Role of Rho-Kinase Gene Polymorphisms and Protein Expressions in Colorectal Cancer Development

Pathobiology ◽  
2013 ◽  
Vol 80 (3) ◽  
pp. 138-145 ◽  
Author(s):  
Ibrahim Sari ◽  
Betul Berberoglu ◽  
Esma Ozkara ◽  
Serdar Oztuzcu ◽  
Celaletdin Camci ◽  
...  
2012 ◽  
Vol 1 (1) ◽  
pp. 37-47
Author(s):  
Karam Singh Boparai ◽  
Yark Hazewinkel ◽  
Evelien Dekker

Biomédica ◽  
2019 ◽  
Vol 39 (1) ◽  
pp. 205-211
Author(s):  
Miriam Partida ◽  
Melva Gutiérrez ◽  
María De la Luz Ayala ◽  
Nelly Margarita Macías ◽  
Carlos Rogelio Alvizo ◽  
...  

Introduction: Obesity and colorectal cancer could be linked by adipocytokines, which are proteins associated with cell proliferation. High levels of the adipocytokine leptin promote the development of colorectal cancer through its receptor.Objective: To determine the association between c.326A>G and c.668A>G LEPR gene polymorphisms and colorectal cancer.Materials and methods: DNA was extracted from the peripheral blood of 147 patients with sporadic colorectal cancer and 134 healthy people. Genotypes were obtained by PCRRFLP and the association was determined by the odds ratio (OR) test using the SPSS™, version 10.0, program. Haplotype frequencies and linkage disequilibrium were estimated by the Arlequin, version 3.5, software.Results: Both polymorphisms were in Hardy-Weinberg equilibrium. Only the c.326A>G heterozygous genotype revealed an increased risk for colorectal cancer development (OR=1.81, 95% CI=1.04-3.16, p=0.04). The AG haplotype showed a significant association with colorectal cancer (OR=0.58, 95% CI=0.35-0.96, p<0.03). Linkage disequilibrium between the variants was only evident for the patients group (r2=0.36). Conclusion: Our results suggest that AG individuals heterozygous for the c.326A>G LEPR variant have a higher risk of colorectal cancer development whereas the AG haplotype (c.326A/c.668G) has a protective effect in the Mexican population.


Author(s):  
J. Heijmans ◽  
N.V. Büller ◽  
V. Muncan ◽  
G.R. van den Brink

2020 ◽  
Vol 11 (12) ◽  
pp. 3580-3587
Author(s):  
Shu-Qin Li ◽  
Yang Yu ◽  
Yan Zhang ◽  
Yan-Ping Sun ◽  
Xin-xing Li ◽  
...  

2020 ◽  
Vol 31 (1) ◽  
pp. 10-16
Author(s):  
Mitsukuni Suenaga ◽  
Shu Cao ◽  
Wu Zhang ◽  
Satoshi Matsusaka ◽  
Satoshi Okazaki ◽  
...  

Oncotarget ◽  
2017 ◽  
Vol 8 (62) ◽  
pp. 105472-105478 ◽  
Author(s):  
Wei Cui ◽  
Feng Li ◽  
Qiang Yuan ◽  
Gang Chen ◽  
Cailing Chen ◽  
...  

2017 ◽  
Vol 10 (5) ◽  
pp. 417-428 ◽  
Author(s):  
Sofia Oke ◽  
Alberto Martin

The intestinal microbiota consists of a dynamic organization of bacteria, viruses, archaea, and fungal species essential for maintaining gut homeostasis and protecting the host against pathogenic invasion. When dysregulated, the intestinal microbiota can contribute to colorectal cancer development. Though the microbiota is multifaceted in its ability to induce colorectal cancer, this review will focus on the capability of the microbiota to induce colorectal cancer through the modulation of immune function and the production of microbial-derived metabolites. We will also explore an experimental technique that is revolutionizing intestinal research. By elucidating the interactions of microbial species with epithelial tissue, and allowing for drug screening of patients with colorectal cancers, organoid development is a novel culturing technique that is innovating intestinal research. As a cancer that remains one of the leading causes of cancer-related deaths worldwide, it is imperative that scientific findings are translated into the creation of effective therapeutics to treat colorectal cancer.


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