The phase behavior of polyisoprene-polystyrene (PI-PS) diblock copolymers near the orderdisorder transition was investigated using dynamic mechanical measurements, transmission electron microscopy, and small-angle X-ray and neutron scattering at polyisoprene volume fractions 0.33 < /pi < 0.42. Two new ordered morphologies have been documented between hexagonally packed cylinders (HEX) and lamellae (LAM). At low temperatures a hexagonally perforated layered (HPL) microstructure occurs, that transforms into a bicontinuous cubic phase characterized by laid space group symmetry near the orderdisorder transition (ODT). The ordered-bicontinuous double diamind (OBDD) phase was not found at any temperature or composition studied. We demonstrate that the bicontinuous laid phase exists at equilibrium over a narrow range of compositions, 0.35 5 /pi 5 0.40 bounded by the HEX, LAM, HPL, and disordered states, and is restricted to within about 60 °C of the ODT, suggesting the importance of finite size effects. This cubic phase also exhibits pronounced metastability, remaining intact for extended periods of time after cooling below the Iaid-HEX or 7a3d-HPL phase boundary. Cooling from above the ODT to below the PS glass transition temperature leads to a vitrified form of the laid state.

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BACKGROUND: Insulin-like growth factor 1 (IGF1) promotes breast cancer and disease progression. Bioavailability of IGF1 is modulated by IGF-binding proteins (IGFBPs). IGFBP4 inhibits IGF1 activity but cleavage by pregnancy-associated plasma protein-A (PAPP-A) protease releases active IGF1. METHODS: Expression of IGF pathway components and PAPP-A was assessed by western blot or RT -PCR. IGFBP4 (dBP4) resistant to PAPP-A cleavage, but retaining IGF-binding capacity, was used to block IGF activity in vivo. 4T1.2 mouse mammary adenocarcinoma cells transfected with empty vector, vector expressing wild-type IGFBP4 or vector expressing dBP4 were implanted in the mammary fat pad of BALB/c mice and tumour growth was assessed. Tumour angiogenesis and endothelial cell apoptosis were assessed by immunohistochemistry. RESULTS: 4T1.2 cells expressed the IGF1R receptor and IGFBP4. PAPP-A was expressed within mammary tumours but not by 4T1.2 cells. Proliferation and vascular endothelial growth factor (VEGF) production by 4T1.2 cells was increased by IGF1(E3R) (recombinant IGF1 resistant to binding by IGFBPs) but not by wild-type IGF1. IGF1-stimulated microvascular endothelial cell proliferation was blocked by recombinant IGFBP4. 4T1.2 tumours expressing dBP4 grew significantly more slowly than controls or tumours expressing wild-type IGFBP4. Inhibition of tumour growth by dBP4 was accompanied by the increased endothelial cell apoptosis. CONCLUSION: Protease-resistant IGFBP4 blocks IGF activity, tumour growth and angiogenesis .

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