Genentech Inc., is a biotechnology corporation which became a subsidiary of Roche in 2009. Genentech Research and Early Development operates as an independent center within Roche.As of August 2013, Genentech employed more than 12,300 people. In July 2014, Genentech announced its acquisition of Seragon for up to $1.725 billion. Wikipedia.
Curis and Genentech | Date: 2017-02-22
Novel inhibitors of IAP that are useful as therapeutic agents for treating malignancies and have the general formula I:R and R are as described herein.
Genentech | Date: 2017-02-15
Methods for treating multiple sclerosis (MS) with a CD20 antibody using special dosing regimens and protocols are described. Articles of manufacture for use in such methods are also described.
Genentech | Date: 2017-03-15
The present invention concerns affinity matured CRIg variants. In particular, the invention concerns CRIg variants having increased binding affinity to C3b and retaining selective binding to C3b over C3.
Genentech | Date: 2017-01-04
The present invention is directed to novel polypeptides having sequence identity with IL-17 and to nucleic acid molecules encoding those polypeptides. Also provided herein are vectors and host cells comprising those nucleic acid sequences, chimeric polypeptides molecules comprising the polypeptides of the present invention fused to heterologous polypeptide sequences, antibodies which bind to the polypeptides of the present invention and to methods for producing the polypeptides of the present invention. Further provided herein are methods for treating degenerative cartilaginous disorders.
Genentech and Hoffmann-La Roche | Date: 2017-03-08
The invention relates to anti-Factor D antibody variants, their production and their use in the preparation of compositions and medicaments for treatment of diseases and disorders associated with excessive or uncontrolled complement activation.
Genentech | Date: 2017-04-19
The invention provides anti-EphB4 anti-bodies, and compositions comprising and methods of using these antibodies.
EMBO Journal | Year: 2012
Aberrant regulation of the Wnt signalling pathway has emerged as a prevalent theme in cancer biology. This chapter summarizes the research that provides a proof of concept for inhibiting Wnt signalling in cancer, the potential means by which this could be achieved, and some recent advances towards this goal. A brief discussion of molecular diagnostics and possible safety concerns is also provided. © 2012 European Molecular Biology Organization.
Cold Spring Harbor Perspectives in Biology | Year: 2012
Aberrant regulation of the Wnt signaling pathway is a prevalent theme in cancer biology. From the earliest observation that Wnt overexpression could lead to malignant transformation of mouse mammary tissue to the most recent genetic discoveries gleaned from tumor genome sequencing, the Wnt pathway continues to evolve as a central mechanism in cancer biology. This article summarizes the evidence supporting a role for Wnt signaling in human cancer. This includes a review of the genetic mutations affecting Wnt pathway components, as well as some of epigenetic mechanisms that alter expression of genes relevant to Wnt. I also highlight some research on the cooperativity of Wnt with other signaling pathways in cancer. Finally, some emphasis is placed on laboratory research that provides a proof of concept for the therapeutic inhibition of Wnt signaling in cancer. © 2012 Cold Spring Harbor Laboratory Press; all rights reserved.
Nature genetics | Year: 2010
To understand the genetic predisposition to selective immunoglobulin A deficiency (IgAD), we performed a genome-wide association study in 430 affected individuals (cases) from Sweden and Iceland and 1,090 ethnically matched controls, and we performed replication studies in two independent European cohorts. In addition to the known association of HLA with IgAD, we identified association with a nonsynonymous variant in IFIH1 (rs1990760G>A, P = 7.3 x 10(-10)) which was previously associated with type 1 diabetes and systemic lupus erythematosus. Variants in CLEC16A, another known autoimmunity locus, showed suggestive evidence for association (rs6498142C>G, P = 1.8 x 10(-7)), and 29 additional loci were identified with P < 5 x 10(-5). A survey in IgAD of 118 validated non-HLA autoimmunity loci indicated a significant enrichment for association with autoimmunity loci as compared to non-autoimmunity loci (P = 9.0 x 10(-4)) or random SNPs across the genome (P < 0.0001). These findings support the hypothesis that autoimmune mechanisms may contribute to the pathogenesis of IgAD.
Nature Genetics | Year: 2012
A new exome sequencing study of individuals with hepatocellular carcinoma (HCC) reveals imprints of mutagenic exposure and identifies new genes contributing to tumorigenesis. This work joins several recent publications reporting whole-genome, exome and RNA sequencing in HCC, which together provide a comprehensive genomic landscape and new insights into the etiology of liver cancer. © 2012 Nature America, Inc. All rights reserved.