BackgroundNew Zealand Māori have a poorer outcome from breast cancer than non-Māori, yet prognostic data are sparse. The objective of this study was to quantify levels of prognostic factors in a cohort of self-declared Māori and European breast cancer patients from Christchurch, New Zealand.Methods and ResultsClinicopathological and survival data from 337 consecutive breast cancer patients (27 Māori, 310 European) were evaluated. Fewer tumours were high grade in Māori women than European women (p = 0.027). No significant ethnic differences were detected for node status, tumour type, tumour size, human epidermal growth factor receptor, oestrogen and progesterone receptor (ER/PR) status, or survival.In addition, tumour and serum samples from a sub-cohort of 14 Māori matched to 14 NZ European patients were analyzed by immunohistochemistry and enzyme linked immunosorbent assay for molecular prognostic factors. Significant correlations were detected between increased grade and increased levels of hypoxia inducible factor-1 (HIF-1α), glucose transporter-1 (GLUT-1), microvessel density (MVD) and cytokeratins CK5/6 (p < 0.05). High nodal status correlated with reduced carbonic anhydrase IX (CA-IX). Negative ER/PR status correlated with increased GLUT-1, CA-IX and MVD. Within the molecular factors, increased HIF-1α correlated with raised GLUT-1, MVD and CK5/6, and CK5/6 with GLUT-1 and MVD (p < 0.05). The small number of patients in this sub-cohort limited discrimination of ethnic differences.ConclusionsIn this Christchurch cohort of breast cancer patients, Māori women were no more likely than European women to have pathological or molecular factors predictive of poor prognosis. These data contrast with data from the North Island NZ, and suggest potential regional differences.

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: The drug combination of cis-dichlorodiammineplatinum (II) ( CDDP ) and 5-fluorouracil (5-FU) is widely used in various cancer treatments. To better understand the benefits of this treatment regime, we analyzed the cell cycle profiles and p53-p21-pRB cascade in three gastric cancer cell lines : MKN45, MKN74 (both expressing wild type p53), and MKN28 (expressing a mutant p53).Treatment with the drug combination caused different responses in the MKN45 and MKN74 cell lines : MKN45 cells accumulated in the G 1 phase of the cell cycle and showed fewer cells in the S phase. MKN74 cells accumulated at the G1-S transition. CDDP alone caused G2-M arrest in both cell lines. The drug combination did not affect the p53 levels but increased the p21 protein levels in both cell lines. Corresponding to the 01 accumulation, unphosphorylated pRB was predominant in the MKN45 cells, and corresponding to the observed S-G2M retardation, phosphorylated pRB was predominant in the MKN74 cells. No drug combination effect was observed in MKN28 cells. These results suggest that there are several sites of action for the drug combination in cells expressing wild-type p53 and indicate that the combined drug effect is greater in cells expressing wild-type p53 than in those expressing a mutant p53.