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Assaying Circulating-Tumor DNA To Predict Recurrence of Localized Colon Cancer.

© Digestive Medicine Research. All rights reserved. Dig Med Res 2020 | http://dx.doi.org/10.21037/dmr.2020.04.02 Colorectal cancer (CRC) is a genetic disease in which cells have accumulated multiple changes in the genome to advantage excessive uncontrolled proliferation for morphological growth and capability for metastases (1,2). The genetic and epigenetic changes commence in affected stem cells to generate precursor adenomas, with additional changes accruing that advance the histology and malignant potential to an early stage cancer, and further progression to advanced stage cancer. Directly assaying human CRCs demonstrate hypermutated tumors in ~15% of cases that are driven most commonly by epigenetic silencing of the DNA mismatch repair gene MLH1 causing coding exon frameshift mutations, and non-hypermutated tumors in ~85% of cases that commonly show mutations of APC, KRAS, and TP53 genes as principal drivers (2-4). These two major genetic pathways for CRC development and progression show differences in histology, immune infiltration, location within the colon, patient outcome, and response and approach to treatment (5-10). The march towards more accurate precision medicine for patients with CRC is deemed worthy as the genetics of CRC are further characterized, and despite the fact that tumors can be heterogeneous while at the same time be genetically unique for each patient (2,11). Screening is the principal approach in preventing CRC (12,13); once CRC develops, surgical resection is the primary method for attempted cure of the patient (for patients with low rectal tumors, they first receive neoadjuvant chemoradiotherapy) (7,14). However, among those patients who undergo curative surgery and adjuvant treatment, as many as 40% may recur or relapse metachronously (15,16). The mechanism for recurrence is presumed through the occurrence of microscopic metastases that are not apparent by currently-utilized diagnostic techniques at the time of initial staging. Methods that can detect the presence of residual disease after attemptive curative surgery will change surveillance and management of patients, and can categorize patients for enhanced surveillance and additional treatments from those who don’t possess micrometastases. This will require the use of accurate and highly predictable biomarkers as compared to the current use of radiographic imaging and current use of the serum marker carcinoembryonic antigen (CEA) to diagnose recurrence, as both are not sensitive enough for the purpose of detecting micrometastases (Table 1). In addition, neither radiographic imaging or CEA can fully quantitate patient tumor burden nor specify changes in the genetic and epigenetic profile of the patient’s tumor that might have resulted from initial treatments towards curing the tumor. This last point had been only previously possible with direct assay of the primary and/or metastatic tissue, and could not be re-performed after tumor resection or significant regression of tumor size. Thus, more ideal biomarkers that can detect residual disease after curative Editorial Commentary