ArticlePloS one2014
Role of leukocyte cell-derived chemotaxin 2 as a biomarker in hepatocellular carcinoma.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Global research trends and hotspots for leukocyte cell-derived chemotaxin-2 from the past to 2023: a combined bibliometric review.Frontiers in immunology · 2024Pooled it
- LECT2: A pleiotropic and promising hepatokine, from bench to bedside.Journal of cellular and molecular medicine · 2022Review
- Wnt/-Catenin Signaling and Liver Regeneration: Circuit, Biology, and Opportunities.Gene expression · 2021Review
- LECT2 Protects Nile Tilapia (Frontiers in immunology · 2021Article
- LECT 2 Antagonizes FOXM1 Signaling via Inhibiting MET to Retard PDAC Progression.Frontiers in cell and developmental biology · 2021Article
- Clinical role of serum programmed death ligand 1 in patients with hepatocellular carcinoma: Where does it come from?Surgery today · 2020Article
- Article
- Loss of Wnt Secretion by Macrophages Promotes Hepatobiliary Injury after Administration of 3,5-Diethoxycarbonyl-1, 4-Dihydrocollidine Diet.The American journal of pathology · 2019Article
- Leukocyte cell derived chemotaxin-2 (Lect2) as a predictor of survival in adult acute liver failure.Translational gastroenterology and hepatology · 2019Article
- Leukocyte Cell-Derived Chemotaxin-2: It's Role in Pathophysiology and Future in Clinical Medicine.Clinical and translational science · 2017Review
- Targeting β-catenin in hepatocellular cancers induced by coexpression of mutant β-catenin and K-Ras in mice.Hepatology (Baltimore, Md.) · 2017Article
- Review
- Leukocyte Cell-Derived Chemotaxin 2-Associated Amyloidosis: A Recently Recognized Disease with Distinct Clinicopathologic Characteristics.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
- β-Catenin Signaling and Roles in Liver Homeostasis, Injury, and Tumorigenesis.Gastroenterology · 2015Review
- Complete response of Ctnnb1-mutated tumours to β-catenin suppression by locked nucleic acid antisense in a mouse hepatocarcinogenesis model.Journal of hepatology · 2015Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
We sought to identify a secreted biomarker for β-catenin activation commonly seen in hepatocellular carcinoma (HCC). By examination of our previously published genearray of hepatocyte-specific β-catenin knockout (KO) livers, we identified secreted factors whose expression may be β-catenin-dependent. We verified expression and secretion of the leading factor in HCC cells transfected with mutated (Hep3BS33Y)-β-catenin. Serum levels of biomarker were next investigated in a mouse model of HCC with β-catenin gene (Ctnnb1) mutations and eventually in HCC patients. Leukocyte cell-derived chemotaxin-2 (LECT2) expression was decreased in KO livers. Hep3BS33Y expressed and secreted more LECT2 in media as compared to Hep3BWT. Mice developing HCC with Ctnnb1 mutations showed significantly higher serum LECT2 levels. However patients with CTNNB1 mutations showed LECT2 levels of 54.28 ± 22.32 ng/mL (Mean ± SD; n = 8) that were insignificantly different from patients with non-neoplastic chronic liver disease (32.8 ± 21.1 ng/mL; n = 15) or healthy volunteers (33.2 ± 7.2 ng/mL; n = 11). Intriguingly, patients without β-catenin mutations showed significantly higher serum LECT2 levels (54.26 ± 22.25 ng/mL; n = 46). While β-catenin activation was evident in a subset of non-mutant β-catenin HCC group with high LECT2 expression, serum LECT2 was unequivocally similar between β-catenin-active and -normal group. Further analysis showed that LECT2 levels greater than 50 ng/ml diagnosed HCC in patients irrespective of β-catenin mutations with specificity of 96.1% and positive predictive value of 97.0%. Thus, LECT2 is regulated by β-catenin in HCC in both mice and men, but serum LECT2 reflects β-catenin activity only in mice. Serum LECT2 could be a potential biomarker of HCC in patients.
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