'A foundation-hatched black elite’: Obama, the US establishment and foreign policy

US foreign policy has a largely unacknowledged racial dimension due to the racial characteristics of the US foreign policy establishment, and in shared mindsets in a soon-to-be ‘majority-minority’ nation. White Anglo-Saxon Protestant (WASP) racial-ethnic and class factors produce managed change through socialisation in an attenuated meritocratic order, adapting to challenges to elite dominance by incorporating rising talent, without altering broader patterns of power. The greatest success of such a system would be the assimilation of the most elite minority individuals, even as the bulk of those groups’ members continue to experience discrimination. Such success would be compounded by election to the highest office of a minority US president extolling the virtues of post-racial politics. President Barack Obama represents a ‘Wasp-ified’ black elite, assimilated into the extant structures of power that remain wedded to a more secular, non-biologically-racial, version of Anglo-Saxonism or, more broadly, liberal internationalism. Hence, it should occasion little surprise that there has been so little change in US foreign policies during Obama’s two-term presidency

MMTV-Wnt1 and -ΔN89β-Catenin Induce Canonical Signaling in Distinct Progenitors and Differentially Activate Hedgehog Signaling within Mammary Tumors

Canonical Wnt/β-catenin signaling regulates stem/progenitor cells and, when perturbed, induces many human cancers. A significant proportion of human breast cancer is associated with loss of secreted Wnt antagonists and mice expressing MMTV-Wnt1 and MMTV-ΔN89β-catenin develop mammary adenocarcinomas. Many studies have assumed these mouse models of breast cancer to be equivalent. Here we show that MMTV-Wnt1 and MMTV-ΔN89β-catenin transgenes induce tumors with different phenotypes. Using axin2/conductin reporter genes we show that MMTV-Wnt1 and MMTV-ΔN89β-catenin activate canonical Wnt signaling within distinct cell-types. ΔN89β-catenin activated signaling within a luminal subpopulation scattered along ducts that exhibited a K18+ER−PR−CD24highCD49flow profile and progenitor properties. In contrast, MMTV-Wnt1 induced canonical signaling in K14+ basal cells with CD24/CD49f profiles characteristic of two distinct stem/progenitor cell-types. MMTV-Wnt1 produced additional profound effects on multiple cell-types that correlated with focal activation of the Hedgehog pathway. We document that large melanocytic nevi are a hitherto unreported hallmark of early hyperplastic Wnt1 glands. These nevi formed along the primary mammary ducts and were associated with Hedgehog pathway activity within a subset of melanocytes and surrounding stroma. Hh pathway activity also occurred within tumor-associated stromal and K14+/p63+ subpopulations in a manner correlated with Wnt1 tumor onset. These data show MMTV-Wnt1 and MMTV-ΔN89β-catenin induce canonical signaling in distinct progenitors and that Hedgehog pathway activation is linked to melanocytic nevi and mammary tumor onset arising from excess Wnt1 ligand. They further suggest that Hedgehog pathway activation maybe a critical component and useful indicator of breast tumors arising from unopposed Wnt1 ligand