocytes were also significantly protected against BCNU-induced clastogenicity both in the presence (P Ͻ 0.001) and absence of O 6 -beG (P Ͻ 0.05). The primitive, multipotent spleen colony-forming cells (CFU-S) in these animals also showed moderate (1.6-fold, P = 0.034) protection in the absence of O 6 -beG but in the presence of the inactivator they remained as sensitive to BCNU toxicity as those in the control animals (P = 0.133). This result contrasts with previous findings demonstrating significant hATPA/GAmediated, O 6 -beG-resistant protection against the toxicity and clastogenicity of a number of O 6 -alkylating agents, including temozolomide, fotemustine and chlorozotocin. The possibility that our strategy for protective gene therapy may be highly agent and cell-type specific is unexpected and has possible implications for clinical trials of this approach using BCNU or related agents.

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Secondary Malignancies Following Cancer Chemotherapy

Cited by 105 publications

References 35 publications

Toxicidad ocular de la quimioterapia sistémica anticancerosa

Toxicidad ocular de la quimioterapia sistémica anticancerosa

Human cytidine deaminase as an ex vivo drug selectable marker in gene-modified primary bone marrow stromal cells

Protection of committed murine haemopoietic progenitors against BCNU toxicity does not predict protection of primitive, multipotent spleen colony-forming cells – implications for chemoprotective gene therapy

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