Oncology is one of the most important fields of personalized medicine as a majority of efforts in this field have recently centered on targeted cancer drug development. New tools are continuously being developed that promise to make cancer treatment more efficacious while causing fewer side effects. Like most industries, the biopharmaceutical industry is also following certain global trends and these are analyzed in this article. As academia and industry are mutually dependent on each other, researchers in the field should be aware of those trends and the immediate consequences for their research. It is important for the future of this field that there is a healthy relationship among all interested parties as the challenges of personalized medicine are becoming ever more complex.
References
[1]
FDA. Drugs@FDA. Available online: http://www.accessdata.fda.gov/scripts/cder/drugsatfda/ (accessed on 7 February 2012).
[2]
Datamonitor. Market and Product Forecasts: Targeted Cancer Therapies—Trend towards Personalized Medicine Will Lead to Market Fragmentation. 2011.
[3]
Futreal, P.A.; Campbell, P.J.; Stratton, M.R. The cancer genome. Nature 2009, 458, 719–724, doi:10.1038/nature07943. 19360079
[4]
Cox, D.R.; Frazer, K.A.; Ballinger, D.G.; Eskin, E.; Halperin, E.; Nilsen, G.B.; Stuve, L.L.; Hinds, D.A. Whole-genome patterns of common DNA variation in three human populations. Science 2005, 307, 1072–1079, doi:10.1126/science.1105436. 15718463
[5]
Medtrack. Medtrack: Biomedical Corporate Intelligence Database. Available online: http://www.medtrack.com/ (accessed on 7 February 2012).
[6]
Thomson Reuters. Thomson Reuters Pharma Database.: New York, NY, USA, 2011; pp. 118–8. Available online: https://www.thomson-pharma.com/ , accessed on 7 February 2012.
[7]
Deininger, M.W.; Guilhot, F.; Talpaz, M.; Schiffer, C.A.; Ottmann, O.G.; Miller, C.B.; Goldman, J.M.; Feldman, E.; Hochhaus, A.; Sawyers, C.L.; et al. Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: Results of a phase II study. Blood 2002, 99, 3530–3539, doi:10.1182/blood.V99.10.3530. 11986204
[8]
Thomas, D.A.; Garcia-Manero, G.; Faderl, S.; Shan, J.; Rios, M.B.; Albitar, M.; Giles, F.J.; O’Brien, S.; Cortes, J.; Kantarjian, H.M.; et al. Imatinib mesylate (STI571) therapy for Philadelphia chromosome-positive chronic myelogenous leukemia in blast phase. Blood 2002, 99, 3547–3553, doi:10.1182/blood.V99.10.3547. 11986206
[9]
Ohno-Jones, S.; Capdeville, R.; Kantarjian, H.; Lydon, N.B.; Ford, J.M.; Buchdunger, E.; Peng, B.; Resta, D.J.; Talpaz, M.; Druker, B.J.; et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N. Engl. J. Med. 2001, 344, 1031–1037, doi:10.1056/NEJM200104053441401. 11287972
[10]
Rudoltz, M.; Radich, J.P.; Müller, M.C.; Goldman, J.M.; Foroni, L.; Branford, S.; Druker, B.J.; Guilhot, F.; O’Brien, S.G.; Hochhaus, A.; et al. IRIS Investigators. Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia. Leukemia 2009, (23), 1054–1061.
[11]
Lindblom, A.; Koskenvesa, P.; Flogeg？rd, M.; Bj？reman, M.; Almqvist, A.; Stentoft, J.; Remes, K.; Markev？rn, B.; Gedde-Dahl, T.; Simonsson, B.; et al. Combination of pegylated IFN-α2b with imatinib increases molecular response rates in patients with low- or intermediate-risk chronic myeloid leukemia. Blood 2011, 118, 3228–3235, doi:10.1182/blood-2011-02-336685. 21685374
[12]
Minna, J.D.; Papadimitrakopoulou, V.; Herbst, R.S.; Peng, Z.; Sun, D.; Bornmann, W.G.; Bekele, B.N.; Fang, B.; Dai, B.; Meng, J.; et al. Combination treatment with MEK and AKT inhibitors is more effective than each drug alone in human non-small cell lung cancer in vitro and in vivo. PLOS One 2010, (5), 3228–3235, doi:10.1371/journal.pone.0014124.
[13]
Novartis. Novartis Oncology Products. Available online: http://www.novartisoncology.com/novartis-oncology-products/ (accessed on 7 February 2012).
[14]
J？nne, P.A.; Engelman, J.A. Mechanisms of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer. Clin. Cancer Res. 2008, 14, 2895–2899, doi:10.1158/1078-0432.CCR-07-2248. 18483355
[15]
Murray, S.; Papadimitriou, C.A.; Kosmidis, P.; Bafaloukos, D.; Siannis, F.; Kanaloupiti, D.; Dahabreh, I.J.; Linardou, H. Assessment of somatic k-RAS mutations as a mechanism associated with resistance to EGFR-targeted agents: A systematic review and meta-analysis of studies in advanced non-small-cell lung cancer and metastatic colorectal cancer. Lancet Oncol. 2008, 9, 962–972, doi:10.1016/S1470-2045(08)70206-7. 18804418
[16]
Marchant, J. Key Trends in Drug-Diagnostic Co-Development; Business Insight Ltd.: Dallas, TX, USA, 2009; pp. 118–8.
Gray, N.S.; Yang, P.L.; Zhang, J. Targeting cancer with small molecule kinase inhibitors. Nat. Rev. Cancer 2009, 9, 28–39, doi:10.1038/nrc2559. 19104514
[19]
Carmichael, J.; Friedlander, M.; Weitze, J.N.; Audeh, M.W.; Domchek, S.; Garber, J.E.; Robson, M.; Tutt, A. Phase II trial of the oral PARP inhibitor olaparib in BRCA-deficient advanced breast cancer. J. Clin. Oncol. ASCO Annual Meeting Proceedings (Post-Meeting Edition) 2009, (27(15S)), 358–362.
[20]
Tutt, A.; Carmichael, J.; Weitzel, J.N.; Scott, C.; Bell-McGuinn, K.M.; Powell, B.; Friedlander, M.; Penson, R.T.; Audeh, M.W. Phase II trial of the oral PARP inhibitor olaparib (AZD2281) in BRCA-deficient advanced ovarian cancer. J. Clin. Oncol. ASCO Annual Meeting Proceedings (Post-Meeting Edition). 2009, (27 (15S)), 358–362.
[21]
Rüegg, C.; Del Conte, G.; Guibal, A.; Sessa, C. Biomarkers of angiogenesis for the development of antiangiogenic therapies in oncology: Tools or decorations? Nat. . Clin. Pract. Oncol. 2008, 5, 378–391, doi:10.1038/ncponc1150.
[22]
Sawyers, C.L.; Rao, P.N.; Paquette, R.; Hsu, N.; Ellwood, K.; Mohammed, M.; Gorre, M.E. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science 2001, 293, 876–880, doi:10.1126/science.1062538. 11423618
[23]
Maiti, T.K.; Mallick, S.K.; Bhutia, S.K. Tumour escape mechanisms and their therapeutic implications in combination tumour therapy. Cell Biol. Int. 2010, 34, 553–563, doi:10.1042/CBI20090206. 20384587
[24]
Mietlowski, W.; Rae, P.; Manley, P.; Tanaka, C.; Wassmann, B.; O’Brien, S.; Bhalla, K.; Wunderle, L.; Giles, F.; Kantarjian, H.; et al. Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL. N. Engl. J. Med. 2006, 354, 2542–2551, doi:10.1056/NEJMoa055104. 16775235
[25]
Carlson, R.H. Ponatinib effective in heavily pretreated CML patients with T3151 mutation. Oncol. Times UK 2011, 8, 17–18.
[26]
Kaufman, P.A., Jr.; Paik, S., Jr.; Martino, S., Jr.; Tan-Chiu, E., Jr.; Davidson, N.E., Jr.; Geyer, C.E., Jr.; Suman, V.J.; Bryant, J.; Perez, E.A.; Romond, E.H.; et al. Trastuzumab plus adjuvant chemotherapy for operable HER2-positive breast cancer. N. Engl. J. Med. 2005, 353, 1673–1684, doi:10.1056/NEJMoa052122. 16236738
[27]
Esteva, F.J.; Nahta, R. Herceptin: Mechanisms of action and resistance. Cancer Lett. 2006, 232, 123–138, doi:10.1016/j.canlet.2005.01.041. 16458110
[28]
Kozin, S.V.; Kalva, S.P.; Sahani, D.V.; Chung, D.C.; Tong, R.T.; Munn, L.L.; Duda, D.G.; di Tomaso, E.; Boucher, Y.; Willett, C.G.; et al. Direct evidence that the VEGF-specific antibody bevacizumab has antivascular effects in human rectal cancer. Nat. Med. 2004, 10, 145–147, doi:10.1038/nm988. 14745444
[29]
Hassel, J.C.; Schadendorf, D.; Robert, C.; Gonzalez, R.; Haanen, J.B.; Sosman, J.A.; Weber, R.W.; McDermott, D.F.; O’Day, S.J.; Hodi, F.S.; et al. ？Improved survival with ipilimumab in patients with metastatic melanoma. N. Engl. J. Med. 2010, 363, 711–723, doi:10.1056/NEJMoa1003466. 20525992
[30]
Sussman, L. Matching targeted therapies to tumor’s specific gene mutations key to personalized cancer treatment. Eurekalert. Available online: http://www.eurekalert.org/pub_releases/2011-06/uotm-mtt060311.php (accessed on 20 January 2012).
[31]
Mills, G.B.; Hennessy, B.T.; Gonzalez-Angulo, A.M. Future of personalized medicine in oncology: A systems biology approach. J. Clin. Oncol. 2010, 28, 2777–2783, doi:10.1200/JCO.2009.27.0777. 20406928
