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Colorectal cancer (CRC) is a global health challenge, and patient education plays a crucial role in its early detection and treatment. Despite progress in AI technology, as exemplified by transformer-like models such as ChatGPT, there remains a lack of in-depth understanding of their efficacy for medical purposes. We aimed to assess the proficiency of ChatGPT in the field of popular science, specifically in answering questions related to CRC diagnosis and treatment, using the book "Colorectal Cancer: Your Questions Answered" as a reference. In general, 131 valid questions from the book were manually input into ChatGPT. Responses were evaluated by clinical physicians in the relevant fields based on comprehensiveness and accuracy of information, and scores were standardized for comparison. Not surprisingly, ChatGPT showed high reproducibility in its responses, with high uniformity in comprehensiveness, accuracy, and final scores. However, the mean scores of ChatGPT's responses were significantly lower than the benchmarks, indicating it has not reached an expert level of competence in CRC. While it could provide accurate information, it lacked in comprehensiveness. Notably, ChatGPT performed well in domains of radiation therapy, interventional therapy, stoma care, venous care, and pain control, almost rivaling the benchmarks, but fell short in basic information, surgery, and internal medicine domains. While ChatGPT demonstrated promise in specific domains, its general efficiency in providing CRC information falls short of expert standards, indicating the need for further advancements and improvements in AI technology for patient education in healthcare. [ABSTRACT FROM AUTHOR]

Colorectal tumors often create an immunosuppressive microenvironment that prevents them from responding to immunotherapy. Cannabidiol (CBD) is a non-psychoactive natural active ingredient from the cannabis plant that has various pharmacological effects, including neuroprotective, antiemetic, anti-inflammatory, and antineoplastic activities. This study aimed to elucidate the specific anticancer mechanism of CBD by single-cell RNA sequencing (scRNA-seq) and single-cell ATAC sequencing (scATAC-seq) technologies. Here, we report that CBD inhibits colorectal cancer progression by modulating the suppressive tumor microenvironment (TME). Our single-cell transcriptome and ATAC sequencing results showed that CBD suppressed M2-like macrophages and promoted M1-like macrophages in tumors both in strength and quantity. Furthermore, CBD significantly enhanced the interaction between M1-like macrophages and tumor cells and restored the intrinsic anti-tumor properties of macrophages, thereby preventing tumor progression. Mechanistically, CBD altered the metabolic pattern of macrophages and related anti-tumor signaling pathways. We found that CBD inhibited the alternative activation of macrophages and shifted the metabolic process from oxidative phosphorylation and fatty acid oxidation to glycolysis by inhibiting the phosphatidylinositol 3-kinase-protein kinase B signaling pathway and related downstream target genes. Furthermore, CBD-mediated macrophage plasticity enhanced the response to anti-programmed cell death protein-1 (PD-1) immunotherapy in xenografted mice. Taken together, we provide new insights into the anti-tumor effects of CBD. [Display omitted] • CBD shapes the TME to prevent tumor progression. • CBD-induced metabolic reprogramming inhibits alternative activation of macrophage. • CBD inhibits PI3K-Akt signaling to downregulate anti-inflammatory gene expression. • CBD enhances the response to anti-PD-1 immunotherapy. [ABSTRACT FROM AUTHOR]

This document is a retraction notice from the journal Cancer Management & Research. The article being retracted is titled "SHP-2 Interacts with CD81 and Regulates the Malignant Evolution of Colorectal Cancer by Inhibiting Epithelial–Mesenchymal Transition" by Yuan et al. (2020). The retraction is due to concerns about the duplication of images from Figure 2 with images from unrelated articles. The authors were unable to provide an explanation or data for the study, leading to the decision to retract the article. The retracted article will remain online but will be marked as "Retracted." [Extracted from the article]

Gastrointestinal tract cancers have high incidence and mortality in China, but their molecular characteristics have not been fully investigated. We sequenced 432 tumor samples from the colorectum, stomach, pancreas, gallbladder, and biliary tract to investigate cancer-related mutations and detail the landscape of microsatellite instability (MSI), tumor mutation burden (TMB), and chromosomal instability (CIN). We observed the highest TMB in colorectal and gastric cancers and the lowest TMB in gastrointestinal stromal tumors (GISTs). Twenty-four hyper-mutated tumors were identified only in colorectal and gastric cancers, with a significant enrichment of mutations in the polymerase genes (POLE , POLD1 , and POLH) and mismatch repair (MMR) genes. Additionally, CIN preferentially occurred in colorectal and gastric cancers, while pancreatic, gallbladder, and biliary duct cancers had a much lower CIN. High CIN was correlated with a higher prevalence of malfunctions in chromosome segregation and cell cycle genes, including the copy number loss of WRN , NAT1 , NF2 , and BUB1B , and the copy number gain of MYC , ERBB2 , EGFR , and CDK6. In addition, TP53 mutations were more abundant in high-CIN tumors, while PIK3CA mutations were more frequent in low-CIN tumors. In colorectal and gastric cancers, tumors with MSI demonstrated much fewer copy number changes than microsatellite stable (MSS) tumors. In colorectal and gastric cancers, the molecular characteristics of tumors revealed the mutational diversity between the different anatomical origins of tumors. This study provides novel insights into the molecular landscape of Chinese gastrointestinal cancers and the genetic differences between tumor locations, which could be useful for future clinical patient stratification and targeted interventions. [ABSTRACT FROM AUTHOR]

Purpose: Colon cancer is a common malignant tumor of the digestive system. This project verified the negative role of protein tyrosine phosphatase (SHP-2) in the regulation of colon cancer and further clarified the key targets and molecular mechanisms in the regulation process. Patients and Methods: The expression levels of SHP-2 in colon cancer tissues, adjacent tissues, normal colon cell lines, and cancer cell lines were detected via Quantitative Real-time PCR (qRT-PCR). The effect of SHP-2 on colon cancer cell function was verified using cell proliferation, Transwell, scratch, and apoptotic assays. CD81 was identified as the interaction protein of SHP-2 by immunoprecipitation. Results: The expression of SHP-2 was decreased in colorectal cancer compared with that in adjacent tissues. This expression was also decreased in colon cancer cells compared with that in intestinal epithelial cells. In addition, the tumor tissues of patients with metastatic colon cancer exhibited downregulated expression of SHP-2 compared with those of patients with non-metastatic colon cancer. Cell proliferation, Transwell, scratch, and apoptotic assay showed that the overexpression of SHP-2 inhibited proliferation, adhesion, and metastasis of colon cancer cell lines and promoted apoptosis. CO-IP proved that SHP-2 could interact with CD81 and inhibit the function of CD81. Recovery experiments confirmed that the overexpression of CD81 reversed the anti-cancer effect of SHP-2. Conclusion: Overexpression of SHP-2 inhibited malignant progression of colon cancer. Mechanism experiments showed that the anti-cancer effect of SHP-2 was realized through the interaction with CD81. This study elucidated the molecular mechanism of SHP-2 regulation in colon cancer and provided guidance for the diagnosis and prognosis assessment of colon cancer. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is the third most common cancer globally. Regorafenib, a multi-target kinase inhibitor, has been approved for treating metastatic colorectal cancer patients who have undergone at least two prior standard anti-cancer therapies. However, regorafenib efficacy as a single agent remains suboptimal. A promising target at the crossroads of multiple signaling pathways is the Src homology 2 domain-containing protein tyrosine phosphatase (SHP2). However, a combination approach using SHP2 inhibitors (SHP099) and anti-angiogenic drugs (Regorafenib) has not been reported in current research. In this study, we conducted in vitro experiments combining SHP099 and regorafenib and established an MC-38 colon cancer allograft mouse model. Our results revealed that co-treatment with SHP099 and regorafenib significantly inhibited cell viability and altered the biological characteristics of tumor cells compared with treatment alone in vitro. Furthermore, the combination strategy demonstrated superior therapeutic efficacy compared to monotherapy with either drug. This was evidenced by reduced tumor size, decreased proliferation, increased apoptosis, normalized tumor microvasculature, and improved antitumor immune response in vivo. These findings suggest that the combination of an SHP2 inhibitor and regorafenib is a promising therapeutic approach for patients with colorectal cancer. • Regorafenib monotherapy extends colorectal cancer survival, but duration is brief. • SHP2 inhibitors shows encouraging outcomes in multiple clinical trials. • Initial Exploration: Anti-angiogenic drugs combined with SHP099 for anti-tumor effects. • Medications combination boosts anti-tumor effects and enhances immunity. [ABSTRACT FROM AUTHOR]

Cytokine-induced killer (CIK) cells are ex vivo generated heterogeneous NK-like T-lymphocytes, which have anti-tumor effects in vitro and in vivo. This present study was conducted to evaluate the effects of autologous CIK cell immunotherapy on the prognosis of colorectal cancer patients. Progression-free survival (PFS), overall survival (OS) and immune cells were assessed. We found that the percentages of CD8 + , CD3 + CD56 + , CD3 − CD56 + cell subsets were significantly increased from 19.7 ± 6.3%, 13.8 ± 7.9%, 1.0 ± 1.2% to 35.8 ± 11.6% ( P < 0.001), 20.9 ± 12.5 ( P < 0.001), 14.4 ± 9.5% ( P < 0.001), respectively in the CIK group after 14 days of incubation. The median PFS and median OS in the CIK group were 25.8 months and 41.3 months respectively, while 12.0 months and 30.8 months in the control group. The PFS and OS curves of the CIK group and control group indicated that there were also statistically differences between two groups in PFS (log-rank, P = 0.01) and OS (log-rank, P = 0.037). Our results indicate that CIK cell immunotherapy in combination with chemotherapy can reduce the recurrence rate and promote the survival time of patients with colorectal cancer. [ABSTRACT FROM AUTHOR]