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. 2006 Jan 9:4:3.
doi: 10.1186/1479-5876-4-3.

Adding pharmacogenomics to the development of new marine-derived anticancer agents

José Jimeno  1 , Miguel Aracil, Juan Carlos Tercero
Affiliations

Adding pharmacogenomics to the development of new marine-derived anticancer agents

José Jimeno et al. J Transl Med. .

Abstract

Nature has always been a highly productive tool in the development of anticancer therapies. Renewed interest in the potential of this tool has recently been sparked by the realization that the marine ecosystem can be used for the discovery and development of new compounds with clinical potential in advanced resistant tumors. These compounds can be incorporated into combination approaches in a chronic therapy scenario. Our marine anticancer program is using the sea to develop new agents with activity in resistant solid tumors and to identify new cellular targets for therapeutic intervention. This review describes the integration of different pharmacogenomic tools in the development of Yondelis, Aplidin and Kahalalide F, three marine-derived compounds currently in Phase II or III development. Our results are reinforcing the targeted selectivity of these agents and opening the gates for customized therapies in cancer patients in the near future.

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Figures

Figure 1
Figure 1
Chemical structure of Yondelis™.
Figure 2
Figure 2
Strategy of the proposed pharmacogenomic program of Yondelis™ in sarcoma patients: Gene expression profiles of tumor samples from sarcoma patients treated with Yondelis will be retrospectively analyzed and correlated with their clinical outcome. The DNA repair capability will be analyzed in blood samples of the same patients in order to be used as surrogate marker of response. The putative correlation found between GEP and clinical outcome will be prospectively analyzed in sarcoma patients and further studied in other tumors.
Figure 3
Figure 3
Chemical structure of Aplidin®.
Figure 4
Figure 4
Aplidin® in vitro differentiation of sensitive and resistant leukemic blasts.
Figure 5
Figure 5
Molecular signatures of sensitivity to Aplidin (APLD) in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) patient blasts.
Figure 6
Figure 6
Chemical structure of Kahalalide F.
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