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For instance, the detection of minimal residual dis- ease, after potentially curative therapy, may lead to second-line salvage therapies in sarcomas, prostate cancer, and colorectal cancer.
ed candidate rearrangements or chromosomal alterations that could be detected in all colorectal and breast cancer plasma samples analyzed but not in the plasma samples from healthy individuals (nor in a large number of additional normal genomes).
For early- stage disease, the sensitivity of ctDNA approaches has been shown to be =50% in patients with localized colorectal, breast, esophageal, and pancreatic tumors (15, 96, 97), suggesting that this approach may be feasible for early detection in these and other tumor types.
* EGFR-directed therapies in colorectal cancer and PIK3CA-
Understanding, circumventing, and ultimately treating acquired resistance to targeted therapies will require monitoring for multiple molecular mechanisms; acquired drug resistance- associated mutations (such as the T790M-EGFR mutation in lung cancer or emergence of KRAS mutations in colorectal cancer; refs. 101-104) will be measured by either ctDNA or CTC analyses, whereas more complex mechanisms (including EMT or transversions from non-small cell to small cell histolo- gies; ref. 17) will require whole-cell analyses.
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