Canine cutaneous mast cell tumor (MCT) is very common disease in dogs, this is more aggressive than in other species. The biologic behavior of MCT is highly variable and a more accurate prognosis for these tumors needs to performed. The proto-oncogene c-kit is known to play a critical role in development and function of mast cells (MC). The aim of this study was to evaluate the expression of immunohistochemical pattern of c-kit in MCTs and to correlate these results with MC density (MCD) and intratumoral microvessel density (MVD). Our results confirm that a more aggressive biologic behavior of canine MCT is associated with the increased c-kit expression, further suggesting a new role for c-kit, as a useful marker, in diagnostic pathology and in tumor progression.

Download full-text PDF

Source
http://dx.doi.org/10.1080/08923970801949265DOI Listing

Publication Analysis

Top Keywords

proto-oncogene c-kit
8
canine cutaneous
8
cutaneous mast
8
mast cell
8
biologic behavior
8
c-kit
5
expression proto-oncogene
4
c-kit correlation
4
correlation morphological
4
morphological evaluations
4

Similar Publications

Background: Simulated microgravity environment can lead to gastrointestinal motility disturbance. The pathogenesis of gastrointestinal motility disorders is closely related to the stem cell factor (SCF)/c-kit signaling pathway associated with intestinal flora and Cajal stromal cells. Moreover, intestinal flora can also affect the regulation of SCF/c-kit signaling pathway, thus affecting the expression of Cajal stromal cells.

View Article and Find Full Text PDF

Artemisinin Suppressed Melanoma Recurrence and Metastasis after Radical Surgery through the KIT/PI3K/AKT Pathway.

Int J Biol Sci

January 2025

Cancer Center and Center of Reproduction, Development & Aging, Institute of Translation Medicine, Faculty of Health Sciences, University of Macau, Taipa, Macau, China.

Cancer radical surgery is the primary treatment for melanoma, but almost all malignant melanoma patients get recurrence and metastasis after surgery and are eventually dead. This clinical dilemma appeals to better drugs for post-surgery therapy. Artemisinin is a safe and effective antimalarial drug used in the clinic for decades.

View Article and Find Full Text PDF

Folic Acid-Modified Milk Exosomes Delivering c-Kit siRNA Overcome EGFR-TKIs Resistance in Lung Cancer by Suppressing mTOR Signaling and Stemness.

Int J Biol Sci

January 2025

Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, China, 610041.

Article Synopsis
  • The study addresses a common issue in lung cancer treatment, where patients develop resistance to EGFR-TKIs like gefitinib, leading to worse outcomes.
  • The researchers developed a novel therapy using folic acid-modified milk exosomes loaded with c-kit siRNA (FA-mExo-siRNA-c-kit) to counteract this resistance by targeting the c-kit gene, which is linked to stemness traits in cancer cells.
  • Results showed that this approach not only reduced c-kit expression and stemness characteristics but also slowed tumor growth and improved survival in experimental models, highlighting its potential as a new treatment strategy for resistant lung cancer.
View Article and Find Full Text PDF
Article Synopsis
  • Gastrointestinal stromal tumors (GISTs) are rare cancers linked to mutations in the c-KIT gene, with one common mutation being a deletion in exon 11, as seen in an 82-year-old male patient diagnosed in June 2023.
  • The patient subsequently received a low-dose imatinib treatment protocol, starting at 400 mg/day and tapering down to 200 mg/day, which resulted in a reduction of the tumor size over several months.
  • The study suggests that low-dose imatinib can be an effective treatment option for GIST patients with the W557_K558 deletion, especially for those who cannot tolerate higher doses.
View Article and Find Full Text PDF

The heterogeneous form of malignancy in the myeloid lineage of normal hematopoietic stem cells (HSCs) is characterized as acute myeloid leukemia (AML). The t(9;11) reciprocal translocation (p22;q23) generates MLL-AF9 oncogene, which results in myeloid-based monoblastic AML with frequent relapse and poor survival. MLL-AF9 binds with the C-Myb promoter and regulates AML onset, maintenance, and survival.

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!