Background: Inflammatory myofibroblastic tumours (IMTs) are rare sarcomas that were first described in the lung. They are composed of myofibroblastic mesenchymal spindle cells accompanied by an inflammatory infiltrate of plasma cells. Complete resection is the treatment of choice. There is currently no standard treatment for inoperable or recurrent disease. Expression of ALK protein triggered by ALK gene rearrangement at chromosome 2p23 has been found in 36%-60% of IMTs.

Case Report: We report a rapid early response to crizotinib as neoadjuvant therapy, enabling surgical excision of a large ALK-translocated IMT, which resulted in complete disease clearance. To the best of our knowledge, this is the first case in the literature of a patient with IMT in whom crizotinib was used successfully in the neoadjuvant or curative setting.

Download full-text PDF

Source
http://dx.doi.org/10.5301/tj.5000245DOI Listing

Publication Analysis

Top Keywords

inflammatory myofibroblastic
8
alk gene
8
gene rearrangement
8
crizotinib neoadjuvant
8
neoadjuvant crizotinib
4
crizotinib advanced
4
advanced inflammatory
4
myofibroblastic tumour
4
tumour alk
4
rearrangement background
4

Similar Publications

While the C-X-C motif chemokine ligand 5 (CXCL5) is recognized as an inflammatory mediator and a potent attractant for immune cells, its functions within the human prostate remain unclear. This study explored the expression, functions, and regulatory mechanisms of CXCL5 in prostate stroma and cancer cells. CXCL5 secreted from prostate cancer cells enhanced neutrophil migration.

View Article and Find Full Text PDF

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 PDF

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 PDF
Article Synopsis
  • This research explores the activation of hepatic stellate cells (HSCs) across different types of chronic liver disease (CLD), finding that their activation follows similar mechanisms regardless of the injury type.
  • A single-cell RNA-sequencing atlas was created to categorize HSCs into three profiles: quiescent, initiatory, and myofibroblasts, indicating consistent activation patterns in both mice and humans.
  • The study highlights key transcription factors and novel ligands involved in HSC activation, paving the way for new insights and potential treatments for liver fibrosis.
View Article and Find Full Text PDF

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 PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!