Fucoidan has many biological activities, including the inhibitory effect on the development of various cancer types. This study showed that lipopolysaccharide-induced inflammation in FHC cells (normal human colonic epithelial cells) could be reversed using fucoidan at different concentrations. The fucoidan-induced anti-inflammatory effect was also confirmed through experiments in mice. Compared to the mice of the model group, the ratio of Firmicutes/Bacteroidetes in feces increased and the diversity of gut microbial composition was restored in mice after fucoidan intervention. In colorectal cancer (CRC) cells DLD-1 and SW480, fucoidan inhibited cell proliferation and promoted cell apoptosis. It also blocked the cell cycle of DLD-1 and SW480 at the G0/G1 phase. The animal model of inflammation-related CRC showed that the incidence of tumors in mice was significantly reduced by fucoidan intervention. Furthermore, the administration of fucoidan decreased the expression levels of inflammatory factors such as TNF-α IL-6 and IL-1β in the colonic tissues. Therefore, fucoidan can effectively prevent the development of colitis-associated CRC.
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http://dx.doi.org/10.1021/acs.jafc.2c02357 | DOI Listing |
World J Surg Oncol
January 2025
Colorectal Surgery Department, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University/ Hunan Cancer Hospital, No. 283 Tongzipo Road, Yuelu District, Changsha, Hunan, 410013, China.
Objective: The clinical benefits of neoadjuvant bevacizumab plus chemotherapy in locally advanced gastric cancer patients are controversial. This study intended to evaluate the efficacy and safety of neoadjuvant bevacizumab plus chemotherapy in these patients.
Methods: In this retrospective study, 71 locally advanced gastric cancer patients receiving neoadjuvant bevacizumab plus chemotherapy or neoadjuvant chemotherapy alone were divided into bevacizumab plus chemo group (N = 23) and chemo group (N = 48).
BMC Cancer
January 2025
Department of Laboratory Medicine, Affiliated Gaozhou People's Hospital, Guangdong Medical University, Maoming, 525200, P.R. China.
Background: DNA hypomethylation and uracil misincorporation into DNA, both of which have a very important correlation with colorectal carcinogenesis. Folate plays a crucial role in DNA synthesis, acting as a coenzyme in one-carbon metabolism, which involves the synthesis of purines, pyrimidines, and methyl groups. MTHFR, a key enzyme in folate metabolism, has been widely studied in relation to neural tube defects and hypertension, but its role in colorectal cancer remains underexplored.
View Article and Find Full Text PDFBMC Med Res Methodol
January 2025
Leeds Institute of Clinical Trials Research, University of Leeds, Clarendon Way, Leeds, LS2 9NL, UK.
Background: Early detection and diagnosis of cancer are vital to improving outcomes for patients. Artificial intelligence (AI) models have shown promise in the early detection and diagnosis of cancer, but there is limited evidence on methods that fully exploit the longitudinal data stored within electronic health records (EHRs). This review aims to summarise methods currently utilised for prediction of cancer from longitudinal data and provides recommendations on how such models should be developed.
View Article and Find Full Text PDFJ Gastrointest Cancer
January 2025
Computer Science, Changchun University of Science and Technology, Changchun, 130022, Jilin, China.
Objectives: To address the issue that most microsatellite-stable (MSS) and proficient mismatch repair (pMMR) metastatic colorectal cancer (mCRC) patients have minimal response to immunotherapy, this meta-analysis evaluated the efficacy and safety of durvalumab and tremelimumab with concomitant treatment in treating MSS/pMMR metastatic colorectal cancer.
Methods: All included trials were prospective studies with a median patient age of 63 years, of which 94.2% were MSS/pMMR mCRC patients, with a male to female ratio of 1.
Cell Death Differ
January 2025
Department of Colorectal and Anal Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.
Hyperactivation of the YAP/TEAD transcriptional complex in cancers facilitates the development of an immunosuppressive tumor microenvironment. Herein, we observed that the transcription factor SP1 physically interacts with and stabilizes the YAP/TEAD complex at regulatory genomic loci in colorectal cancer (CRC). In response to serum stimulation, PKCζ (protein kinase C ζ) was found to phosphorylate SP1 and enhance its interaction with TEAD4.
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