Circulating tumor cells (CTCs) are a valuable biomarker for the diagnosis, prognosis, and therapeutic management of gastrointestinal (GI) cancers. A major challenge in GI cancer treatment is the high rate of metastasis, which significantly contributes to cancer-related mortality. CTCs are crucial in the metastatic cascade, serving as indicators of tumor progression. Therefore, the detection and molecular characterization of CTCs have prognostic potential for identifying early-stage GI cancers and assessing metastatic probability, enabling timely treatment. Moreover, CTC analysis offers a minimally invasive method for real-time monitoring of tumors.Clinicians can adjust therapeutic strategies accordingly by tracking changes in CTC count and molecular profile. Despite this promising application, no standardized protocol for CTC isolation in GI tract cancers has been established, which poses a barrier to routine clinical use. This review explores the current CTC detection methodologies, their clinical relevance in GI cancer management, and the potential integration of CTC analysis into personalized medicine. We also discuss the challenges and future directions in CTC research, focusing on clinical validation and the development of standardized procedures to fully realize the utility of CTC count for improving patient care.

Background: This study aimed to identify the specific T cell co-stimulatory and co-inhibitory factors that play prognostic roles in patients with glioblastoma. Additionally, the unique histone H3 modification enzymes that regulate the expression levels of these specific costimulatory and co-inhibitory factors were investigated. Methods: The medical records of 84 patients newly diagnosed with glioblastoma at our institution from January 2006 to December 2020 were retrospectively reviewed.Immunohistochemical (IHC) staining for T cell co-stimulatory factors (CD27, CD28, CD137, OX40, and ICOS), T cell co-inhibitory factors (CTLA4, PD1, PD-L1, TIM3, and CD200R), and histone H3 lysine modification enzymes (MLL4, RIZ, EZH1, NSD2, KDM5c, JMJD1a, UTX, and JMJD5) was performed on archived paraffin-embedded tissues obtained by biopsy or resection. Quantitative real time-polymerase chain reaction (qRT-PCR) was performed for specific factors, which demonstrated causal relationships, in order to validate the findings of the IHC examinations. Results: The mean follow-up duration was 27.5 months (range, 4.1–43.5 months). During this period, 76 patients (90.5%) died, and the mean OS was 19.4 months (95% confidence interval, 16.3–20.9 months). Linear positive correlations were observed between the expression levels of CD28 and JMJD1a (R2 linear = 0.982) and those of CD137 and UTX (R2 linear = 1.528). Alternatively, significant negative correlations were observed between the expression levels of CTLA4 and RIZ (R2 linear = −1.746) and those of PD-L1 and EZH1 (R2 linear = −2.118); relationships were confirmed by qRT-PCR. In the multivariate analysis, increased expression levels of CD28 (P = 0.042), and CD137 (P = 0.009), and decreased expression levels of CTLA4 (P = 0.003), PD-L1 (P = 0.020), and EZH1 (P = 0.040) were significantly associated with longer survival. Conclusion These findings suggest that the expression of certain T cell co-stimulatory factors, such as CD28 and CD 137, and co-inhibitory factors, such as CTLA4 and PD-L1 are associated with prognosis of glioblastoma patients.