The Role of Intratumor Microbiomes in Cervical Cancer Metastasis

Abstract

Background: Intratumor microbiomes can influence tumorigenesis and progression. The relationship between intratumor microbiomes and cervical cancer metastasis, however, remains unclear. Methods: We examined 294 cervical cancer samples together with information on microbial expression, identified metastasis-associated microbiomes, and used machine learning methods to validate their predictive ability on tumor metastasis. The tumors were subsequently typed based on differences in microbial expression. Differentially expressed genes in different tumor types were combined to construct a tumor-prognostic risk score model and a multiparameter nomogram model. In addition, we performed a functional enrichment analysis of differentially expressed genes to infer the mechanism of action between microbiomes and tumor cells. Results: Based on the 15 differentially expressed microbiomes, machine learning models were able to correctly predict the risk of cervical cancer metastasis. In addition, both the risk score and the nomogram model accurately predicted tumor prognosis. Differences in the expression of endogenous genes in tumors can influence the distribution of the intracellular microbiomes. Conclusions: Intratumoral microbiomes in cervical cancer are associated with tumor metastasis and influence disease prognosis. A change in gene expression within tumor cells is responsible for differences in the microbial populations within the tumor.

A Case Report of Complete Androgen Insensitivity Syndrome Rising a Concern About the Time of Surgery and the Role of Parents' Behavior

“…[11] Many of them have a medical history of hernia surgery and/or masses in the inguinal canals that are found to be testes during surgery. [12,13] The majority of CAIS patients lack pubic and axillary hair, while breasts and female adiposity develop normally because of the conversion of testosterone to estradiol. [14] A milestone in the management of CAIS is the decision of whether or not to remove the testes due to an increased risk of gonadal tumor development [15,16].…”

A perspective on emerging therapies in metastatic colorectal cancer: Focusing on molecular medicine and drug resistance

“…Due to the conflicting reported findings in research based on renal cell carcinoma that claim an ambiguous function for antibiotics in VEGF-blockade treatment, the impact of the microbiota on anti-VEGF medicines is still up for dispute. 143,144…”

“…This effect could be due to the significant reduction in the variety and density of gut microbes caused by antibiotics. Due to the conflicting reported findings in research based on renal cell carcinoma that claim an ambiguous function for antibiotics in VEGF‐blockade treatment, the impact of the microbiota on anti‐VEGF medicines is still up for dispute 143,144 …”

Intratumoral Microbiome: Foe or Friend in Reshaping Tumor Microenvironment Landscape?

“…Moreover, a cohort analysis in patients with metastatic cervical cancer revealed that an intratumoral microbiome signature comprising of Robiginitomaculum, Microbispora, Klebsiella, and Micromonospora was correlated with increased expression of the surface receptors PD-1 and CTLA-4, and the egl-9 family hypoxia-inducible factor 1 (EGLN1), as well as with worse disease prognosis. Interestingly, EGLN1 expression is negatively correlated with CD8+ T cell infiltration within the TME, while positively associated with accumulation of CD4+ resting memory T cells, M0 macrophages and activated mast cells, which partly explains the negative predictive value of this microbiome subset on the disease outcome, via remodeling the hypoxic and immune TME niches [201]. Noteworthy, the potential role of microbiome as a multileveled regulator of distinct TME segments is further illustrated by a recent study showing that gut microbiota regulate the expression of the addressin MAdCAM-1 in intestinal endothelial and lymphoid tissues, thus controlling the egress of enterotropic α4β7+/IL-17+ regulatory T cells to tumor tissues, by modulating the interaction between MAdCAM-1 and α4β7 [202].…”