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• W2023488654 abstract "In her Research News article “Systems for identifying new drugs are often faulty” (7 Nov., p. [1041][1]), Trisha Gura describes numerous studies with xenograft models used in drug sensitivity screens that have failed to detect active compounds to take into clinical trials. She hypothesizes that by applying our rapidly accumulating knowledge of the molecular pathways involved in cancer susceptibility and resistance to this problem, a new rational approach will lead to more specific and efficacious drugs. We submit that the failure to identify potent anticancer compounds with xenograft testing does not result from the lack of tumor models that are genetically matched at a given susceptibility locus, or the site of tumor implantation; instead, the problem lies in the microphysiology of the tumor. If test compounds are physically or metabolically impeded from being uniformly distributed throughout the tumor because of temporarily closed blood vessels or decreased proliferation of tumor cells in poorly perfused regions, then no compound will ever achieve its in vitro killing potential in vivo. If one uses an agent, namely, ionizing radiation, which gives the same dose to all cancer cells, xenograft response is well predicted by the level of DNA damage to the cells. This response of xenografted tumors to ionizing radiation is often measured by a clonogenic assay method, where tumors treated in vivo are dissociated into a single-cell suspension and plated for their ability to form a multicellular colony from a single cell. Numerous studies have demonstrated that the ability to control tumor growth is tightly linked with its clonogenic efficiency. This holds true for tumors that die by activating their endogenous pathway for apoptotic cell death ([1][2]). Rational drug design that takes into account tumor physiology will truly be the next major frontier in cancer therapy.1. [↵][3]1. B. G. Wouters, 2. A. J. Giaccia, 3. N. C. Denko, 4. J. M. Brown , Cancer Res. 57, 4703 (1997). [OpenUrl][4][Abstract/FREE Full Text][5] [1]: /lookup/doi/10.1126/science.278.5340.1041 [2]: #ref-1 [3]: #xref-ref-1-1 View reference 1 in text [4]: {openurl}?query=rft.jtitle%253DCancer%2BResearch%26rft.stitle%253DCancer%2BRes.%26rft.issn%253D0008-5472%26rft.aulast%253DWouters%26rft.auinit1%253DB.%2BG.%26rft.volume%253D57%26rft.issue%253D21%26rft.spage%253D4703%26rft.epage%253D4706%26rft.atitle%253DLoss%2Bof%2Bp21Waf1%252FCip1%2BSensitizes%2BTumors%2Bto%2BRadiation%2Bby%2Ban%2BApoptosis-independent%2BMechanism%26rft_id%253Dinfo%253Apmid%252F9354425%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [5]: /lookup/ijlink/YTozOntzOjQ6InBhdGgiO3M6MTQ6Ii9sb29rdXAvaWpsaW5rIjtzOjU6InF1ZXJ5IjthOjQ6e3M6ODoibGlua1R5cGUiO3M6NDoiQUJTVCI7czoxMToiam91cm5hbENvZGUiO3M6NjoiY2FucmVzIjtzOjU6InJlc2lkIjtzOjEwOiI1Ny8yMS80NzAzIjtzOjQ6ImF0b20iO3M6MjM6Ii9zY2kvMjc5LzUzNDcvMTAuNS5hdG9tIjt9czo4OiJmcmFnbWVudCI7czowOiIiO30=" @default.
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• W2023488654 date "1998-01-02" @default.
• W2023488654 modified "2023-09-24" @default.
• W2023488654 title "Cancer Therapy and Tumor Physiology" @default.
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• W2023488654 doi "https://doi.org/10.1126/science.279.5347.10e" @default.
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