Princeton University

Genentech, Inc.

Other

Memorial Sloan Kettering Cancer Center

Affymetrix, Inc.

Icahn School of Medicine at Mount Sinai

The Simons Center for Systems Biology at the Institute for Advanced Study

Laessig, Michael

Arnold J Levine

Diane Pennica

Thomas E Shenk

Cathy A Finlay

Austin L Gurney

William I Wood

Audrey Goddard

Kenneth J Hillan

David Botstein

Margaret Ann Roy

Robert L Cohen

David A Lawrence

Taha Merghoub

Jedd David Wolchok

Kurt C Gish

David H Mack

Carlos Cordon-Cardo

Timothy A Chan

Maureen Elizabeth Murphy

Uri Alon

Edward Yat Tom

Mark A Labow

Steven B Baim

Michael Laessig

Steven D Leach

Marta Luksza

Vinod P Balachandran

Benjamin D Greenbaum

Systems and methods for determining the likely responsiveness of a human cancer subject to a checkpoint blockade immunotherapy regimen are provided. Sequencing reads are obtained from samples from the subject representative of the cancer. A human leukocyte antigen type and a plurality of clones is determined from the sequencing reads. For each clone, an initial frequency Xin the one or more samples is determined and a corresponding clone fitness score of the clone is computed, thereby computing clone fitness scores. Each such fitness score is computed by identifying neoantigens in the respective clone, computing a recognition potential for each neoantigen, and determining the corresponding clone fitness score of the respective clone as an aggregate of these recognition potentials. A total fitness, quantifying the likely responsiveness of the subject to the regimen, is computed by summing the clone fitness scores across the plurality of clones.

Neoantigens and uses thereof for treating cancer

Wnt-1-Induced Secreted Proteins (WISPs) are provided, whose genes are induced at least by Wnt-1. Also provided are nucleic acid molecules encoding those polypeptides, as well as vectors and host cells comprising those nucleic acid sequences, chimeric polypeptide molecules comprising the polypeptides fused to heterologous polypeptide sequences, antibodies which bind to the polypeptides, and methods for producing the polypeptides.

WISP polypeptides and nucleic acids encoding same

DNAs are provided, whose genes are induced at least by Wnt-1. Also provided are nucleic acid molecules encoding those polypeptides, as well as vectors and host cells comprising those nucleic acid sequences, chimeric polypeptide molecules comprising the polypeptides fused to heterologous polypeptide sequences, antibodies which bind to the polypeptides, and methods for producing the polypeptides.

Polypeptides and nucleic acids encoding same

Systems and methods for enhanced quantitative analysis of hybridization intensity measurements obtained from oligonucleotide probes and other probes exposed to target samples are provided by virtue of the present invention. One embodiment ameliorates the effects of high frequency noise superimposed on a hybridization intensity measurement signal measured over successive probe alignments to a target sample sequence. Detection of expressed genes and ESTs and quantitative measurement of expression level may be improved. Mutation detection and base calling may be improved.

Quantitative analysis of hybridization patterns and intensities in oligonucleotide arrays

Many genes are identified as being p53-regulated which were not heretofore known to be p53-regulated. This includes both genes whose expression is induced and genes whose expression is repressed by the expression of wild-type p53. Monitoring expression of these genes is used to provide indications of p53 status in a cell. Such monitoring can also be used to screen for useful anti-cancer therapeutics, as well as for substances which are carcinogenic. Defects in p53 can be bypassed by supplying p53 induced genes to cells. Defects in p53 can also be bypassed by supplying antisense constructs to p53-repressed genes.

P53-regulated genes

Method for detecting pre-cancerous or cancerous cells using P90

The present invention relates to novel chimeric transactivating proteins comprising a functional portion of a DNA binding protein and a functional portion of a transcriptional activator protein. The chimeric transactivating proteins of the invention offer a variety of advantages, including the specific activation of expression of genes engineered to comprise transactivator responsive elements, thereby achieving exceptionally high levels of gene expression. Furthermore, in various embodiments of the invention, the transactivator proteins may be used to increase expression of some genes while repressing the expression of others, thus permitting a greater degree of control of gene expression patterns than other currently available systems. In preferred embodiments of the invention, the function of the chimeric transactivator proteins may be induced, for example, by chemical agents (e.g. IPTG) or changes in temperature. In a preferred specific embodiment of the invention, the ability to switch transactivator function on and off may be utilized in the context of transgenic animals and to develop cell lines capable of differentiation.

Eukaryotic cells comprising a DNA sequence encoding a bacterial-viral

A panel of probes detects and distinguishes between sets of human p53 gene or protein mutations that frequently occur or are selected for in pre-cancer and cancer cells Each set of mutations gives rise to a phenotype that is different from that of wild-type p53 and of at least one other set of p53 mutations.

Methods for detecting mutant p53

A panel of probes that detect and distinguish between sets of human p53 gene or protein mutations that frequently occur or are selected for in pre-cancer and cancer cells, each set giving rise to a phenotype that is different from that of wild-type p53 and of at least one other set of p53 mutants.

Methods of diagnosing pre-cancer or cancer states using probes for

Growing community of inventors

Princeton, NJ, United States of America

Arnold J Levine