Dietary glycaemic index, glycaemic load and breast cancer risk: a systematic review and meta-analysis

This systematic review aimed to examine if an association exists between dietary glycaemic index (GI) and glycaemic load (GL) intake and breast cancer risk. A systematic search was conducted in Medline and Embase and identified 14 relevant studies up to May 2008. Adjusted relative risk estimates comparing breast cancer risk for the highest versus the lowest category of GI/GL intake were extracted from relevant studies and combined in meta-analyses using a random-effects model. Combined estimates from six cohort studies show non-significant increased breast cancer risks for premenopausal women (relative risk (RR) 1.14, 95% CI 0.95-1.38) and postmenopausal women (RR 1.11, 95% CI 0.99-1.25) consuming the highest versus the lowest category of GI intake. Evidence of heterogeneity hindered analyses of GL and premenopausal risk, although most studies did not observe any significant association. Pooled cohort study results indicated no association between postmenopausal risk and GL intake (RR 1.03, 95% CI 0.94-1.12). Our findings do not provide strong support of an association between dietary GI and GL and breast cancer risk. © 2008 Cancer Research UK.


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Hoxa6 potentiates short-term hemopoietic cell proliferation and extended self-renewal.

Hemopoietic progenitor cells express clustered homeobox (Hox) genes in a pattern characteristic of their lineage and stage of differentiation. In general, HOX expression tends to be higher in more primitive and lower in lineage-committed cells. These trends have led to the hypothesis that self-renewal of hemopoietic stem/progenitor cells is HOX-dependent and that dysregulated HOX expression underlies maintenance of the leukemia-initiating cell. Gene expression profile studies support this hypothesis and specifically highlight the importance of the HOXA cluster in hemopoiesis and leukemogenesis. Within this cluster HOXA6 and HOXA9 are highly expressed in patients with acute myeloid leukemia and form part of the "Hox code" identified in murine models of this disease. We have examined endogenous expression of Hoxa6 and Hoxa9 in purified primary progenitors as well as four growth factor-dependent cell lines FDCP-Mix, EML, 32Dcl3, and Ba/F3, representative of early multipotential and later committed precursor cells respectively. Hoxa6 was consistently higher expressed than Hoxa9, preferentially expressed in primitive cells and was both growth-factor and cell-cycle regulated. Enforced overexpression of HOXA6 or HOXA9 in FDCP-Mix resulted in increased proliferation and colony formation but had negligible effect on differentiation. In both FDCP-Mix and the more committed Ba/F3 precursor cells overexpression of HOXA6 potentiated factor-independent proliferation. These findings demonstrate that Hoxa6 is directly involved in fundamental processes of hemopoietic progenitor cell development.