PERSPECTIVES with cancer are not all the same and personalized approach to their care. 005 23. e.P.AMechani and future 60637.Us tcimitedtocnroling doe10.1038h318l 66, 20 26 trial desion N ment andng 28 As a con ch Genome Atlas 6 31. rugtargets than ever before.Indeed,the era (BOX nidable and 9 se to and clinically discrete tumour subsets Anincreasing number of drug targets . ncer [r a 12. rD10759 randomi nd pre N.et al P s that nd 14 tumour regr r ly cal d 220 es of 16 in many trials. ew para 18. 4290. 21582005 19. atory 22 LLINKS ARE ACTIVE IN THE ONLNE PDE together to meet these challenges.Patients 947-9572009 366 MAY 2010 VOLUME 9 www.nature.com/reviews/drugdisc 2010 Matmillan Publishers Limited.All rizhts reserve also resistant to EGFR-directed antibodies. These data raise the possibility of further limiting the use of these agents to patients with wild-type genetic markers in each of these segments of the EGFR signalling pathway36. Ongoing and future clinical trials with cetuximab will be limited to enrolling patients with KRAS wild-type tumours, thereby increasing the possibility of demon￾strating benefit from the drug by excluding a non-responsive patient population. Conclusion Personalized cancer care is rapidly becoming a reality in the clinical assessment and management of patients. As a consequence, the expectation is that this approach will improve treatment efficacy, reduce toxicity and minimize cost. Ongoing genome￾profiling activities such as the National Cancer Institute’s Cancer Genome Atlas and the Sanger Institute’s Cancer Genome Project hold promise to reveal more drug targets than ever before. Indeed, the number will grow even more as epigenetic targets are identified. With more than 800 anticancer drugs already in clinical devel￾opment, the challenges of the targeted therapy era (BOX 2) are formidable and include the following: • The identification of more biologically and clinically discrete tumour subsets. • An increasing number of drug targets and agents in development. • Greater use of placebo controls and randomized trials that require more patients and present greater recruitment challenges. • A longer time to reach time-to-event end points for agents that do not produce tumour regression. • More expensive clinical documentation to record progression events. • The availability of multiple lines of effective therapy making it challenging to demonstrate a survival advantage in many trials. • Greater regulatory complexity for studies that seek approval of both drugs and diagnostic tests. 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DATABASES entrez Gene: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=gene BrAF | CYP2D6 | eGFr | erCC1 | Her2 | KrAs | MGMT | PTeN | UGT1A1 OMiM: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMiM Breast cancer | chronic myeloid leukaemia | colorectal cancer | gastointestinal stromal tumours | non-small cell lung cancer FURTHER InFORMATIOn Accelerating Development and Approval of targeted cancer therapies: http://www.brookings.edu/~/media/ Files/events/2009/0914_clinical_cancer_research/ Panel3%20ApresFiNAL.pdf the Brookings institute: http://www.brookings.edu the cancer Genome Atlas: http://cancergenome.nih.gov the cancer Genome Project: http://www.sanger.ac.uk/genetics/CGP All links Are AcTive in The online PDf Pers P ectives 366 | MAY 2010 | vOLUME 9 www.nature.com/reviews/drugdisc © 2010 Macmillan Publishers Limited. All rights reserved