Journal of Breast Cancer · 2020 · 13 citations · 23 references
MedicineOncologyBreast OncologyChemotherapyMolecular OncologyBiomarker ValidationToxicity Risk AssessmentBreast Cancer ChemotherapyBreast Cancer PrognosisBreast Cancer Response AssessmentChemotherapy Response AssessmentGamma-glutamyl TransferaseHormone Receptor - Positive Breast CancerHormone Receptor-positive DiseasePost-neoadjuvant Therapy
PURPOSE: Gamma-glutamyl transferase (GGT) has been reported as being involved in tumor progression. Previous studies documented a potential relationship between serum GGT level and survival outcome in several types of human malignancies. However, the association between serum GGT levels and response to neoadjuvant chemotherapy (NAC) has not yet been reported. The present study aimed to evaluate the association between pre-therapeutic serum GGT level and the efficacy, long-term survival, and adverse reactions of NAC and to investigate its role in predicting NAC sensitivity in patients with breast cancer. METHODS: test and multivariate logistic regression model were used to analyze the correlation between pre-therapeutic serum GGT levels and adverse reactions. RESULTS: Pre-therapeutic serum GGT levels were associated with pCR among breast cancer patients treated with NAC. Multivariate analysis showed that low-level GGT significantly increased pCR rate. Patients in the high-level GGT group had poorer survival than those in the low-level GGT group. Subgroup analysis demonstrated that serum GGT level was potentially related to RFS and DFS in the hormone receptor-positive group. Low levels of GGT are significantly associated with a higher incidence of neutropenia. CONCLUSION: Pre-therapeutic serum GGT level is an independent and novel biomarker for predicting the efficiency, prognosis, and adverse reactions to NAC in breast cancer patients. Patients with low pre-therapeutic serum GGT levels are more likely to have higher pCR rates, better RFS and DFS, and higher hematologic toxicity. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02199418, NCT02221999.
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Cisplatin nephrotoxicity: molecular mechanisms.
Marie H. Hanigan, Prasad Devarajan · PubMed · 2003 · 390 citations
Medicine, Oncology, Pharmacology +17
Yi Chen, Kai Chen, Xiaoyun Xiao et al. · BMC Cancer · 2016 · 157 citations · Full text
Medicine, Oncology, Breast Oncology +14