He skillfully used these points in electoral campaigns against the SPD, which was more sympathetic to co-existence with the GDR and the post-war borders. Adenauer opposed recognition of the rival German Democratic Republic or the Oder-Neisse line. He worked to restore the West German economy from the destruction of World War II to a central position in Europe, presiding over the German economic miracle together with his Minister of Economics, Ludwig Erhard, and was a driving force in re-establishing national military forces (the Bundeswehr) and intelligence services (the Bundesnachrichtendienst) in West Germany in 19.
A shrewd and strategic politician, Adenauer was deeply committed to a Western-oriented foreign policy and restoring the position of West Germany on the world stage. He displayed a strong dedication to a broad vision of market-based liberal democracy and anti-communism. Īdenauer belied his age by his intense work habits and his uncanny political instinct. During his years in power, West Germany achieved democracy, stability, international respect and economic prosperity ( Wirtschaftswunder, German for "economic miracle").
In the early years of the Federal Republic, he switched focus from denazification to recovery, and led his country from the ruins of World War II to becoming a productive and prosperous nation that forged close relations with France, the United Kingdom and the United States. From 1946 to 1966, he was the first leader of the Christian Democratic Union (CDU), a Christian democratic party he co-founded, which under his leadership became the dominant force in the country.Ī devout Roman Catholic and member of the Catholic Centre Party, Adenauer was a leading politician in the Weimar Republic, serving as Mayor of Cologne (1917–1933) and as president of the Prussian State Council (1922–1933). ©2017 American Association for Cancer Research.Konrad Hermann Joseph Adenauer ( German: ( listen) 5 January 1876 – 19 April 1967) was a German statesman who served as the first chancellor of West Germany from 1949 to 1963. Treatment of myxoid liposarcoma cell lines with several IGF-IR inhibitors resulted in significant growth inhibition in vitro and in vivo Conclusions: Our preclinical study substantiates the fundamental role of the IGF-IR/PI3K/Akt signaling pathway in myxoid liposarcoma pathogenesis and provides a mechanism-based rationale for molecular- targeted approaches in myxoid liposarcoma cancer therapy.
Conversely, RNAi-mediated FUS-DDIT3 knockdown in myxoid liposarcoma cells led to an inactivation of IGF-IR/PI3K/Akt signaling associated with diminished IGF2 mRNA expression. In HT1080 fibrosarcoma cells, overexpression of FUS-DDIT3 induced aberrant IGF-IR/PI3K/Akt pathway activity, which was dependent on transcriptional induction of the IGF2 gene. Results: A comprehensive subset of myxoid liposarcoma specimens showed elevated expression and phosphorylation levels of various IGF-IR/PI3K/Akt signaling effectors. An established myxoid liposarcoma avian chorioallantoic membrane model was used for in vivo confirmation of the preclinical in vitro results. FUS-DDIT3 dependency and biological function of the IGF-IR/PI3K/Akt signaling cascade were analyzed using a HT1080 fibrosarcoma-based myxoid liposarcoma tumor model and multiple tumor-derived myxoid liposarcoma cell lines. Experimental Design: Immunohistochemical evaluation of key effectors of the IGF-IR/PI3K/Akt signaling axis was performed in a comprehensive cohort of myxoid liposarcoma specimens. We here investigate the functional role of FUS-DDIT3 in IGF-IR/PI3K/Akt signaling driving myxoid liposarcoma pathogenesis. The resulting chimeric FUS-DDIT3 fusion protein plays a crucial role in myxoid liposarcoma pathogenesis however, its specific impact on oncogenic signaling pathways remains to be substantiated. Over 90% of myxoid liposarcoma are characterized by a reciprocal t(12 16)(q13 p11) translocation. Purpose: Myxoid liposarcoma is an aggressive disease with particular propensity to develop hematogenic metastases.
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