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In gerelateerde artikelen een aantal artikelen als preventie. Maar zie ook deze search op onze website met microbioom in de titel als zoekopdracht: https://kanker-actueel.nl/search.html?search_text=microbioom&search_in=title&page=1

En deze search met darmflora in de titel: https://kanker-actueel.nl/search.html?search_text=darmflora&search_in=title

20 juli 2026: Bron: Cell medisch tijdschrift d.d. 14 juli 2026, met dank aan Pieter die me deze studie doorstuurde

Bacteroides uniformis, een bacterie uit het darmmicrobioom, blijkt een positieve invloed te kunnen hebben op de immuunrespons van immuuntherapie tegen kanker bij muizen met een melanoom. De specifieke bacterie Bacteroides uniformis zet het aminozuur tryptofaan om in indolen, wat de antitumorimmuniteit bij muizen versterkte.

Hoewel nog slechts een muizenstudie blijkt deze nieuwe studie van onderzoekers van de Universiteit van Nebraska-Lincoln, de eerste studie die aantoont dat metabolieten geproduceerd door bepaalde bacteriën in de darm een positieve invloed kunnen hebben op de immuunrespons van het lichaam tegen kanker.

"Eerder onderzoek heeft aangetoond dat darmbacteriën het immuunsysteem beïnvloeden en kunnen helpen bij de bestrijding van kanker", aldus Ze'ev Ronai, directeur van het Translational Research Institute aan Cedars-Sinai en hoogleraar chirurgie, die samen met dr. Amanda Ramer-Tait de studie leidde. "Onze nieuwe bevindingen zijn een belangrijke stap voorwaarts, omdat ze ons een specifiek metaboliet opleveren dat kan worden gebruikt voor toekomstige therapieën."

"Ons idee is dat we in de toekomst interventies kunnen ontwikkelen op basis van het darmmicrobioom of het dieet, die gunstige microben of de benodigde voedingsstoffen leveren om de respons van een patiënt op immuuntherapie te verbeteren", aldus onderzoekster dr. Amanda Ramer-Tait. "Wat vooral veelbelovend is, is dat deze aanpak potentieel verder reikt dan melanoom, omdat indolen ook een belangrijke rol spelen bij het verbeteren van de immuunrespons op andere vormen van kanker."

Het volledige studierapport is gratis in te zien of als PDF te downloaden, klik daarvoor op de titel van het abstract:

Article Online now 102921 July 14, 2026 Open access

Tryptophan degradation by intestinal Bacteroides induces anti-tumor immunity and limits melanoma growth

Ximena Diaz Olea 1,2,3,12 ∙ Kristin Beede 4,12 ∙ Gabriel Pereira 5 ∙ … ∙ Jennifer Wargo 11 ∙ Amanda E. Ramer-Tait 4 Send email to aramer-tai2@unl.edu ∙ Ze’ev A. Ronai 1,2,13 Send email to zeev.ronai@csmc.edu … Show more

Affiliations & Notes

Article Info

Highlights

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Tryptophan degradation by B. rodentium/B. uniformis enzymes induces anti-tumor immunity

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TnaA degrades tryptophan to indoles, which inhibit melanoma

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Indole induces immune cell infiltration into melanoma, inhibiting their growth

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Increase in abundance of TnaA and ArAT seen in responders to ICB

Summary

Study of gut microbiota control of anti-tumor immunity (ATI) identifies Bacteroides rodentium and the human-related Bacteroides uniformis species to be capable of inducing ATI and limiting melanoma development in germ-free (GF), complex microbiome, or wild-type (WT) mice. Enhanced CD8+ T cell infiltration within tumors of mice harboring B. rodentium coincides with increased expression of immune-stimulating pathways. Metabolomic analyses identify lower tryptophan levels in the cecal samples of GF mice harboring B. rodentium. In silico genomic reconstruction reveals that B. rodentium and B. uniformis harbor tryptophanase A (TnaA) and aromatic aminotransferase genes, which degrade tryptophan to indoles. Administration of B. uniformis harboring TnaA mutant fails to inhibit melanoma growth. Notably, administration of indoles effectively induces ATI and inhibits melanoma development. Correspondingly, the levels of bacterially encoded tryptophan-degrading enzymes are higher in cohorts of patients with melanoma responding to immunotherapy. These findings identify indoles as tryptophan breakdown products capable of inducing ATI resulting in melanoma inhibition.

Graphical abstract

Limitations of the study

While our data suggest that the canonical transcriptional signatures of AhR, GPCR, or PXR activation are not strongly induced following B. rodentium or indole administration, further work is needed to define the mechanisms underlying indoles’ ability to induce ATI. It is important to note that a partial, context-dependent, or cell type-specific AhR/GPCR/PXR signaling cannot be excluded. Based on our finding, it will be also important to determine whether enhanced administration of ArAT or TnaA, or their combination, could offer an effective means to induce ATI, a subject tor future studies.

Resource availability

Lead contact

Requests for further information and resources should be directed to and will be fulfilled by the lead contact, Ze’ev A. Ronai (zeev.ronai@csmc.edu).

Materials availability

Reagents generated in this study will be made available on request, but we may require payment and/or a completed materials transfer agreement if there is potential for commercial application. There are restrictions to the availability of TnaA-mutant B. uniformis because of the lack of an external centralized repository for its distribution and our need to maintain the stock. We are glad to share this mutant bacterial strain with reasonable compensation by requestor for its processing and shipping.

Data and code availability

Data

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RNA sequencing data have been deposited at GEO under accession number GEO: GSE293242. 16S sequencing data have been deposited at NCBI SRA under BioProject ID: PRJNA1474073. Metabolomics data have been deposited at Metabolomic Workbench study ST004939 (project PR003168, doi: https://doi.org/10.21228/M86273). These data are publicly available as of the date of publication. Microscopy data reported in this paper will be shared by the lead contact upon request.

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This paper analyzes existing, publicly available data, accessible in the references Gunjur et al.,36 Lee et al.,37 Liu et al.,45 Dohlman et al.,60 and Mimpen et al.61 for the analyses performed by NKI collaborators and accessible in the references Spencer et al.43 and Gopalakrishnan et al.62 for the analyses performed by MDACC.

Code.

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This paper does not report original code.

Additional information

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Any additional information required to reanalyze the data reported in this paper is available from the lead contact upon request.

Acknowledgments

We thank members of the Ronai lab for extensive discussions. We thank Dr. Cosimo Commisso of Sanford Burnham Medical Discovery Institute, for providing us with the KP65 cells. We also thank Lorin Chin of the Cedars Sinai Microbiome Institute as well as Mason Mandolfo and Robert Schmaltz of the University of Nebraska-Lincoln for their assistance with bacterial cultures and animal studies and Dina Abbasian of the University of Pennsylvania for metabolic analyses. Support by the Cedars-Sinai shared resources in genomics, vivarium, and microbiome studies is greatly appreciated. We gratefully acknowledge support by NCI grant R35CA197465 (to Z.A.R.), by gift from the Hervey Family/San Diego Foundation (to Z.A.R.), by grant R21CA249822 (to A.E.R.-T. and H.K.), and by funding from the Buffett Cancer Center funds (to A.E.R.-T.) via NCI grant CA036727.

Author contributions

X.D.O., A.E.R.-T., and Z.A.R. conceived the study; X.D.O., K.B., and G.P. performed the experiments; D.S. and C.P. performed metabolite analyses; A.K.S. and A.M. analyzed bacterial 16S rRNA gene sequencing data; S.K. oversaw spa tial analysis, T.W.Z. and A.S. performed bioinformatic analyses; N.J.A., J.W., E.E.V., and M.P.M. analyzed indicated patient stool samples. E.M., S.D., A.O., M.B.F., O.H., A.E.R.-T., N.J.A., J.W., and Z.A.R analyzed the data; X.D.O., A.E.R.-T., and Z.A.R. wrote the manuscript with contributions from all authors.