Chemoprotection of normal tissues by transfer of drug resistance genes
Rafferty, J. A. ; Hickson, I. ; Chinnasamy, N. ; Lashford, L. S. ; Margison, G. P. ; Dexter, T. M. ; Fairbairn, L. J.
Springer
Published 1996
Springer
Published 1996
| ISSN: |
1573-7233
|
|---|---|
| Keywords: |
myelosuppression ; therapy-related malignancy ; chemoprotection ; MDR-1 ; ATase ; retrovirus
|
| Source: |
Springer Online Journal Archives 1860-2000
|
| Topics: |
Medicine
|
| Notes: |
Abstract The effectiveness of many types of antitumour agent is limited by (i) acute dose limiting cytotoxicity, principally myelosuppression but also lung, liver and gastrointestinal tract toxicity, (ii) the risk of therapy related secondary malignancy and (iii) the inherent or acquired drug-resistance of tumour cells. As the management of the acute toxic effects improve, the more insidious effects, and particularly haematological malignancies, are anticipated to increase. Furthermore, attempts to overcome tumour cell resistance to treatment can lead to increased collateral damage in normal tissues. One approach to circumventing both the acute toxic and chronic carcinogenic effects of chemotherapy would be to use gene therapy to achieve high levels of expression of drug resistance proteins in otherwise drug-sensitive tissues. To date the products of the multi-drug resistance (MDR-1) and the human O 6-alkylguanine-DNA-alkyltransferase (ATase) gene have been used in reclinical experiments to demonstrate proof of principle, and the former of these is now being tested in a clinical situation. Here we discuss the potential of drug-resistance gene therapy to provide chemoprotection to normal tissues and examine the prospects for a dual approach which combines this with pharmacological sensitisation of tumours to chemotherapeutic agents.
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| Type of Medium: |
Electronic Resource
|
| URL: |
| _version_ | 1798296895067521024 |
|---|---|
| autor | Rafferty, J. A. Hickson, I. Chinnasamy, N. Lashford, L. S. Margison, G. P. Dexter, T. M. Fairbairn, L. J. |
| autorsonst | Rafferty, J. A. Hickson, I. Chinnasamy, N. Lashford, L. S. Margison, G. P. Dexter, T. M. Fairbairn, L. J. |
| book_url | http://dx.doi.org/10.1007/BF00046348 |
| datenlieferant | nat_lic_papers |
| hauptsatz | hsatz_simple |
| identnr | NLM196747767 |
| issn | 1573-7233 |
| journal_name | Cancer and metastasis reviews |
| materialart | 1 |
| notes | Abstract The effectiveness of many types of antitumour agent is limited by (i) acute dose limiting cytotoxicity, principally myelosuppression but also lung, liver and gastrointestinal tract toxicity, (ii) the risk of therapy related secondary malignancy and (iii) the inherent or acquired drug-resistance of tumour cells. As the management of the acute toxic effects improve, the more insidious effects, and particularly haematological malignancies, are anticipated to increase. Furthermore, attempts to overcome tumour cell resistance to treatment can lead to increased collateral damage in normal tissues. One approach to circumventing both the acute toxic and chronic carcinogenic effects of chemotherapy would be to use gene therapy to achieve high levels of expression of drug resistance proteins in otherwise drug-sensitive tissues. To date the products of the multi-drug resistance (MDR-1) and the human O 6-alkylguanine-DNA-alkyltransferase (ATase) gene have been used in reclinical experiments to demonstrate proof of principle, and the former of these is now being tested in a clinical situation. Here we discuss the potential of drug-resistance gene therapy to provide chemoprotection to normal tissues and examine the prospects for a dual approach which combines this with pharmacological sensitisation of tumours to chemotherapeutic agents. |
| package_name | Springer |
| publikationsjahr_anzeige | 1996 |
| publikationsjahr_facette | 1996 |
| publikationsjahr_intervall | 8004:1995-1999 |
| publikationsjahr_sort | 1996 |
| publisher | Springer |
| reference | 15 (1996), S. 365-383 |
| schlagwort | myelosuppression therapy-related malignancy chemoprotection MDR-1 ATase retrovirus |
| search_space | articles |
| shingle_author_1 | Rafferty, J. A. Hickson, I. Chinnasamy, N. Lashford, L. S. Margison, G. P. Dexter, T. M. Fairbairn, L. J. |
| shingle_author_2 | Rafferty, J. A. Hickson, I. Chinnasamy, N. Lashford, L. S. Margison, G. P. Dexter, T. M. Fairbairn, L. J. |
| shingle_author_3 | Rafferty, J. A. Hickson, I. Chinnasamy, N. Lashford, L. S. Margison, G. P. Dexter, T. M. Fairbairn, L. J. |
| shingle_author_4 | Rafferty, J. A. Hickson, I. Chinnasamy, N. Lashford, L. S. Margison, G. P. Dexter, T. M. Fairbairn, L. J. |
| shingle_catch_all_1 | Rafferty, J. A. Hickson, I. Chinnasamy, N. Lashford, L. S. Margison, G. P. Dexter, T. M. Fairbairn, L. J. Chemoprotection of normal tissues by transfer of drug resistance genes myelosuppression therapy-related malignancy chemoprotection MDR-1 ATase retrovirus myelosuppression therapy-related malignancy chemoprotection MDR-1 ATase retrovirus Abstract The effectiveness of many types of antitumour agent is limited by (i) acute dose limiting cytotoxicity, principally myelosuppression but also lung, liver and gastrointestinal tract toxicity, (ii) the risk of therapy related secondary malignancy and (iii) the inherent or acquired drug-resistance of tumour cells. As the management of the acute toxic effects improve, the more insidious effects, and particularly haematological malignancies, are anticipated to increase. Furthermore, attempts to overcome tumour cell resistance to treatment can lead to increased collateral damage in normal tissues. One approach to circumventing both the acute toxic and chronic carcinogenic effects of chemotherapy would be to use gene therapy to achieve high levels of expression of drug resistance proteins in otherwise drug-sensitive tissues. To date the products of the multi-drug resistance (MDR-1) and the human O 6-alkylguanine-DNA-alkyltransferase (ATase) gene have been used in reclinical experiments to demonstrate proof of principle, and the former of these is now being tested in a clinical situation. Here we discuss the potential of drug-resistance gene therapy to provide chemoprotection to normal tissues and examine the prospects for a dual approach which combines this with pharmacological sensitisation of tumours to chemotherapeutic agents. 1573-7233 15737233 Springer |
| shingle_catch_all_2 | Rafferty, J. A. Hickson, I. Chinnasamy, N. Lashford, L. S. Margison, G. P. Dexter, T. M. Fairbairn, L. J. Chemoprotection of normal tissues by transfer of drug resistance genes myelosuppression therapy-related malignancy chemoprotection MDR-1 ATase retrovirus myelosuppression therapy-related malignancy chemoprotection MDR-1 ATase retrovirus Abstract The effectiveness of many types of antitumour agent is limited by (i) acute dose limiting cytotoxicity, principally myelosuppression but also lung, liver and gastrointestinal tract toxicity, (ii) the risk of therapy related secondary malignancy and (iii) the inherent or acquired drug-resistance of tumour cells. As the management of the acute toxic effects improve, the more insidious effects, and particularly haematological malignancies, are anticipated to increase. Furthermore, attempts to overcome tumour cell resistance to treatment can lead to increased collateral damage in normal tissues. One approach to circumventing both the acute toxic and chronic carcinogenic effects of chemotherapy would be to use gene therapy to achieve high levels of expression of drug resistance proteins in otherwise drug-sensitive tissues. To date the products of the multi-drug resistance (MDR-1) and the human O 6-alkylguanine-DNA-alkyltransferase (ATase) gene have been used in reclinical experiments to demonstrate proof of principle, and the former of these is now being tested in a clinical situation. Here we discuss the potential of drug-resistance gene therapy to provide chemoprotection to normal tissues and examine the prospects for a dual approach which combines this with pharmacological sensitisation of tumours to chemotherapeutic agents. 1573-7233 15737233 Springer |
| shingle_catch_all_3 | Rafferty, J. A. Hickson, I. Chinnasamy, N. Lashford, L. S. Margison, G. P. Dexter, T. M. Fairbairn, L. J. Chemoprotection of normal tissues by transfer of drug resistance genes myelosuppression therapy-related malignancy chemoprotection MDR-1 ATase retrovirus myelosuppression therapy-related malignancy chemoprotection MDR-1 ATase retrovirus Abstract The effectiveness of many types of antitumour agent is limited by (i) acute dose limiting cytotoxicity, principally myelosuppression but also lung, liver and gastrointestinal tract toxicity, (ii) the risk of therapy related secondary malignancy and (iii) the inherent or acquired drug-resistance of tumour cells. As the management of the acute toxic effects improve, the more insidious effects, and particularly haematological malignancies, are anticipated to increase. Furthermore, attempts to overcome tumour cell resistance to treatment can lead to increased collateral damage in normal tissues. One approach to circumventing both the acute toxic and chronic carcinogenic effects of chemotherapy would be to use gene therapy to achieve high levels of expression of drug resistance proteins in otherwise drug-sensitive tissues. To date the products of the multi-drug resistance (MDR-1) and the human O 6-alkylguanine-DNA-alkyltransferase (ATase) gene have been used in reclinical experiments to demonstrate proof of principle, and the former of these is now being tested in a clinical situation. Here we discuss the potential of drug-resistance gene therapy to provide chemoprotection to normal tissues and examine the prospects for a dual approach which combines this with pharmacological sensitisation of tumours to chemotherapeutic agents. 1573-7233 15737233 Springer |
| shingle_catch_all_4 | Rafferty, J. A. Hickson, I. Chinnasamy, N. Lashford, L. S. Margison, G. P. Dexter, T. M. Fairbairn, L. J. Chemoprotection of normal tissues by transfer of drug resistance genes myelosuppression therapy-related malignancy chemoprotection MDR-1 ATase retrovirus myelosuppression therapy-related malignancy chemoprotection MDR-1 ATase retrovirus Abstract The effectiveness of many types of antitumour agent is limited by (i) acute dose limiting cytotoxicity, principally myelosuppression but also lung, liver and gastrointestinal tract toxicity, (ii) the risk of therapy related secondary malignancy and (iii) the inherent or acquired drug-resistance of tumour cells. As the management of the acute toxic effects improve, the more insidious effects, and particularly haematological malignancies, are anticipated to increase. Furthermore, attempts to overcome tumour cell resistance to treatment can lead to increased collateral damage in normal tissues. One approach to circumventing both the acute toxic and chronic carcinogenic effects of chemotherapy would be to use gene therapy to achieve high levels of expression of drug resistance proteins in otherwise drug-sensitive tissues. To date the products of the multi-drug resistance (MDR-1) and the human O 6-alkylguanine-DNA-alkyltransferase (ATase) gene have been used in reclinical experiments to demonstrate proof of principle, and the former of these is now being tested in a clinical situation. Here we discuss the potential of drug-resistance gene therapy to provide chemoprotection to normal tissues and examine the prospects for a dual approach which combines this with pharmacological sensitisation of tumours to chemotherapeutic agents. 1573-7233 15737233 Springer |
| shingle_title_1 | Chemoprotection of normal tissues by transfer of drug resistance genes |
| shingle_title_2 | Chemoprotection of normal tissues by transfer of drug resistance genes |
| shingle_title_3 | Chemoprotection of normal tissues by transfer of drug resistance genes |
| shingle_title_4 | Chemoprotection of normal tissues by transfer of drug resistance genes |
| sigel_instance_filter | dkfz geomar wilbert ipn albert fhp |
| source_archive | Springer Online Journal Archives 1860-2000 |
| timestamp | 2024-05-06T09:59:21.393Z |
| titel | Chemoprotection of normal tissues by transfer of drug resistance genes |
| titel_suche | Chemoprotection of normal tissues by transfer of drug resistance genes |
| topic | WW-YZ |
| uid | nat_lic_papers_NLM196747767 |