Competing endogenous RNA network crosstalk reveals novel molecular markers in colorectal cancer

2018 ◽  
Vol 119 (8) ◽  
pp. 6869-6881 ◽  
Author(s):  
Nehal Samir ◽  
Marwa Matboli ◽  
Hanaa El‐Tayeb ◽  
Ahmed El‐Tawdi ◽  
Mohmed K. Hassan ◽  
...  
2019 ◽  
Vol 84 (4) ◽  
pp. 350-359 ◽  
Author(s):  
Shanshan Qin ◽  
Yingchun Gao ◽  
Yijun Yang ◽  
Lei Zhang ◽  
Ting Zhang ◽  
...  

Swiss Surgery ◽  
2001 ◽  
Vol 7 (6) ◽  
pp. 243-248
Author(s):  
Scheunemann ◽  
Hosch ◽  
Kutup ◽  
Izbicki

Die Einführung von immunhisto-/zytochemischen und molekularbiologischen bzw. zytogenetischen Methoden in der onkologische Forschung hat trotz vieler nach wie vor bestehender offener Fragen insgesamt zu einem besseren Verständnis der genetischen Ursachen der Tumorentstehung geführt. Darüber hinaus ergaben sich in verschiedenen Studien Hinweise für eine prognostische Relevanz von bestimmten (zyto)genetischen Veränderungen bzw. residualen Tumorzellen in Lymphknoten oder Knochenmark. Bevor diese Untersuchungen jedoch in den klinischen Alltag Einzug halten und therapeutische Konsequenzen abgeleitet werden können, sind weitere prospektive Studien mit groáen Patientenfallzahlen sowie vereinheitlichte und methodologisch praktikable Untersuchungstechniken zu fordern.


2013 ◽  
Vol 2 (2) ◽  
pp. 95-97
Author(s):  
Beatriz Carvalho ◽  
Linda JW Bosch ◽  
Manon Van Engeland ◽  
Gerrit A Meijer

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Rani Kanthan ◽  
Jenna-Lynn Senger ◽  
Selliah Chandra Kanthan

Despite multiple screening techniques, including colonoscopy, flexible sigmoidoscopy, radiological imaging, and fecal occult blood testing, colorectal cancer remains a leading cause of death. As these techniques improve, their sensitivity to detect malignant lesions is increasing; however, detection of precursor lesions remains problematic and has generated a lack of general acceptance for their widespread usage. Early detection by an accurate, noninvasive, cost-effective, simple-to-use screening technique is central to decreasing the incidence and mortality of this disease. Recent advances in the development of molecular markers in faecal specimens are encouraging for its use as a screening tool. Genetic mutations and epigenetic alterations that result from the carcinogenetic process can be detected by coprocytobiology in the colonocytes exfoliated from the lesion into the fecal matter. These markers have shown promising sensitivity and specificity in the detection of both malignant and premalignant lesions and are gaining popularity as a noninvasive technique that is representative of the entire colon. In this paper, we summarize the genetic and epigenetic fecal molecular markers that have been identified as potential targets in the screening of colorectal cancer.


Author(s):  
Jie Zhang ◽  
Xiao-Yan Li ◽  
Ping Hu ◽  
Yuan-Sheng Ding

Previous study indicates that long noncoding RNA NORAD could serve as a competing endogenous RNA to pancreatic cancer metastasis. However, its role in colorectal cancer (CRC) needs to be investigated. In the present study, we found that the expression of NORAD was significantly upregulated in CRC tissues. Furthermore, the expression of NORAD was positively related with CRC metastasis and patients’ poor prognosis. Knockdown of NORAD markedly inhibited CRC cell proliferation, migration, and invasion but induced cell apoptosis in vitro. In vivo experiments also indicated an inhibitory effect of NORAD on tumor growth. Mechanistically, we found that NORAD served as a competing endogenous RNA for miR-202-5p. We found that there was an inverse relationship between the expression of NORAD and miR-202-5p in CRC tissues. Moreover, overexpression of miR-202-5p in SW480 and HCT116 cells significantly inhibited cellular proliferation, migration, and invasion. Taken together, our study demonstrated that the NORAD/miR-202-5p axis plays a pivotal function on CRC progression.


2018 ◽  
Vol 59 (5-6) ◽  
pp. 361-370 ◽  
Author(s):  
Pridvi Kandagatla ◽  
Lilias H. Maguire ◽  
Karin M. Hardiman

Colorectal cancer (CRC) lymph node metastases are common but their genetics and the mechanism whereby these metastases occur are not well understood. Here we present recent data regarding genetic heterogeneity in primary CRCs and their metastasis. In addition, we explain the different potential models describing the mechanisms of metastasis and the data supporting them. Multiple studies have also revealed a variety of prognostic molecular markers that are associated with lymph node metastasis in CRC. A better understanding of genetic heterogeneity and the mechanisms of metastasis is critical to predicting clinical response and resistance to targeted therapy.


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