scholarly journals The correlation between intestinal microbiota and colorectal cancer

2021 ◽  
Vol 99 (5-6) ◽  
pp. 339-341
Author(s):  
E. M. Lipnitsky ◽  
Yu. S. Medkova ◽  
E. A. Akhmetgalieva ◽  
D. N. Borisova

The study of intestinal and oral microflora and their metabolites playing an important role in intestinal homeostasis, has led to the identification of species closely related to the development of colorectal cancer, intracellular correlations of fungi and bacteria compared to control. The correlation between oral microbiota and intestinal microflora, as well as associated with the mucous membrane of the large intestine, was revealed. It was noted that the use of eu- and probiotics improved the immunological indices and the structure of the intestinal microbiota. Thus, studying the oral and intestinal microbiota and its metabolites may prove to be a simple, accessible and informative method for the early diagnosis of colon cancer. However, most studies indicate only changes in the quantitative and qualitative composition of the microbiota, hardly revealing its cause-effect relations with the processes of tumor formation in the colon. Therefore, it is necessary to continue studies of this problem.

Author(s):  
Ju. G. Samoilova ◽  
O. A. Oleynik ◽  
E. V. Sagan ◽  
I. N. Vorozhtsova ◽  
T. A. Filippova ◽  
...  

This review summarizes the results from national and international studies regarding the quantitative and qualitative composition of intestinal microbiota in health and the dominance of certain bacteria in the intestinal microbiota of obese children. Moreover, we discuss the relationships between the development of obesity and the changes in the composition and metabolic activity of intestinal microbiota in children. These analyses are of scientific interest from the perspective of finding new targets and approaches to conservative management aimed at preventing and treating obesity through the restoration of intestinal microflora.


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.


ESMO Open ◽  
2020 ◽  
Vol 5 (6) ◽  
pp. e001001
Author(s):  
Lisa Salvatore ◽  
Marco Imperatori ◽  
Ermenegildo Arnoldi ◽  
Carlo Carnaghi ◽  
Stefano Cordio ◽  
...  

About 75% of colorectal cancers are diagnosed as early stage, in which radical surgery is achievable. In the last decade, in Italy, the overall incidence of colorectal cancer has remained stable, while mortality gradually decreased, which is attributable to early diagnosis and improved medical, surgical and locoregional treatments. The Italian Medical Oncology Association formulated guidelines to manage early-stage colon cancer, including screening, diagnosis, treatment and follow-up, which we herein present.


mBio ◽  
2013 ◽  
Vol 4 (6) ◽  
Author(s):  
Joseph P. Zackular ◽  
Nielson T. Baxter ◽  
Kathryn D. Iverson ◽  
William D. Sadler ◽  
Joseph F. Petrosino ◽  
...  

ABSTRACT Recent studies have shown that individuals with colorectal cancer have an altered gut microbiome compared to healthy controls. It remains unclear whether these differences are a response to tumorigenesis or actively drive tumorigenesis. To determine the role of the gut microbiome in the development of colorectal cancer, we characterized the gut microbiome in a murine model of inflammation-associated colorectal cancer that mirrors what is seen in humans. We followed the development of an abnormal microbial community structure associated with inflammation and tumorigenesis in the colon. Tumor-bearing mice showed enrichment in operational taxonomic units (OTUs) affiliated with members of the Bacteroides, Odoribacter, and Akkermansia genera and decreases in OTUs affiliated with members of the Prevotellaceae and Porphyromonadaceae families. Conventionalization of germfree mice with microbiota from tumor-bearing mice significantly increased tumorigenesis in the colon compared to that for animals colonized with a healthy gut microbiome from untreated mice. Furthermore, at the end of the model, germfree mice colonized with microbiota from tumor-bearing mice harbored a higher relative abundance of populations associated with tumor formation in conventional animals. Manipulation of the gut microbiome with antibiotics resulted in a dramatic decrease in both the number and size of tumors. Our results demonstrate that changes in the gut microbiome associated with inflammation and tumorigenesis directly contribute to tumorigenesis and suggest that interventions affecting the composition of the microbiome may be a strategy to prevent the development of colon cancer. IMPORTANCE The trillions of bacteria that live in the gut, known collectively as the gut microbiome, are important for normal functioning of the intestine. There is now growing evidence that disruptive changes in the gut microbiome are strongly associated with the development colorectal cancer. However, how the gut microbiome changes with time during tumorigenesis and whether these changes directly contribute to disease have not been determined. We demonstrate using a mouse model of inflammation-driven colon cancer that there are dramatic, continual alterations in the microbiome during the development of tumors, which are directly responsible for tumor development. Our results suggest that interventions that target these changes in the microbiome may be an effective strategy for preventing the development of colorectal cancer.


Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2060
Author(s):  
Bo-Ram Jin ◽  
Hyo-Jung Kim ◽  
Seo-Ah Sim ◽  
Minho Lee ◽  
Hyo-Jin An

Many researchers have argued that Western diet (WD)-induced obesity accelerates inflammation and that inflammation is a link between obesity and colorectal cancer (CRC). This study investigated the effect of WDs on the development and progression of colitis-associated colon cancer (CAC) and the efficacy of the anti-obesity agent orlistat on WD-driven CAC in mice. The results revealed that the WD exacerbated CAC in azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced mice, which showed increased mortality, tumor formation, and aggravation of tumor progression. Furthermore, WD feeding also upregulated inflammation, hyperplasia, and tumorigenicity levels through the activation of STAT3 and NF-κB signaling in an AOM/DSS-induced mouse model. In contrast, treatment with orlistat increased the survival rate and alleviated the symptoms of CAC, including a recovery in colon length and tumor production decreases in WD-driven AOM/DSS-induced mice. Additionally, orlistat inhibited the extent of inflammation, hyperplasia, and tumor progression via the inhibition of STAT3 and NF-κB activation. Treatment with orlistat also suppressed the β-catenin, slug, XIAP, Cdk4, cyclin D, and Bcl-2 protein levels in WD-driven AOM/DSS-induced mice. The results of this study indicate that orlistat alleviates colon cancer promotion in WD-driven CAC mice by suppressing inflammation, especially by inhibiting STAT3 and NF-κB activation.


Author(s):  
Robb M. Gavalis ◽  
Hua Xing ◽  
Peter Y. Wong ◽  
Lothar Lilge ◽  
Caroline G. L. Cao

Colonoscopy is currently the gold standard for diagnosing colorectal cancer and inflammatory bowel disease. During a colonoscopy, a flexible endoscope is inserted into the patient’s colon to inspect the inner wall of the large intestine, from the rectum to the caecum. This procedure is very important for cancer screening and can yield early diagnosis. Colon cancer is 85–95% successfully treated if detected early; however, there is only a 30% compliance rate for the procedure in the United States. This low compliance rate for the examination is largely due to its uncomfortable nature, caused by difficulties in blind scope manipulation, and “looping” of the endoscope which can lead to stretching and perforation of the bowel [1] (Figure 1).


Swiss Surgery ◽  
2003 ◽  
Vol 9 (1) ◽  
pp. 3-7 ◽  
Author(s):  
Gervaz ◽  
Bühler ◽  
Scheiwiller ◽  
Morel

The central hypothesis explored in this paper is that colorectal cancer (CRC) is a heterogeneous disease. The initial clue to this heterogeneity was provided by genetic findings; however, embryological and physiological data had previously been gathered, showing that proximal (in relation to the splenic flexure) and distal parts of the colon represent distinct entities. Molecular biologists have identified two distinct pathways, microsatellite instability (MSI) and chromosomal instability (CIN), which are involved in CRC progression. In summary, there may be not one, but two colons and two types of colorectal carcinogenesis, with distinct clinical outcome. The implications for the clinicians are two-folds; 1) tumors originating from the proximal colon have a better prognosis due to a high percentage of MSI-positive lesions; and 2) location of the neoplasm in reference to the splenic flexure should be documented before group stratification in future trials of adjuvant chemotherapy in patients with stage II and III colon cancer.


2014 ◽  
Vol 23 (2) ◽  
pp. 161-170 ◽  
Author(s):  
Claudiu Margaritescu ◽  
Daniel Pirici ◽  
Irina Cherciu ◽  
Alexandru Barbalan ◽  
Tatiana Cârtâna ◽  
...  

Background & Aims: Colorectal cancer represents the third most common malignancy and the fourth most common cause of cancer death worldwide. The existence of drug-resistant colon cancer stem cells is thought to be one of the most important reasons behind treatment failure in colon cancer, their existence putatively leading to metastasis and recurrences. The aim of our study was to investigate the immunoexpression patterns of CD133 and CD166 in colon carcinoma, both individually and in combination, assessing their significance as prognostic markers.Methods. A total of 45 retrospective colon adenocarcinoma cases were investigated by enzymatic and multiple fluorescence immunohistochemistry for their CD133 and CD166 expression and colocalization.Results. Both CD133 and CD166 were expressed to different extents in all cancer specimens, with apredominant cytoplasmic pattern for CD133 and a more obvious membranous-like pattern for CD166.Overall, when comparing their reactivity for the tumoral tissue, CD166 expression areas seemed to be smaller than those of CD133. However, there was a direct correlation between CD133 and CD166 expression levels throughout the entire spectrum of lesions, with higher values for dysplastic lesions. Colocalization of CD133/ CD166 was obvious at the level of cells membranes, with higher coeficients in high grade dysplasia, followed by well and moderate differentiated tumours.Conclusions. CD133/CD166 colocalization is an early event occurring in colon tumorigenesis, with thehighest coeficients recorded for patients with high grade dysplasia, followed by well differentiated tumours. Thus, we consider that the coexpression of these two markers could be useful for further prognostic andtherapeutically stratification of patients with colon cancer.Abbreviations: AJCC - American Joint Committee on Cancer; CCD - charge-coupled device camera sensor; CD133 - prominin-1 (PROM1); CD166 - Activated Leukocyte Cell Adhesion Molecule (ALCAM); CRC - colorectal cancer; CSC - cancer stem cells; DAB - 3,3'-diaminobenzidine chromogen; DAPI - 4',6-diamidino- 2-phenylindole; HE - Hematoxylin and eosin staining; HGD - high grade dysplasia; HRP - horseradish peroxidase; LGD - low grade dysplasia; SDS - sodium dodecyl sulfate*Part of this work has been accepted as a poster presentation at the Digestive Disease Week (DDW) meeting, Chicago, IL, USA May 3-6, 2014


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