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In addition to influencing the progression anddevelopment of cancer by regulating inflammation and other immune pathways,resident gut bacteria seem to influence the efficacy of many cancer therapiesthat are intended to work in coherencewith host immunity to eliminate tumours. Some of the cancer drugs, such as oxaliplatin chemotherapy and CpG-oligonucleotide immunotherapy, work by increasing inflammation.

If the microbiome is changed in such a way that inflammation is decreasing, these therapeutic agents are less effective. Cancer-cell surface proteins bind to receptors on T cells to inhibit them from killing cancer cells. Checkpoint inhibitors that block this binding of activated T cells to cancer cells are affected by members of the microbiota that mediate these same cell interactions. Cyclophosphamide Chemotherapy corrupts the gut epithelial barrier, causing the gut to leak certain bacteria. Bacteria gather in lymphoid tissue just outside the gut and spur generation of T helper 1 and T helper 17 cells that migrate to a tumour and kill it. The capability of Salmonella, Clostridia,and other anaerobic bacteria to target tumoursfor their preferential copy, causing to tumourregression (7).  Previously it was demonstratedthat a protozoan parasite, Toxoplasma gondii,when injected into melanoma-bearing mice, caused suppression of tumour by blocking angiogenesis (formation ofblood vessels).

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The inhibition of angiogenesis in the tumour was due to the producing of infection-induced antiangiogenicsoluble factors that make hypoxic conditionsin the tumours, causing to their necrosis(13). Since different anaerobic bacteria have been reported to allow tumourregression (7, 14)and since such bacteria proliferate mainly in the anaerobic core of the tumours,Dang et al. (7) usedthe chemotherapeutic agent mitomycin C and the antivascular agent dolastatin-10in combination with the spores of an attenuated anaerobic bacterium, Clostridiumnovyi, to treat colorectal cancercells. The rationale behind this combined therapy (called combinationbacteriolytic therapy or COBALT) was that, while the anaerobic bacteria grew inthe anaerobic zone of the core of the tumours, the antivascular agent wouldcreate more extensive hypoxic areas for bacterial growth and starve the tumoursof oxygen and essential nutrients while the chemotherapeutic agent attacked thetumour cells in the well-perfused, nonnecrotic outside cells of the tumours, leadingto their total destruction (7, 14).The results of such a study were highly impressive.

In the absence of thebacteria, but in the presence of mitomycin C and dolastatin-10, the tumours persisted for a longer time and showedlimited regression, while containing the bacteria led to extensivedisappearance of the tumours within a short period of time and, in some cases,complete dissolution of the tumours, leaving the animals without tumour.Similar results were shown with a melanoma tumourcell line (7).A downside of this combination therapy was the high level of toxicity, where 15to 45% of the mice died within a few days after the treatment began, presumablydue to the release of the highly toxic metabolic products of the disintegratingtumours (7).

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