Abstract | BACKGROUND: METHODS: In the nontumour-bearing liver, the presence of SOS was studied histopathologically. The genotype was determined by a semi-nested PCR. RESULTS: Thirty-two of the 55 (58%) patients showed SOS lesions, consisting of 27% mild, 22% moderate and 9% severe lesions. The GSTM1-null genotype was present in 25 of the 55 (46%). Multivariate analysis showed that the GSTM1-null genotype significantly correlated with the presence of (moderate-severe) SOS (P=0.026). CONCLUSION: The GSTM1-null genotype is an independent risk factor for SOS. This finding allows us, in association with other risk factors, to conceive a potential risk profile predicting whether the patient is at risk of developing SOS, before starting oxaliplatin, and subsequently might result in adjustment of treatment.
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Authors | C P H Vreuls, S W M Olde Damink, G H Koek, A Winstanley, E Wisse, R H E Cloots, M A J van den Broek, C H C Dejong, F T Bosman, A Driessen |
Journal | British journal of cancer
(Br J Cancer)
Vol. 108
Issue 3
Pg. 676-80
(Feb 19 2013)
ISSN: 1532-1827 [Electronic] England |
PMID | 23287989
(Publication Type: Journal Article)
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Chemical References |
- Antineoplastic Agents
- Organoplatinum Compounds
- Oxaliplatin
- glutathione S-transferase T1
- Glutathione Transferase
- glutathione S-transferase M1
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Topics |
- Adult
- Aged
- Aged, 80 and over
- Antineoplastic Agents
(adverse effects)
- Colorectal Neoplasms
(drug therapy, genetics, pathology)
- Female
- Follow-Up Studies
- Genotype
- Glutathione Transferase
(genetics)
- Hepatic Veno-Occlusive Disease
(etiology)
- Humans
- Liver Neoplasms
(drug therapy, genetics, secondary)
- Male
- Middle Aged
- Organoplatinum Compounds
(adverse effects)
- Oxaliplatin
- Polymerase Chain Reaction
- Polymorphism, Genetic
(genetics)
- Prognosis
- Risk Factors
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