| License: Creative Commons Attribution 4.0 PDF - Published Version (2MB) |
- URN to cite this document:
- urn:nbn:de:bvb:355-epub-554598
- DOI to cite this document:
- 10.5283/epub.55459
Abstract
The concept of post-therapy metastatic spread, cancer repopulation and acquired tumor cell resistance (M-CRAC) rationalizes tumor progression because of tumor cell heterogeneity arising from post-therapy genetic damage and subsequent tissue repair mechanisms. Therapeutic strategies designed to specifically address M-CRAC involve tissue editing approaches, such as low-dose metronomic ...

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