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Andrea E. Murmann
Researcher at Northwestern University
Publications - 51
Citations - 2970
Andrea E. Murmann is an academic researcher from Northwestern University. The author has contributed to research in topics: Cancer cell & Cancer. The author has an hindex of 19, co-authored 48 publications receiving 2576 citations. Previous affiliations of Andrea E. Murmann include Heidelberg University & University of Chicago.
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Journal ArticleDOI
The role of let-7 in cell differentiation and cancer
TL;DR: The role of let-7 in normal development and differentiation is discussed, the regulation oflet-7 expression, cancer-relevantLet-7 targets, and the relationship between let-8 and drug sensitivity are highlighted, and an overview of the relationships between deregulated let- 7 expression and tumorigenesis is provided.
Journal ArticleDOI
Molecular ordering of the initial signaling events of CD95
Alicia Algeciras-Schimnich,Le Shen,Bryan C. Barnhart,Andrea E. Murmann,Janis K. Burkhardt,Marcus E. Peter +5 more
TL;DR: The data indicate that the signal initiation by CD95 is a complex process actively regulated at various levels, providing a number of new drug targets to specifically modulate CD95 signaling.
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MicroRNAs Reprogram Normal Fibroblasts into Cancer-Associated Fibroblasts in Ovarian Cancer
Anirban K. Mitra,Marion Zillhardt,Youjia Hua,Payal Tiwari,Andrea E. Murmann,Marcus E. Peter,Ernst Lengyel +6 more
TL;DR: Results indicate that ovarian cancer cells reprogram fibroblasts to become CAFs through the action of miRNAs, which may represent novel therapeutic targets in the tumor microenvironment.
Journal ArticleDOI
The role of CD95 and CD95 ligand in cancer
Marcus E. Peter,Abbas Hadji,Abbas Hadji,Andrea E. Murmann,Sonia Brockway,William Putzbach,Abhinandan Pattanayak,Paolo Ceppi +7 more
TL;DR: Five different ways in which inhibiting or eliminating CD95L, rather than augmenting, may be beneficial for cancer therapy alone or in combination with standard chemotherapy or immune therapy are discussed.
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miR-200c regulates induction of apoptosis through CD95 by targeting FAP-1
TL;DR: It is demonstrated that miR-200c sensitizes cells to apoptosis mediated by CD95, and the apoptosis inhibitor FAP-1 is identified as a target for miR -200c, providing a molecular mechanism to explain both the downregulation of CD95 expression and the reduction in sensitivity of cells to CD95-mediated apoptosis that is observed during tumor progression.