Entity

Time filter

Source Type

Emeryville, CA, United States

Liu H.,University of California at San Francisco | Liu H.,Eureka Therapeutics | Radisky D.C.,Mayo Clinic Cancer Center | Yang D.,University of California at San Francisco | And 4 more authors.
Nature Cell Biology | Year: 2012

Overexpression of MYC transforms cells in culture, elicits malignant tumours in experimental animals and is found in many human tumours. We now report the paradoxical finding that this powerful oncogene can also act as a suppressor of cell motility, invasiveness and metastasis. Overexpression of MYC stimulated proliferation of breast cancer cells both in culture and in vivo as expected, but inhibited motility and invasiveness in culture, and lung and liver metastases in xenografted tumours. We show further that MYC represses transcription of both subunits of α vβ 3 integrin, and that exogenous expression of β 3 integrin in human breast cancer cells that do not express this integrin rescues invasiveness and migration when MYC is downregulated. These data uncover an unexpected function of MYC, provide an explanation for the hitherto puzzling literature on the relationship between MYC and metastasis, and reveal a variable that could influence the development of therapies that target MYC. © 2012 Macmillan Publishers Limited. All rights reserved. Source


Trademark
Eureka Therapeutics | Date: 2016-01-20

Pharmaceutical preparations of chimeric immune cell antigen receptors for therapeutic use for the treatment of cancers, for the treatment of proliferative cell diseases, and in transplantation.


Patent
Eureka Therapeutics | Date: 2011-11-29

The present disclosure provides compositions and methods comprising cells producing glycoproteins with variant glycosylation patterns. The methods and compositions may be used in producing antibodies and proteins of therapeutic value.


Patent
Sloan Kettering Cancer Center and Eureka Therapeutics | Date: 2015-05-28

The present invention provides antigen binding proteins that specifically bind to Wilms tumor protein (WT1), including humanized, chimeric and fully human antibodies against WT1, antibody fragments, chimeric antigen receptors (CARs), fusion proteins, and conjugates thereof. The antigen binding proteins and antibodies bind to HLA-A0201-restricted WT1 peptide. Such antibodies, fragments, fusion proteins and conjugates thereof are useful for the treatment of WT1 associated cancers, including for example, breast cancer, ovarian cancer, prostate cancer, chronic myelocytic leukemia, multiple myeloma, acute lymphoblastic leukemia (ALL), acute myeloid/myelogenous leukemia (AML) and myelodysplastic syndrome (MDS). In more particular embodiments, the anti-WT1/A antibodies may comprise one or more framework region amino acid substitutions designed to improve protein stability, antibody binding and/or expression levels.


Patent
Eureka Therapeutics and Sloan Kettering Cancer Center | Date: 2012-04-02

The present invention provides antigen binding proteins that specifically bind to Wilms tumor protein (WT1), including humanized, chimeric and fully human antibodies against WT1, antibody fragments, chimeric antigen receptors (CARs), fusion proteins, and conjugates thereof. The antigen binding proteins and antibodies bind to HLA-A0201-restricted WT1 peptide. Such antibodies, fragments, fusion proteins and conjugates thereof are useful for the treatment of WT1 associated cancers, including for example, breast cancer, ovarian cancer, prostate cancer, chronic myelocytic leukemia, multiple myeloma, acute lymphoblastic leukemia (ALL), acute myeloid/myelogenous leukemia (AML) and myelodysplastic syndrome (MDS). In more particular embodiments, the anti-WT1/A antibodies may comprise one or more framework region amino acid substitutions designed to improve protein stability, antibody binding and/or expression levels.

Discover hidden collaborations