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dc.contributor.authorRedmond, S M
dc.contributor.authorJoncourt, F
dc.contributor.authorBuser, K
dc.contributor.authorZiemiecki, A
dc.contributor.authorAltermatt, H J
dc.contributor.authorFey, M
dc.contributor.authorMargison, Geoffrey P
dc.contributor.authorCerny, T
dc.date.accessioned2010-06-11T08:49:20Z
dc.date.available2010-06-11T08:49:20Z
dc.date.issued1991-04-15
dc.identifier.citationAssessment of P-glycoprotein, glutathione-based detoxifying enzymes and O6-alkylguanine-DNA alkyltransferase as potential indicators of constitutive drug resistance in human colorectal tumors. 1991, 51 (8):2092-7 Cancer Res.en
dc.identifier.issn0008-5472
dc.identifier.pmid1672623
dc.identifier.urihttp://hdl.handle.net/10541/104657
dc.description.abstractDrug resistance is a major problem in cancer chemotherapy. Treatment protocols generally include a number of different cytotoxic drugs given in combination. Therefore, drug resistance in the tumor is likely to result from the coexpression of several cellular activities able to prevent cell killing by any of the drugs used. In this study we have measured several potential drug resistance mechanisms consisting of the multidrug resistance gene product P-glycoprotein, glutathione, glutathione-transferase and -peroxidase, and the DNA repair enzyme O6-alkylguanine-DNA-alkyltransferase in samples of colon carcinoma and normal adjacent mucosa from 23 untreated patients. All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient. The significance was highest for glutathione peroxidase (P less than or equal to 0.0005). Individual patients, however, showed very different patterns, with none, several, or all monitored resistance mechanisms elevated in the tumor. The implications both in the choice of drugs and in the use of resistance modifying agents to improve therapy for the individual patient are discussed.
dc.language.isoenen
dc.subjectColonic Canceren
dc.subjectBiological Tumour Markersen
dc.subject.meshAged
dc.subject.meshBacterial Proteins
dc.subject.meshColonic Neoplasms
dc.subject.meshDrug Resistance
dc.subject.meshEscherichia coli Proteins
dc.subject.meshFemale
dc.subject.meshGlutathione
dc.subject.meshGlutathione Peroxidase
dc.subject.meshGlutathione Transferase
dc.subject.meshHumans
dc.subject.meshIntestinal Mucosa
dc.subject.meshMale
dc.subject.meshMembrane Glycoproteins
dc.subject.meshO(6)-Methylguanine-DNA Methyltransferase
dc.subject.meshP-Glycoprotein
dc.subject.meshPilot Projects
dc.subject.meshTranscription Factors
dc.subject.meshTumor Markers, Biological
dc.titleAssessment of P-glycoprotein, glutathione-based detoxifying enzymes and O6-alkylguanine-DNA alkyltransferase as potential indicators of constitutive drug resistance in human colorectal tumors.en
dc.typeArticleen
dc.contributor.departmentInstitute for Clinical & Experimental Cancer Research, Berne, Switzerland.en
dc.identifier.journalCancer Researchen
html.description.abstractDrug resistance is a major problem in cancer chemotherapy. Treatment protocols generally include a number of different cytotoxic drugs given in combination. Therefore, drug resistance in the tumor is likely to result from the coexpression of several cellular activities able to prevent cell killing by any of the drugs used. In this study we have measured several potential drug resistance mechanisms consisting of the multidrug resistance gene product P-glycoprotein, glutathione, glutathione-transferase and -peroxidase, and the DNA repair enzyme O6-alkylguanine-DNA-alkyltransferase in samples of colon carcinoma and normal adjacent mucosa from 23 untreated patients. All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient. The significance was highest for glutathione peroxidase (P less than or equal to 0.0005). Individual patients, however, showed very different patterns, with none, several, or all monitored resistance mechanisms elevated in the tumor. The implications both in the choice of drugs and in the use of resistance modifying agents to improve therapy for the individual patient are discussed.


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