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found reduced enrichment of Actinobacteria in the gut microbiome of lung cancer patients. In our and others’ research, lung cancer patients had different gut and respiratory microbiome compositions compared to their healthy controls. It is possible that with more data we eventually identify specific bacterial functional networks, or metabolomes, associated with these clinical outcomes. More granular findings include association of Bacteroides, Coprococcus, Corynebacterium, Enterococcus, and Neisseria enrichment with higher likelihood of CRC development, although the causative mechanisms remain unclear. At the phylum level, decreased relative abundance of Firmicutes has been associated with CRC. Studies of colorectal cancer (CRC) patients have associated decreased α-diversity, or overall species enrichment, of the gut microbiome with tumorigenesis. They can be very narrow, attributing one or two bacterial genera to tumor development other studies implicate alterations in the abundance of an entire phylum or even the overall number of detectable taxonomic species in a microbiome. The breadth of findings tying microbiome composition to carcinogenesis vary widely.
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Alterations in Microbiome Composition Are Associated with Carcinogenesis Using this framework, we can begin to appreciate the search for links connecting the microbiome, cancer, and the efficacy and toxicity of immunotherapy, its possible treatment.Ģ.1.
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On a daily basis, our microbiome-and the metabolomic networks formed within it-are instrumental in mitigating the body’s inflammatory state, but its composition can be affected by external insults. Lastly, the microbiome is increasingly associated with disease states, including neuropsychiatric and inflammatory bowel diseases, and, as we will discuss, cancer. It is not simply the presence of the microbiome that mitigates these outcomes-specific bacterial genera are responsible for critical functions. The gut microbiome also affects the metabolism of medications, utilizing a wide variety of enzymatic actions including but not limited to reduction, decarboxylation, demethylation, deamination, and hydrolysis of prodrugs. There is increasing study of the microbiome’s role in gluconeogenesis and lipid metabolism. Specific bacteria in the gut are responsible for digestion and metabolism in a symbiotic manner. The microbiome has already been recognized for its significant role in human metabolism. The microbiome has emerged as a possible therapeutic avenue as well as conduit for understanding mechanisms by which ICI effects are modulated: why do some patients develop crippling toxicities from treatment, while others virtually none? How can we explain the variance in outcomes between patients with similar cancers and tumor PD-L1 expression following treatment with the same drug? Is the oft-noted association between development of irAEs with response to ICI therapy in actuality describing two phenomena that can be decoupled? In short, the current state of immunotherapy in oncology leaves much room for improvement. These phenomena are associated with ICI activation of T cells throughout the body, potentially leading to a multitude of occasionally life-threatening autoinflammatory organopathies. Unfortunately, this suboptimal chance of benefit is accompanied by increased risk of immune-related adverse effects (irAEs). Despite low response rates, patients whose cancers regress under ICI therapy may be more likely to enjoy longer progression-free survival. Save for specific tumor traits such as genomic microsatellite instability (MSI-H), high programmed cell death ligand-1 (PD-L1) expression, or other genetically hypermutated (POLε) states, it appears that only a minority of patients respond to ICI therapy. As indications for immune checkpoint inhibitors (ICI) for treatment of malignancies have broadened, outcomes remain variable and difficult to predict.