Dana-farber-cancer Institute Inc.

Harvard College

Thomas M Roberts

Jean Zhao

Timothy Alan Springer

Mark S Ptashne

Keith C Backman

Gail D Lauer

Takashi K Kishimoto

Gordon James Freeman

Bruce M Spiegelman

Jeffrey Charles Way

William C Hahn

Avram Lev Robinson-Mosher

John Blenis

David E Hill

Jesse S Boehm

Haoxuan Tong

Johann Bergholz

Frederick J King

David F Harris

Erding Hu

Joanne Chan

The present invention is based, in part, on the identification of novel FI.3K-mTORCI-S6K 1 signaling pathway biomarkers predictive of responsiveness to anti-cancer therapies.

P13K-MTORC1-S6K1 signaling pathway biomarkers predictive of anti-cancer responses

The present invention relates to methods for treating PTEN deficient epithelial cancers using a combination of anti-PI3Kbeta and anti-immune checkpoint agents.

Methods for treating PTEN deficient epithelial cancers using a combination of anti-PI3KBETA and anti-immune checkpoint agents

Provided herein are nucleic acids, proteins, vectors, cells, kits, devices and methods useful for identifying regulatable proteins that are able to complement components of cellular signaling pathways. Also provided are compositions and methods using these complementing genes directly as markers for cancer diagnosis or prognosis and as targets for anti-neoplastic therapeutics. Further provided are methods for using changes caused by expression of the complementing genes to indirectly identify associated genes to be used as markers for cancer diagnosis or prognosis and as targets for anti-neoplastic therapeutics.

Compositions and methods for identifying transforming and tumor suppressor genes

The present invention relates to novel SH3 domain binding protein, referred to herein a DEF polypeptides. The DEF polypeptides comprise several motifs including a src SH3 consensus binding sequence, four ankyrin repeats, one zinc finger domain and six copies of a proline-rich tandem repeat. DEF polypeptides may function as mediators of SH3 domain-dependent signal transduction pathways and, thus may mediate multiple signaling events such as cellular gene expression, cytoskeletal architecture, protein trafficking and endocytosis, cell adhesion, migration, proliferation and differentiation. Described herein are isolated and antisense nucleic acids molecules, recombinant expression vectors, host cells and non-human transgenic animals containing an insertion or a disruption of the DEF gene. Diagnostic, screening and therapeutic methods utilizing the compositions of the invention are also provided

Differentiation enhancing factors and uses therefor

The invention relates to therapeutic methods of using a substantially pure protein comprising the .beta.-subunit of a human glycoprotein involved in cellular adhesion, or a biologically active fragment thereof, or analog thereof. These therapeutic methods are useful for treating auto immune diseases and allograft rejection.

Methods for treating various disease states by reducing adhesion of

The present invention discloses a cDNA sequence which encodes the beta-subunit of LFA-1. The present invention further discloses fragments of the cDNA sequence which are capable of recognizing a restriction length polymorphism within the LFA-1 sequence.

Cloning LFA-1

This invention is a process to produce specific proteins coded for by eukaryotic (or prokaryotic) DNA in bacteria. The invention, which uses recombinant DNA techniques, produces proteins in their natural, functional state unencumbered by extraneous peptides.

Fused hybrid gene

Protein synthesis

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Cambridge, MA, United States of America

Thomas M Roberts