Cancer Genetics and Epigenetics, 2025, Vol.13, No.6, 287-299 http://medscipublisher.com/index.php/cge 289 has strong predictive value. The latest recurrence prediction models have begun to combine these molecular markers with traditional clinicopathological factors, thereby improving the accuracy of risk assessment and providing a basis for formulating more individualized postoperative follow-up and treatment plans (Gao et al., 2023; Tang et al., 2025). 2.3 Differences in individual recurrence patterns The recurrence patterns of different colorectal cancer patients vary significantly, which is influenced by multiple factors such as the location, stage, molecular characteristics of the primary tumor and the perioperative treatment status. The recurrence time and location of patients vary. Although the peak of recurrence mostly occurs within 2 years after surgery, the recurrence time varies greatly due to different individual risk factors (Ryu et al., 2023; Kawashima et al., 2025). For instance, the overall recurrence rate and local recurrence rate of rectal cancer are usually higher than those of colon cancer. In addition, special cases such as anastomotic fistula and tumor invasion of the surgical margin will further change the recurrence pattern (Imaoka et al., 2025). In addition, surgery-related complications such as intraoperative bleeding and postoperative infection may also increase the possibility of local recurrence, indicating that the risk of recurrence is jointly affected by multiple factors (Takagi et al., 2025). The interaction of genes, epigenetics and environmental factors makes the differences in recurrence patterns more obvious. Some patients have a rapid disease progression when they relapse, and multiple metastatic foci may appear. Some patients may have a later recurrence time or only present with a single metastatic lesion. In such cases, the condition can still be controlled through radical salvage therapy (Liu, 2025). At present, machine learning models and morphological maps integrating a large number of clinicopathological and molecular indicators have shown higher accuracy in predicting individual recurrence risk and recurrence patterns (Tang et al., 2025). Understanding and attaching importance to such individual differences is of great significance for adjusting the monitoring frequency, screening patients in need of adjuvant therapy, and improving the long-term survival effect of colorectal cancer patients (Ryu et al., 2023; Huang et al., 2025). 3 The Principle and Detection Technology of ctDNA 3.1 The origin, biological characteristics and release mechanism of ctDNA Circulating tumor DNA (ctDNA) is small segments of free DNA released by tumor cells into the bloodstream. These fragments are mainly produced when tumor cells undergo apoptosis, necrosis or active secretion (Chen et al., 2025; Shim et al., 2025). In patients with colorectal cancer, the amount of ctDNA generally reflects the tumor burden and growth status. The larger and faster the tumor grows, the more ctDNA there is usually in the blood. Tumors with microsatellite instability typically produce higher levels of ctDNA (Andersen et al., 2024). ctDNA stays in the body for a very short time, usually no more than 2 hours, so it can quickly reflect whether the tumor has changed. Precisely because of this, ctDNA is regarded as a relatively sensitive detection method, capable of identifying extremely small residual lesions or early recurrence, and abnormalities can often be detected several months earlier than imaging examinations. The biological characteristics of ctDNA stem from tumor-specific genes and epigenetic alterations, which distinguish it from normal free DNA. Typically, ctDNA fragments are shorter than normal free DNA and may have unique fragment characteristics, methylation patterns, and the same gene mutations as primary tumors (Chen et al., 2025). The ctDNA fragment is mainly the size of a monomsome, indicating that it mainly originates from apoptosis. However, in rapidly growing or oxygen-deficient tumors, cell necrosis and active release can also produce a portion of ctDNA. The proportion of ctDNA in total free DNA varies greatly. It may be less than 0.01% in early-stage cancer patients, while it can exceed 10% in advanced-stage patients. This characteristic brings both opportunities and challenges to detection. To better use ctDNA as a biomarker in the diagnosis and treatment of colorectal cancer, it is very important to understand its release mechanism and biological differences (Andersen et al., 2024; Zhu, 2025). 3.2 Main testing platforms: dPCR, NGS, personalized panels ctDNA detection requires highly sensitive molecular techniques to identify rare tumor-derived DNA fragments in a large amount of normal free DNA. Currently, the two most commonly used technical platforms in clinical practice and research are digital PCR (dPCR, including droplet digital PCR and DPCR) and next-generation
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