Background: This study aimed to evaluate the value of chitinase activity in prognosticating the occurrence of metastasis in and prognosis of patients with colorectal cancer (CRC).
Methods: The chitinase activity in four different groups, namely 335 CRC patients without distant metastasis at their first visit (Group 1), 51 patients with CRC having synchronous liver metastasis (Group 2), 100 healthy age-matched controls (Group 3) and 40 patients with liver cancer (Group 4), were assayed using an enzyme-linked immunosorbent assay. The Cox proportional hazards ratio model and Kaplan-Meier curve were used to identify the association between chitinase activity and the clinical outcome of CRC patients without metastasis in the training set and testing set at their first visit. An in vitro Transwell experiment was performed to evaluate the migration of colon cancer cells.
Results: Patients with high chitinase activity had a significantly higher metastasis risk than those with low chitinase activity in the training and testing sets during follow-up, both at stage I/II and stage III. Further, multivariate analysis revealed that chitinase activity was an independent risk factor prognosticating liver metastases (P = 0.001). The combination of chitinase activity and lymph node metastasis status increased the accuracy of the prognosis of liver metastases after radical resection (P = 0.454E-011). In addition, chitinase promoted CRC cell migration in vitro.
Conclusions: Chitinase activity can prognosticate the occurrence of metastasis in patients with CRC. Moreover, the combination of chitinase activity and N stage increased the power of prognosticating the occurrence of metastasis. Inhibiting chitinase activity may serve as a new strategy to treat metastases of CRC.
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http://dx.doi.org/10.1186/s12885-019-5834-7 | DOI Listing |
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Wisconsin Alzheimer's Disease Research Center, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI, USA.
Background: Prior studies suggest that obstructive sleep apnea (OSA) may be associated with Alzheimer's disease (AD) pathology, including Aβ42/Aβ40 and p-Tau181. However, less is known about relationships between OSA and non-AD pathology, including neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), S100, chitinase 3-like 1 (YKL40), and soluble triggering receptor expressed on myeloid cells 2 (sTREM2), as well as the effect of potential moderating factors. The present study investigated the relationship between the apnea-hypopnea index (AHI) and cerebrospinal fluid (CSF) biomarkers of AD and related pathology.
View Article and Find Full Text PDFSci Rep
January 2025
School of Crop Production Technology, Institute of Agricultural Technology, Suranaree University of Technology, Nakhon Ratchasima, 30000, Thailand.
Several mungbean (Vigna radiata (L.) Wilczek) cultivars are susceptible to Cercospora leaf spot (CLS) caused by Cercospora canescens Ellis & Martin, and it is necessary to explore resistance sources and understand resistance mechanisms. However, the CLS resistance mechanisms have not yet been explored.
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School of Life Sciences, Yunnan University, Kunming 650500, China.
Chitinase-3-like-1 (Chi3l1), also known as YKL-40 or BRP-39, is a highly conserved mammalian chitinase with a chitin-binding ability but no chitinase enzymatic activity. Chi3l1 is secreted by various cell types and induced by several inflammatory cytokines. It can mediate a series of cell biological processes, such as proliferation, apoptosis, migration, differentiation, and polarization.
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December 2024
Department of Neurology, Medical University of Lodz, Kosciuszki Street 4, 90-419 Lodz, Poland.
Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS) with a complex and not fully understood etiopathological background involving inflammatory and neurodegenerative processes. CHI3L1 has been implicated in pathological conditions such as inflammation, injury, and neurodegeneration, and is likely to play a role in the physiological development of the CNS. CHI3L1 is primarily produced by CNS macrophages, microglia, and activated astrocytes.
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