Changes in gut microbiota and plasma inflammatory factors across the stages of colorectal tumorigenesis: a case-control study

Zhang, Yongzhen; Yu, Xin; Yu, Enda; Wang, Na; Cai, Quan-Cai; Shuai, Qun; Yan, Feihu; Jiang, Lufang; Wang, Hexing; Liu, Jianxiang; Chen, Yue; Li, Zhao‐Shen; Jiang, Qingwu

doi:10.1186/s12866-018-1232-6

Cited by 60 publications

(51 citation statements)

References 55 publications

(60 reference statements)

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“…If the gut microbiota do contribute to the modelling of the TME via providing nutrients or immune modulation then from the data presented here, HCC and CRC have a very different TME. In addition, it can be seen from the Table 10 that HCC spawned from three (Greathouse et al, 2015) *Data taken from (Zhang et al, 2018). different etiologies may also have distinct differences in their TME.…”

Section: Resultsmentioning

confidence: 99%

Gut microbiota alterations are distinct for primary colorectal cancer and hepatocellular carcinoma

et al. 2020

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Colorectal cancer (CRC) and hepatocellular carcinoma (HCC) are the second and third most common causes of death by cancer, respectively. The etiologies of the two cancers are either infectious insult or due to chronic use of alcohol, smoking, diet, obesity and diabetes. Pathological changes in the composition of the gut microbiota that lead to intestinal inflammation are a common factor for both HCC and CRC. However, the gut microbiota of the cancer patient evolves with disease pathogenesis in unique ways that are affected by etiologies and environmental factors. In this review, we examine the changes that occur in the composition of the gut microbiota across the stages of the HCC and CRC. Based on the idea that the gut microbiota are an additional "lifeline" and contribute to the tumor microenvironment, we can observe from previously published literature how the microbiota can cause a shift in the balance from normal → inflammation → diminished inflammation from early to later disease stages. This pattern leads to the hypothesis that tumor survival depends on a less proinflammatory tumor microenvironment. The differences observed in the gut microbiota composition between different disease etiologies as well as between HCC and CRC suggest that the tumor microenvironment is unique for each case.

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Section: Resultsmentioning

confidence: 99%

Gut microbiota alterations are distinct for primary colorectal cancer and hepatocellular carcinoma

et al. 2020

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“…A relationship between commensal bacteria and intestinal carcinogenesis was first suggested in rodent models by Reddy et al in 1974 [19]. In recent studies, detailed microbial profiles gained by high-throughput analyses, like metagenomics sequencing and 16S rDNA sequencing, have revealed that bacteria are associated with CRC [20–23]. However, nothing was reported to our knowledge about cellular immune activation.…”

Section: Discussionmentioning

confidence: 99%

Immune senescence and immune activation in elderly colorectal cancer patients

Giunco

Petrara

Bergamo

et al. 2019

Aging

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In our previous study, we found that low thymic output and short telomere length were associated with a higher risk of tumor in elderly cancer patients. Here, we aimed to examine in depth the impact of immunological and biological senescence and immune activation on disease outcome in elderly patients with colorectal cancer (CRC).Peripheral blood samples from 81 CRC patients were studied for immune activation, immune senescence and recent thymic emigrant(RTE) CD4 and CD8 cells by flow cytometry. T-cell receptor rearrangement excision circle (TREC) levels and telomere lengths were measured by real-time PCR. Plasma levels of microbial translocation markers, LPS and sCD14, were quantified by ELISA. While TREC levels and telomere length were not prognostic of disease outcome, high percentages of immune senescent and immune activated CD8 cells were associated with a higher risk of a negative event (relapse, progression, or death) in all studied patients and disease relapse in I-III staged patients. Levels of sCD14 and LPS were higher in patients who will experience a negative event than in patients who will not. In conclusion, in elderly CRC patients higher immunological senescence and immune activation negatively impact the disease outcome; how these characteristics influence the antineoplastic treatments remains to be investigated.

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“…However, the approach of the disruption of signaling homeostasis-induced crosstalk in the carcinogenesis paradigm "Epistemology of the origin of cancer" is strongly supported by the evidence provided within the various publications of this Special Issue and in terms of the microbiome as dysbiosis with changes in inflammation together with cancer development along the adenomacarcinoma sequence has been provided [54] without any mutation.…”

Section: Microbesmentioning

confidence: 98%

Microbiome and morbid obesity increase pathogenic stimulus diversity

Brücher

Jamall

2019

4open

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The microbiome, the relationship between environmental factors, a high-fat diet, morbid obesity, and host response have been associated with cancer, only a small fraction of which (<10%) are genetically triggered. This nongenetic association is underpinned by a worldwide increase in morbid obesity, which is associated with both insulin resistance and chronic inflammation. The connection of the microbiome and morbid obesity is reinforced by an approximate shift of about 47% in the estimated total number of bacteria and an increase from 38,000,000,000,000 in a reference man to 56,000,000,000,000 in morbid obesity leading to a disruption of the microbial ecology within the gut. Humans contain 6,000,000,000 microbes and more than 90% of the cells of the human body are microorganisms. Changes in the microflora of the gut are associated with the polarization of ion channels by butyrate, thereby influencing cell growth. The decrease in the relative proportion of Bacteroidetes together with a change in the fermentation of carbohydrates by bacteria is observed in morbid obesity. The disruption of homeostasis of the microflora in the obese changes signaling and crosstalk of several pathways, resulting in inflammation while suppressing apoptosis. The interactions between the microbiome and morbid obesity are important to understand signaling and crosstalk in the context of the progression of the six-step sequence of carcinogenesis. This disruption of homeostasis increases remodeling of the extracellular matrix and fibrosis followed by the none-resolvable precancerous niche as the internal pathogenic stimuli continue. The chronic stress explains why under such circumstances there is a greater proclivity for normal cells to undergo the transition to cancer cells.

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Changes in gut microbiota and plasma inflammatory factors across the stages of colorectal tumorigenesis: a case-control study

Cited by 60 publications

References 55 publications

Gut microbiota alterations are distinct for primary colorectal cancer and hepatocellular carcinoma

Gut microbiota alterations are distinct for primary colorectal cancer and hepatocellular carcinoma

Immune senescence and immune activation in elderly colorectal cancer patients

Microbiome and morbid obesity increase pathogenic stimulus diversity

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