Rabbit Anti-Human LECT2 Polyclonal Antibody

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Its pathogenesis is frequently linked to liver inflammation. Gain-of-function mutations in the gene encoding beta-catenin are frequent genetic modifications found in human HCCs. Thus, we investigated whether inflammation was a component of beta-catenin-induced tumorigenesis using genetically modified mouse models that recapitulated the stages of initiation and progression of this tumoral process. Oncogenic beta-catenin signaling was found to induce an inflammatory program in hepatocytes that involved direct transcriptional control by beta-catenin and activation of the NF-kappa B pathway. This led to a specific inflammatory response, the intensity of which determined the degree of tumor aggressiveness. The chemokine-like chemotactic factor leukocyte cell-derived chemotaxin 2 (LECT2) and invariant NKT (iNKT) cells were identified as key interconnected effectors of liver beta-catenin-induced inflammation. In genetic deletion models lacking the gene encoding LECT2 or iNKT cells, hepatic beta-catenin signaling triggered the formation of highly malignant HCCs with lung metastasis. Thus, our results identify inflammation as a key player in beta-catenin-induced liver tumotigenesis. We provide strong evidence that, by activating pro-and antiinflammatory mediators, beta-catenin signaling produces an inflammatory microenvironment that has an impact on tumoral development. Our data are consistent with the fact that most beta-catenin-activated HCCs are of better prognosis.

Amyloidosis is a protein deposition disorder caused by pathologic accumulation of fibrils, leading to organ dysfunction. The newest protein is Leukocyte Cell-derived Chemotaxin 2 Amyloidosis (ALECT2), which shows ethnic predilection for Hispanics, Middle Eastern, and other minority groups. We report a case of 71-year-old Persian male with history of hepatitis B and resected hepatocellular carcinoma who presented with acute onset jaundice and abnormal liver function tests. Liver biopsy performed for diagnostic workup revealed hepatic ALECT2 with distinct signet-ring like globular proteinaceous deposits infiltrating hepatic parenchyma, mimicking epithelioid/histiocytic neoplasm. The infiltrative spherular material was positive for Congo red and negative for pan-keratin stains. Amyloid protein analysis by Liquid Chromatography tandem Mass Spectrometry (LC MS/MS) identified a peptide profile indicative of ALECT2. Although, ALECT2 accounts for the second most common cause of hepatic amyloidosis, only limited cases of hepatic ALECT2 are reported in the literature and little is known about patient management, especially the role of transplant as curative option. In summary, hepatic ALECT2 is an emerging disorder with relative high prevalence that deserves morphologic recognition. The report intends to emphasise distinctive morphology for accurate diagnosis and understanding its pathogenesis, clinical significance, and therapeutic strategies.