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Environmental contaminants #1
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Thanks for the question. I'm happy to respond, clarify a few things, and provide some reassuring data:
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@travisgibson Happy to do this and provide some clarifications:
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It is interesting that even using the overlap with the WIS dataset that had all of these experimental controls, that Rhizobium, typically regarded as a soil microbe, is coming up. Certain species within the Rhizobium genus cause plant tumors, and of these Rhizobium radiobacter can also be found in human infections, including case reports of in cancer patients (https://citeseerx.ist.psu.edu/document?repid=rep1&type=pdf&doi=abf50af543d7357152c1e9c8da9a7097eeef881f). In this study strains of R. radiobacter cultured out of human samples could not cause plant disease and were not found in environmental contaminant controls - suggestive of human adaptation. Is it possible to redo analyses here at the species level to see if the Rhizobium being identified is R. radiobacter? Similarly, a full Bradyrhizobium genome was assembled from the biopsy of a cancer patient who got colitis following a cord blood transplant in this paper (https://www.nejm.org/doi/10.1056/NEJMoa1211115). They found that this organism was highly related to the soil microbe B. japonicum, but was different and named it B. enterica, and again suggested that this isolate might be human adapted. Would it be possible to test if the Bradyrhizobium reads in this analysis are mapping closer to B. enterica than other Bradyrhizobium? This might shed light on whether the "soil bacteria" being identified here are actually these relatives that may be adapted to humans. That both Rhizobium and Bradyrhizobium closely interact with plant hosts to form symbiotic nodules, and that these relationships can "go awry" and form tumors in plants, makes it potentially interesting to explore mechanistically any potential pathway overlap with the mechanisms that these microbes exploit during tumorigenesis in plants and pathways of importance in human tumor formation. May be hard to do but I am just thinking of ways to dig a little more into mechanistic leads using sequence data. |
@clozupone I really like your questions and suggestions. However, it's unfortunately not possible to answer them with the Gihawi et al. data, which was fixed at the genus level and did not share the reads. This main goal of this repository, by re-analyzing their data, was to show that alternative bioinformatic pipelines and reduced feature sets still yield the conclusion that microbiomes are cancer type specific, even when limiting the analyses to 9 'well known' genera. I think there are ways to get to the species/read level and do what you're suggesting/asking about. I'll reach out via email to discuss further. |
I appreciate the attempt, but neither of the studies quoted ruled out contamination |
@mw55309 I have no involvement in those papers and suggest that you reach out to the original authors if you have concerns of contamination. However, I kindly note that the following text in Bhatt et al. 2013 NEJM directly addresses this topic:
In their Supplementary Appendix, they have 2.5 pages (p. 5-7) specifically detailing how they mitigated contamination. It thus seems difficult to conclude that they did not make good faith attempts to rule it out, but I again encourage you to reach out to those authors if it remains a concern for you. |
Thanks for posting this public rebuttal! Good science is open science.
There's been some suggestion that removing environmental contaminants, as done in the original paper, removes the cancer sub-type signal. See attached and the tweet below.
Whilst that analysis is sadly not open, it would be good to respond.
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