c-Kit as a Novel Potential Therapeutic Target in Colorectal Cancer

Shah, Yatrik M.; Brink, Gijs R. van den

doi:10.1053/j.gastro.2015.07.027

Cited by 18 publications

(11 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lee et al, 2015;Mojarad et al, 2016;Ok et al, 2010;Wright et al, 2005), whereas Y. H. Kim et al (2009) did not find any significant differences and Beyond MSI as a prognostic biomarker, two studies have examined the impact of EMAST on oncologic outcomes (Garcia et al, 2012;Koi et al, 2016), although the results have been inconsistent. Garcia et al (2012) & van den Brink, 2015). Also, Tan et al (2015) suggested c-kit signaling obviously promotes proliferation and invasion of CRC and leads to cancer progression and metastasis (Tan et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…c‐Kit is a tyrosine kinase receptor that induces several pathways and is known to play an important role in CRC, including the PI3K, RAS, and JAK/ STAT pathways (Cardoso, Figueira, Correia, Vaz, & Socorro, ). De sousa e melo et al () provided pieces of evidence that CRS subtypes with c‐Kit signature are strongly associated with poor prognosis, maybe by induction of markers of epithelial–mesenchymal transition, such as SNAIL and ZEB1 (Shah & van den Brink, ). Also, Tan et al () suggested c‐kit signaling obviously promotes proliferation and invasion of CRC and leads to cancer progression and metastasis (Tan et al, ).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

MSI‐L/EMAST is a predictive biomarker for metastasis in colorectal cancer patients

Esfahani

Seyedna

Nazemalhosseini‐Mojarad

et al. 2018

Journal Cellular Physiology

View full text Add to dashboard Cite

Background Microsatellite instability (MSI) is a prognostic marker in colorectal cancer (CRC). The biological significance of MSI‐low (MSI‐L) phenotype and its differences with microsatellite stable (MSS) phenotype remains unclear. The aim of this study is indicating the role of mononucleotide repeat in identifying MSI‐L and revealing the association of MSI‐L with elevated microsatellite alterations at selected tetranucleotide repeats (EMAST) and oncologic outcome in CRC patients. Methods MSI and EMAST status were analyzed using three quasimonomorphic panel (BAT‐25, BAT‐26, and NR‐27) and five tetranucleotide repeats (D20S82, D20S85, D9S242, D8S321, and MYCL1), respectively, by capillary electrophoresis method without the need to fluorescent primers. The associations of MSI status with clinicopathological features, EMAST status, metastasis, and overall survival (OS) were investigated. Results Among 159 CRC patient 22.0% were MSI‐H, 40.3% were MSS, 37.7% were MSI‐L, and 41.5% showed EMAST + phenotype. MSI‐L were associated with advanced stages, EMAST+ tumors and worse OS ( p ≤ 0.001). Metastasis was relatively common in MSI‐L/EMAST + CRCs and BAT‐25 were the most unstable marker in these tumors. Conclusions MSI‐L tumors have different clinicopathological features from MSS and MSI‐H tumors. The MSI‐L phenotype is a worse prognostic biomarker in CRC and when accompanied by EMAST could be a predictor for metastasis.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MSI‐L/EMAST is a predictive biomarker for metastasis in colorectal cancer patients

Esfahani

Seyedna

Nazemalhosseini‐Mojarad

et al. 2018

Journal Cellular Physiology

View full text Add to dashboard Cite

show abstract

“…In colorectal adenocarcinomas, C-KIT activation by SCF ligand induces signaling by different pathways including PI3K, RAS, and JAK/STAT [ 31 ]. The C-KIT knockdown in CRC cells is associated with a decrease in tumor growth and colony-forming capacity [ 31 ]. Several reports indicated that C-KIT inhibitors have promising results in CRC prevention and therapy.…”

Section: Discussionmentioning

confidence: 99%

A Unique Coexistence of Rectal Adenocarcinoma and Gastric Antral Gastrointestinal Stromal Tumor: A Case Report and Minireview

et al. 2021

View full text Add to dashboard Cite

Several studies have reported the coexistence of gastric gastrointestinal stromal tumors (GISTs) with many primary carcinomas such as gastric and renal cell carcinomas. However, to date reports about the coexistence of gastric GISTs and colorectal adenocarcinoma are limited. Herein we report a unique case of gastric GIST coexisting synchronously with rectal adenocarcinoma in a 36-year-old male patient who presented with weight loss, vomiting, and bleeding per rectum. Computed tomography (CT) revealed circumferential rectal mass coexistent with an irregular gastric soft tissue mass. The diagnosis of rectal adenocarcinoma and gastric GIST was established by immunohistological evaluation of the colonoscopic (rectum) and CT-guided (stomach) biopsies. The patient received concomitant chemoradiotherapy for the rectal adenocarcinoma and neoadjuvant imatinib for the gastric GIST. This was followed by low anterior resection with total mesorectal excision and wedge resection of the gastric mass. Follow-up of the patient for 1.5 years revealed no evidence of disease recurrence. We also present a minireview of the literature that provides insights into this subject as a separate section.

show abstract

“…KIT, a type III receptor tyrosine kinase, has a crucial role in cancer biology. 30,31 Currently, c-Kit is mainly considered as a stem cell factor. In addition, early studies on c-Kit identified it as an oncogene.…”

Section: Cdc7mentioning

confidence: 99%

<p>Identification of Chemoresistance-Associated Key Genes and Pathways in High-Grade Serous Ovarian Cancer by Bioinformatics Analyses</p>

Xia

Guo

et al. 2020

CMAR

View full text Add to dashboard Cite

High-grade serous ovarian cancer (HGSOC) is the leading cause of death among gynecological malignancies. This is mainly attributed to its high rates of chemoresistance. To date, few studies have investigated the molecular mechanisms underlying this resistance to treatment in ovarian cancer patients. In this study, we aimed to explore these molecular mechanisms using bioinformatics analysis. Methods: We analyzed microarray data set GSE51373, which included 16 platinumsensitive HGSOC samples and 12 platinum-resistant control samples. Differentially expressed genes (DEGs) were identified using RStudio. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using DAVID, and a DEG-associated protein-protein interaction (PPI) network was constructed using STRING. Hub genes in the PPI network were identified, and the prognostic value of the top ten hub genes was evaluated. MGP, one of the hub genes, was verified by immunohistochemistry. Results: All samples were confirmed to be of high quality. A total of 109 DEGs were identified, and the top ten enriched GO terms and four KEGG pathways were obtained. Specifically, the PI3K-AKT signaling pathway and the Rap1 signaling pathway were identified as having significant roles in chemoresistance in HGSOC. Furthermore, based on the PPI network, KIT, FOXM1, FGF2, HIST1H4D, ZFPM2, IFIT2, CCNO, MGP, RHOBTB3, and CDC7 were identified as hub genes. Five of these hub genes could predict the prognosis of HGSOC patients. Positive immunostaining signals for MGP were observed in the chemoresistant samples. Conclusion: Taken together, the findings of this study may provide novel insights into HGSOC chemoresistance and identify important therapeutic targets.

show abstract

c-Kit as a Novel Potential Therapeutic Target in Colorectal Cancer

Cited by 18 publications

References 18 publications

MSI‐L/EMAST is a predictive biomarker for metastasis in colorectal cancer patients

MSI‐L/EMAST is a predictive biomarker for metastasis in colorectal cancer patients

A Unique Coexistence of Rectal Adenocarcinoma and Gastric Antral Gastrointestinal Stromal Tumor: A Case Report and Minireview

<p>Identification of Chemoresistance-Associated Key Genes and Pathways in High-Grade Serous Ovarian Cancer by Bioinformatics Analyses</p>

Contact Info

Product

Resources

About