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. 2013 Dec;15(12):1410-20.
doi: 10.1593/neo.131972.

Cancer subclonal genetic architecture as a key to personalized medicine

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Cancer subclonal genetic architecture as a key to personalized medicine

Alnawaz Rehemtulla. Neoplasia. 2013 Dec.

Abstract

The future of personalized oncological therapy will likely rely on evidence-based medicine to integrate all of the available evidence to delineate the most efficacious treatment option for the patient. To undertake evidence-based medicine through use of targeted therapy regimens, identification of the specific underlying causative mutation(s) driving growth and progression of a patient's tumor is imperative. Although molecular subtyping is important for planning and treatment, intraclonal genetic diversity has been recently highlighted as having significant implications for biopsy-based prognosis. Overall, delineation of the clonal architecture of a patient's cancer and how this will impact on the selection of the most efficacious therapy remain a topic of intense interest.

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References

    1. Agudelo-Garcia PA, De Jesus JK, Williams SP, Nowicki MO, Chiocca EA, Liyanarachchi S, Li PK, Lannutti JJ, Johnson JK, Lawler SE, et al. Glioma cell migration on three-dimensional nanofiber scaffolds is regulated by substrate topography and abolished by inhibition of STAT3 signaling. Neoplasia. 2011;13:831–840. - PMC - PubMed
    1. Bekes EM, Deryugina EI, Kupriyanova TA, Zajac E, Botkjaer KA, Andreasen PA, Quigley JP. Activation of pro-uPA is critical for initial escape from the primary tumor and hematogenous dissemination of human carcinoma cells. Neoplasia. 2011;13:806–821. - PMC - PubMed
    1. Berdiel-Acer M, Bohem ME, Lopez-Doriga A, Vidal A, Salazar R, Martinez-Iniesta M, Santos C, Sanjuan X, Villanueva A, Mollevi DG. Hepatic carcinoma-associated fibroblasts promote an adaptative response in colorectal cancer cells that inhibit proliferation and apoptosis: nonresistant cells die by nonapoptotic cell death. Neoplasia. 2011;13:931–946. - PMC - PubMed
    1. Birbach A, Eisenbarth D, Kozakowski N, Ladenhauf E, Schmidt-Supprian M, Schmid JA. Persistent inflammation leads to proliferative neoplasia and loss of smooth muscle cells in a prostate tumor model. Neoplasia. 2011;13:692–703. - PMC - PubMed
    1. Blando JM, Carbajal S, Abel E, Beltran L, Conti C, Fischer S, DiGiovanni J. Cooperation between Stat3 and Akt signaling leads to prostate tumor development in transgenic mice. Neoplasia. 2011;13:254–265. - PMC - PubMed

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