scholarly journals Recent Advances in Molecular Imaging of Colorectal Tumors

Digestion ◽  
2020 ◽  
pp. 1-8
Author(s):  
Takanori Kashihara ◽  
Naoki Muguruma ◽  
Shota Fujimoto ◽  
Yoshihiko Miyamoto ◽  
Yasushi Sato ◽  
...  

<b><i>Background:</i></b> Recent endoscopic studies have revealed that small colorectal tumors are often overlooked during colonoscopy, indicating that more sensitive detection methods are needed. <b><i>Summary:</i></b> Molecular imaging has received considerable attention as a new endoscopic technique with high sensitivity. It generally employs a fluorescence-labeled compound that specifically binds to a molecule on the tumor. Fluorescent probes for molecular imaging are largely classified as 2 types: a fluorescence-labeled antibody targeting a molecule specifically expressed on the tumor cell surface such as epidermal growth factor receptor or vascular endothelial growth factor (VEGF); and a fluorescence-labeled small molecule compound targeting a molecule specifically expressed in tumor cells including c-Met, glutathione S-transferase, γ-glutamyltranspeptidase, cathepsin, or endothelin A receptor. These probes successfully detected colorectal tumors in several animal studies. Moreover, 3 recent human clinical trials evaluating endoscopic molecular imaging for colorectal tumors have been reported. In one study, a Cy5-labeled synthetic peptide against c-Met was developed, and fluorescent endoscopic observation with this probe detected a greater number of colorectal adenomas than with white light observation. Another trial used IR800-labeled anti-VEGF antibody, which sensitively detected human colorectal adenomas by fluorescent endoscopy. Last, a fluorescent probe with synthetic peptide against BRAF-positive cells was able to visualize sessile serrated lesions. The fluorescent probes accumulated at very high levels in colorectal tumor cells but at lower levels in surrounding nonneoplastic mucosa. <b><i>Key Messages:</i></b> We expect that molecular imaging techniques with fluorescent probes will soon lead to the establishment of a highly sensitive endoscopic method for colorectal tumor detection.

2004 ◽  
Vol 19 (1) ◽  
pp. 97-99 ◽  
Author(s):  
Daniela Jurek ◽  
Natalia Udilova ◽  
Alicja Jozkowicz ◽  
Hans Nohl ◽  
Brigitte Marian ◽  
...  

Neoplasia ◽  
2010 ◽  
Vol 12 (6) ◽  
pp. 443-IN2 ◽  
Author(s):  
Winan J. van Houdt ◽  
Frederik J.H. Hoogwater ◽  
Menno T. de Bruijn ◽  
Benjamin L. Emmink ◽  
Maarten W. Nijkamp ◽  
...  

Langmuir ◽  
2021 ◽  
Author(s):  
Yueyue Chen ◽  
Li Jing ◽  
Qingtao Meng ◽  
Bin Li ◽  
Rui Chen ◽  
...  

2021 ◽  
Vol 22 (9) ◽  
pp. 4960
Author(s):  
Natalia Guillén Díaz-Maroto ◽  
Gemma Garcia-Vicién ◽  
Giovanna Polcaro ◽  
María Bañuls ◽  
Nerea Albert ◽  
...  

Heterotypic interactions between newly transformed cells and normal surrounding cells define tumor’s fate in incipient carcinomas. Once homeostasis has been lost, normal resident fibroblasts become carcinoma-associated fibroblasts, conferring protumorogenic properties on these normal cells. Here we describe the IL1β-mediated interplay between cancer cells and normal colonic myofibroblasts (NCFs), which bestows differential sensitivity to cytotoxic drugs on tumor cells. We used NCFs, their conditioned media (CM), and cocultures with tumor cells to characterize the IL1β-mediated crosstalk between both cell types. We silenced IL1β in tumor cells to demonstrate that such cells do not exert an influence on NCFs inflammatory phenotype. Our results shows that IL1β is overexpressed in cocultured tumor cells. IL1β enables paracrine signaling in myofibroblasts, converting them into inflammatory-CAFs (iCAF). IL1β-stimulated-NCF-CM induces migration and differential sensitivity to oxaliplatin in colorectal tumor cells. Such chemoprotective effect has not been evidenced for TGFβ1-driven NCFs. IL1β induces the loss of a myofibroblastic phenotype in NCFs and acquisition of iCAF traits. In conclusion, IL1β-secreted by cancer cells modify surrounding normal fibroblasts to confer protumorogenic features on them, particularly tolerance to cytotoxic drugs. The use of IL1β-blocking agents might help to avoid the iCAF traits acquisition and consequently to counteract the protumorogenic actions these cells.


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