Inflammatory myofibroblastic tumor (IMT) is an uncommon mesenchymal solid tumor commonly documented in children and young adults. Here, we report a case of IMT in colon confirmed pathologically after laparoscopic anterior resection. A 35-year-old man presented with anal bleeding after defecation for 2 weeks. Colonoscopy demonstrated a mass with shallow ulceration in the central area and irregular margin accompanied by intact mucosa in the descending colon. Computer tomography showed a well-demarcated and homogenous solitary mass in the descending colon. We performed laparoscopic anterior resection. This case was diagnosed as IMT after microscopic examination. The tumor was composed of a proliferation of spindle-shaped cells arranged in the hyaline material with chronic inflammatory cells, composed mainly of plasma cells and lymphocytes. Immunohistochemically, tumor cells were positive for smooth muscle actin, and vimentin, and negative for desmin, CD117 (c-kit), anaplastic lymphoma kinase-1.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3268143 | PMC |
http://dx.doi.org/10.4174/jkss.2012.82.1.45 | DOI Listing |
Int Immunopharmacol
December 2024
Department of Cardiac Surgery, Peking University Third Hospital, Beijing 100191, China. Electronic address:
Chronic heart failure, caused by myocardial fibrosis after acute myocardial infarction (AMI), remains a serious clinical problem that needs urgent resolution. Nitro-oleic acid (OA-NO), an electrophilic nitro-fatty acid found in human plasma, is believed to regulate various pathophysiological functions, particularly anti-inflammation and anti-fibrosis. However, the role of OA-NO in AMI remains unexplored.
View Article and Find Full Text PDFHepatol Commun
November 2024
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Background: Liver fibrosis is caused by chronic toxic or cholestatic liver injury. Fibrosis results from the recruitment of myeloid cells into the injured liver, the release of inflammatory and fibrogenic cytokines, and the activation of myofibroblasts, which secrete extracellular matrix, mostly collagen type I. Hepatic myofibroblasts originate from liver-resident mesenchymal cells, including HSCs and bone marrow-derived CD45+ collagen type I+ expressing fibrocytes.
View Article and Find Full Text PDFJHEP Rep
January 2025
Vrije Universiteit Brussel, Liver Cell Biology research group, Laarbeeklaan 103, 1090 Brussel, Belgium.
Background & Aims: The progression of chronic liver disease (CLD) is characterized by excessive extracellular matrix deposition, disrupting hepatic architecture and function. Upon liver injury, hepatic stellate cells (HSCs) differentiate towards myofibroblasts and become inflammatory, proliferative and fibrogenic. To date, it is still unclear whether HSC activation is driven by similar mechanisms in different aetiologies.
View Article and Find Full Text PDFApoptosis
January 2025
Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Cancer-associated fibroblasts (CAFs) significantly influence tumor progression and therapeutic resistance in colorectal cancer (CRC). However, the distributions and functions of CAF subpopulations vary across the four consensus molecular subtypes (CMSs) of CRC. This study performed single-cell RNA and bulk RNA sequencing and revealed that myofibroblast-like CAFs (myCAFs), tumor-like CAFs (tCAFs), inflammatory CAFs (iCAFs), CXCL14CAFs, and MTCAFs are notably enriched in CMS4 compared with other CMSs of CRC.
View Article and Find Full Text PDFSci Rep
January 2025
Medical Imaging Center, First Affiliated Hospital, Jiamusi University, Jiamusi, Heilongjiang, China.
Chronic hyperglycemia, a hallmark of diabetes, can trigger inflammatory responses in the kidney, leading to diabetic nephropathy (DN). Follistatin-like protein 1 (FSTL1) has emerged as a potential therapeutic target in various kidney diseases. This study investigated the effect of high glucose on FSTL1 expression and its role in oxidative stress and cellular transdifferentiation injury in HK-2 human proximal tubule epithelial cells, a model of DN.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!