Irving L. Weissman
Stanford University
1170 Papers
18.9K Citations
Irving L. Weissman is an academic researcher from Stanford University. The author has contributed to research in topics: Stem cell & Haematopoiesis. The author has an hindex of 201, co-authored 1141 publications. Previous affiliations of Irving L. Weissman include Eli Lilly and Company & Memorial Sloan Kettering Cancer Center.
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Papers
Antibody therapy targeting the CD47 protein is effective in a model of aggressive metastatic leiomyosarcoma
Badreddin Edris,Kipp Weiskopf,Anne Kathrin Volkmer,Jens-Peter Volkmer,Stephen B. Willingham,Humberto Contreras-Trujillo,Jie Liu,Ravindra Majeti,Robert B. West,Jonathan A. Fletcher,Andrew H. Beck,Irving L. Weissman,Matt van de Rijn +12 more
TL;DR: Interference with CD47 increases phagocytosis of two human LMS cell lines, LMS04 and LMS05, in vitro, which suggests that treatment with anti-CD47 antibodies not only reduces primary tumor size but can also be used to inhibit the development of, or to eliminate, metastatic disease.
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Three differentiation states risk-stratify bladder cancer into distinct subtypes.
Jens Peter Volkmer,Jens Peter Volkmer,Debashis Sahoo,Robert K. Chin,Philip Levy Ho,Chad Tang,Antonina V. Kurtova,Stephen B. Willingham,Senthil K. Pazhanisamy,Humberto Contreras-Trujillo,Theresa A. Storm,Yair Lotan,Andrew H. Beck,Benjamin I. Chung,Ash A. Alizadeh,Guilherme Godoy,Seth P. Lerner,Matt van de Rijn,Linda D. Shortliffe,Irving L. Weissman,Keith Syson Chan +20 more
TL;DR: The data indicate that bladder cancer can be subclassified into three subtypes, on the basis of their differentiation states: basal, intermediate, and differentiated, where only the most primitive tumor cell subpopulation within each subtype is capable of generating xenograft tumors and recapitulating downstream populations.
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A monoclonal antibody that recognizes B cells and B cell precursors in mice.
TL;DR: The monoclonal antibody, RA3-2C2, appears to be specific for cells within the B cell lineage, but does not recognize thymocytes, peripheral T cells, or nonlymphoid hematopoietic cells in the spleen or bone marrow.
Glycogen synthase kinase 3β missplicing contributes to leukemia stem cell generation
Annelie Abrahamsson,Ifat Geron,Jason Gotlib,Kim-Hien Dao,Charlene F. Barroga,Isabel G. Newton,Francis J. Giles,Jeffrey Durocher,Remi S. Creusot,Mobin Karimi,Carol D. Jones,James L. Zehnder,Armand Keating,Robert S. Negrin,Irving L. Weissman,Catriona Jamieson +15 more
TL;DR: It is proposed that CP CML is initiated by BCR-ABL expression in an HSC clone but that progression to BC may include missplicing of GSK3β in GMP LSC, enabling unphosphorylated β-catenin to participate in LSC self-renewal.
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