University of California

The University of Texas System

Canji Inc.

Academia Sinica

Taivex Therapeutics Corporation

Wen-Hwa Lee

Eva Y.h.p. Lee

Huei-Jen S. Huang

Jiewen Zhu

Eva Y-h Lee

Phang-Lang Chen

H Michael Shepard

Hongyuan Chen

Eva Y-hp Lee

Xuning Guo

Xiao-Long Qiu

Chun-Mei Hu

Richard J Gregory

Che Ma

Theodore Friedmann

Daniel C Maneval

Jiing-Kuan Yee

Ken N Wills

Chia-Lin Chen

Jin-Yuh Shew

Eva Y H P Lee

Huei-Jen Su Huang

Yumay Chen

David Goodrich

Nan-Ping Wang

Wen-Hsin Lee

Huei-Jen Sue Huang

Eva Y -h P Lee

Chun-Kai Huang

David W Goodrich

Xueling Zhu

Longen Zhou

Duane Johnson

Heng-Hsiung Wu

Nan Ping Wang

Bei Shan

Eva Yhp Lee

Huei-Jen S Huang

Methods and compositions for treatment and therapy of cancer are provided. Specifically, antagonists specific for interleukin-17 receptor B (IL-17RB) and its ligand IL-17B are provided. Potent neutralizing antibodies specific for IL-17RB and methods for their manufacture and use are disclosed. The invention also relates to antisense, RNAi and shRNA compositions for the prevention and treatment of cancer, in particular breast cancer and pancreatic cancer.

Isolated antibodies against interleukin-17 receptor B (IL-17RB) for cancer therapy

The present invention includes novel RAD51 inhibitors. The compounds of the invention may be useful in preventing or treating cancer in a subject in need thereof. The present invention also includes methods of preventing or treating cancer in a subject in need thereof by administering to the subject a therapeutically effective amount of a compound of the invention.

RAD51 inhibitors and uses thereof

Certain embodiments of the present invention provide selected compounds having a molecular structure according to Formula 1:  In Formula 1, Z is &#x2014;CO&#x2014;, &#x2014;SO&#x2014;, or &#x2014;SO&#x2014;; Ar is phenyl, heteroaryl, or heterocycloalkyl; Het is heteroaryl; R is R&#x2033;, X, or NRR; R' is R, or OR; R&#x2033; is R, or OR; Rand Rare each independently H, alkyl, or acyl; Ris H, heteroaryl, or alkyl; Ris H, heteroaryl, or CH(n&#x3e;2); and X is F, Br, I, CN, or NO. In some embodiments, compounds having a molecular structure according to Formula 1 have the property of inhibiting a growth of a cell line selected from HeLa and MB468 with a sub-micromolar IC.

Small molecule modifiers of the Hec1-Nek2 interaction in G2/M

Small molecule modifiers of the HEC1-NEK2 interaction in G2/M

Chronic myelogenous leukemia (CML), and in particular imatinib resistant CML is treated using compositions and methods in which a Rad51-inhibitor and a kinase inhibitor are administered. Most preferably, the Rad51 inhibitor comprises an indolyl isoquinoline structure and the kinase inhibitor is a BCR-ABL inhibitor.

Pharmaceutical compositions containing an indoyl isoquinoline containing compound and uses thereof

Contemplated compounds disrupt interaction between BRCA2 and RAD51, likely by binding to RAD51. Based on the crucial role of the BRCA2-RAD51 complex formation in DNA repair and the role of RAD51 in the control of entry into S-phase from G1, numerous compositions and methods are presented. Among other advantageous uses, contemplated compounds may be employed as protective agents for non-neoplastic cells in chemotherapy before exposure of the cells to a chemotherapeutic drug, and/or as DNA-damage sensitizer for neoplastic cells.

Compositions and methods for disruption of BRCA2-Rad51 interaction

The present invention provides methods and compounds for inhibiting HEC1 activity for the treatment of diseases involving cell hyperproliferation, e.g. cancer. The present invention also provides methods of identifying compounds for inhibiting HEC1 activity.

Methods and compounds for inhibiting Hec1 activity for the treatment of proliferative diseases

Disclosed are methods of controlling cell cycle progression by introducing into a cell to be controlled a composition selected from the group consisting of p56protein, a fragment of the p56protein, and the gene encoding p56protein to alter the cell cycle progression while maintaining the viability of the cell. The p56protein has been found to have the unexpected and surprising characteristic of being soluble in low concentrations of glycerol, thereby enhancing its value in pharmaceutical applications and the gene encoding p56when delivered to the hyperproliferating cell inhibits cellular proliferation.

Method of using an adenoviral vector encoding a retinoblastoma protein to treat hyperproliferating cells

A method for gene therapy for cancers wherein chromosomal location of an inactive or defective cancer suppressing gene is established, a replacement gene which is preferably cloned is then used to replace the inactive or defective cancer suppressing gene in the chromosome. In addition to its uses in therapy, the present invention provides a means for prophylactically treating individuals having a genetic predisposition to cancer and provides an animal model for testing for carcinogenicity of environmental substances.

Products and methods for controlling the suppression of the neoplastic phenotype

This invention relates in general to a phosphoprotein product of the retinoblastoma susceptibility gene. In particular, this invention relates to a phosphoprotein ppRB.sup.110 primarily located in the cell nucleus which has a DNA binding activity. The invention also relates to the amino acid sequence of the phosphoprotein and to the specific purified anti-retinoblastoma phosphoprotein antibody. The invention further relates to a method of diagnosing retinoblastoma and other retinoblastoma gene involved cancers, treating such kind of cancers and regulating the oncogenicity of other genes.

ppRB.sup.110 - nuclear phosphoprotein-the retinoblastoma susceptibility

A method that produces substantial quantities of a desired polypeptide, by delivering genetic material into insect cells. For example, cloned genes, or gene fragments or, derivates may be defined, utilizing as appropriate vector, into host cells for high level production of high purity protein in substantial quantities.

Method for producing retinoblastoma gene protein products

This invention relates in general to a genetic control of retinoblastoma and regulation of carcinogenicity. In particular this invention relates to the cloning, isolation, identification and sequencing of the retinoblastoma gene. The invention also relates to the method of use of the cloned retinoblastoma gene cDNA as a tool for diagnosing retinoblastoma, osteosarcoma and fibrosarcoma. Finally, the invention relates to the control and regulatory mechanisms and functions of the retinoblastoma gene in the oncogenesis.

Retinoblastoma gene-cancer suppressor and regulator

Products and methods for controlling the suppression of the neoplastic

This invention provides a method of preventing or inhibiting the proliferation of a pathologically proliferating cell, wherein the pathological proliferation of the cell is the result of the absence of a functional retinoblastoma protein or polypeptide in the cell. The method requires contacting the cell with an effective amount of retinoblastoma protein or polypeptide. This method also is useful to prevent or treat retinoblastoma or a secondary cancer to retinoblastoma by administering to a patient a functional retinoblastoma protein or polypeptide.

Therapeutic use of the retinoblastoma susceptibility gene product

Growing community of inventors

Newport Coast, CA, United States of America

Wen-Hwa Lee