Towards patient-based cancer therapeutics

A new approach to the discovery of cancer therapeutics is emerging that begins with the cancer patient. Genomic analysis of primary tumors is providing an unprecedented molecular characterization of the disease. The next step requires relating the genetic features of cancers to acquired gene and pathway dependencies and identifying small-molecule therapeutics that target them.

[1]  J. Melo,et al.  The tyrosine kinase inhibitor CGP57148B selectively inhibits the growth of BCR-ABL-positive cells. , 1997, Blood.

[2]  Gerald C. Chu,et al.  P53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation , 2008, Nature.

[3]  A. Iafrate,et al.  Identification of genotype-correlated sensitivity to selective kinase inhibitors by using high-throughput tumor cell line profiling , 2007, Proceedings of the National Academy of Sciences.

[4]  A. Krasnitz,et al.  An Oncogenomics-Based In Vivo RNAi Screen Identifies Tumor Suppressors in Liver Cancer , 2008, Cell.

[5]  M. Wigler,et al.  Identification and Validation of Oncogenes in Liver Cancer Using an Integrative Oncogenomic Approach , 2006, Cell.

[6]  R. Rosenfeld.  Nature , 2009, Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery.

[7]  T. Golub,et al.  Modeling genomic diversity and tumor dependency in malignant melanoma. , 2008, Cancer research.

[8]  Ian Collins,et al.  Probing the Probes: Fitness Factors For Small Molecule Tools , 2010, Chemistry & biology.

[9]  Wei Keat Lim,et al.  The transcriptional network for mesenchymal transformation of brain tumors , 2009, Nature.

[10]  C. Thompson,et al.  Attacking Cancer at Its Root , 2009, Cell.

[11]  A. Joe,et al.  Mechanisms of Disease: oncogene addiction—a rationale for molecular targeting in cancer therapy , 2006, Nature Clinical Practice Oncology.

[12]  Luca Toschi,et al.  Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC. , 2010, Cancer cell.

[13]  Yuri Kotliarov,et al.  Tumor stem cells derived from glioblastomas cultured in bFGF and EGF more closely mirror the phenotype and genotype of primary tumors than do serum-cultured cell lines. , 2006, Cancer cell.

[14]  Michael Peyton,et al.  Synthetic lethal screen identification of chemosensitizer loci in cancer cells , 2007, Nature.

[15]  Ji Luo,et al.  Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction , 2009, Cell.

[16]  Ben S. Wittner,et al.  Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1 , 2009, Nature.

[17]  P. Bach.  Limits on Medicare's ability to control rising spending on cancer drugs. , 2009, The New England journal of medicine.

[18]  S. Schreiber,et al.  Perturbational profiling of a cell-line model of tumorigenesis by using metabolic measurements , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[19]  Stephen V Frye,et al.  The art of the chemical probe. , 2010, Nature chemical biology.

[20]  J. Downing,et al.  Mouse models of human AML accurately predict chemotherapy response. , 2009, Genes & development.

[21]  Laura Tolosi,et al.  Predicting drug susceptibility of non-small cell lung cancers based on genetic lesions. , 2009, The Journal of clinical investigation.

[22]  V. Detours,et al.  Human cancer cell lines: Experimental models for cancer cells in situ? For cancer stem cells? , 2009, Biochimica et biophysica acta.

[23]  S. Aggarwal.  Targeted cancer therapies , 2010, Nature Reviews Drug Discovery.