PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Impact of genistein on the gut microbiome of humanized mice and its role in breast tumor inhibition.

Abstract Since dietary polyphenols can have beneficial effects in prevention and treatment of cancer, we tested the hypothesis that breast cancer patients' intestinal microbiota is modulated by genistein (GE), an isoflavone found in soy, and that microbial alterations may offset the side effects brought about by chemotherapy. We demonstrated successful humanization of germ-free mice by transplanting fecal samples from breast cancer patients before and after chemotherapy. Mice were then grouped based on chemotherapy status and GE or control diet. We did not find any significant differences between pre-chemotherapy and post-chemotherapy bacterial composition and abundances. Germ-free mice on a GE diet showed differences in microbial composition as compared to mice on control diet. Four weeks after introduction of the customized GE diet, there was distinct clustering of GE-fed mice as compared to the control-fed group. In the gut microbiome of GE-treated humanized mice, there was an increase in abundance of genera Lactococcus and Eubacterium. Phylum Verrucomicrobia showed statistically significant (p = 0.02) differences in abundances between the GE-fed and control-fed groups. There was an increase in bacteria belonging to family Lachnospiraceae and Ruminococcaceae in GE-fed mice. Marked changes were observed in GE catabolism in mice humanized with fecal material from two of three patients' post-chemotherapy with complete disappearance of 4-ethylphenol and 2-(4-hydroxyphenol) propionic acid conjugates. The post-tumor samples did not show any distinct clustering of the gut microbiota between the two diet groups. There was an increase in latency of about 25% for tumor growth of the humanized mice that were on a GE diet as compared to humanized mice on a control diet. The average tumor size for the GE group was significantly decreased compared to the non-GE group. Collectively, our results suggest that the intestinal microbiota becomes altered with a GE diet before induction of tumor. Our findings indicate that GE modulates the microbiome in humanized mice that may contribute to its effects on increasing the latency of breast tumor and reducing tumor growth.
PMID
Related Publications

Dietary pomegranate extract and inulin affect gut microbiome differentially in mice fed an obesogenic diet.

Dietary Isomers of Sialyllactose Increase Ganglioside Sialic Acid Concentrations in the Corpus Callosum and Cerebellum and Modulate the Colonic Microbiota of Formula-Fed Piglets.

Complex interactions among diet, gastrointestinal transit, and gut microbiota in humanized mice.

The effect of diet on the human gut microbiome: a metagenomic analysis in humanized gnotobiotic mice.

Resistant Starch Alters the Microbiota-Gut Brain Axis: Implications for Dietary Modulation of Behavior.

Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 29267377
OWN - NLM
STAT- In-Process
LR  - 20171222
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 12
DP  - 2017
TI  - Impact of genistein on the gut microbiome of humanized mice and its role in
      breast tumor inhibition.
PG  - e0189756
LID - 10.1371/journal.pone.0189756 [doi]
AB  - Since dietary polyphenols can have beneficial effects in prevention and treatment
      of cancer, we tested the hypothesis that breast cancer patients' intestinal
      microbiota is modulated by genistein (GE), an isoflavone found in soy, and that
      microbial alterations may offset the side effects brought about by chemotherapy. 
      We demonstrated successful humanization of germ-free mice by transplanting fecal 
      samples from breast cancer patients before and after chemotherapy. Mice were then
      grouped based on chemotherapy status and GE or control diet. We did not find any 
      significant differences between pre-chemotherapy and post-chemotherapy bacterial 
      composition and abundances. Germ-free mice on a GE diet showed differences in
      microbial composition as compared to mice on control diet. Four weeks after
      introduction of the customized GE diet, there was distinct clustering of GE-fed
      mice as compared to the control-fed group. In the gut microbiome of GE-treated
      humanized mice, there was an increase in abundance of genera Lactococcus and
      Eubacterium. Phylum Verrucomicrobia showed statistically significant (p = 0.02)
      differences in abundances between the GE-fed and control-fed groups. There was an
      increase in bacteria belonging to family Lachnospiraceae and Ruminococcaceae in
      GE-fed mice. Marked changes were observed in GE catabolism in mice humanized with
      fecal material from two of three patients' post-chemotherapy with complete
      disappearance of 4-ethylphenol and 2-(4-hydroxyphenol) propionic acid conjugates.
      The post-tumor samples did not show any distinct clustering of the gut microbiota
      between the two diet groups. There was an increase in latency of about 25% for
      tumor growth of the humanized mice that were on a GE diet as compared to
      humanized mice on a control diet. The average tumor size for the GE group was
      significantly decreased compared to the non-GE group. Collectively, our results
      suggest that the intestinal microbiota becomes altered with a GE diet before
      induction of tumor. Our findings indicate that GE modulates the microbiome in
      humanized mice that may contribute to its effects on increasing the latency of
      breast tumor and reducing tumor growth.
FAU - Paul, Bidisha
AU  - Paul B
AD  - Department of Biology, University of Alabama at Birmingham, Birmingham, Alabama, 
      United States of America.
FAU - Royston, Kendra J
AU  - Royston KJ
AD  - Department of Biology, University of Alabama at Birmingham, Birmingham, Alabama, 
      United States of America.
AD  - Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham,
      Alabama, United States of America.
FAU - Li, Yuanyuan
AU  - Li Y
AD  - Department of Biology, University of Alabama at Birmingham, Birmingham, Alabama, 
      United States of America.
AD  - Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham,
      Alabama, United States of America.
FAU - Stoll, Matthew L
AU  - Stoll ML
AD  - Division of Pediatric Rheumatology, University of Alabama at Birmingham,
      Birmingham, Alabama, United States of America.
FAU - Skibola, Christine F
AU  - Skibola CF
AD  - Department of Hematology and Medical Oncology, Emory University School of
      Medicine, Atlanta, Georgia, United States of America.
FAU - Wilson, Landon S
AU  - Wilson LS
AD  - Targeted Metabolomics and Proteomics Laboratory, University of Alabama at
      Birmingham, Birmingham, Alabama, United States of America.
FAU - Barnes, Stephen
AU  - Barnes S
AD  - Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham,
      Alabama, United States of America.
AD  - Targeted Metabolomics and Proteomics Laboratory, University of Alabama at
      Birmingham, Birmingham, Alabama, United States of America.
AD  - Department of Pharmacology and Toxicology, University of Alabama at Birmingham,
      Birmingham, Alabama, United States of America.
AD  - Comprehensive Center for Healthy Aging, University of Alabama at Birmingham,
      Birmingham, Alabama, United States of America.
AD  - Nutrition Obesity Research Center, University of Alabama at Birmingham,
      Birmingham, Alabama, United States of America.
FAU - Morrow, Casey D
AU  - Morrow CD
AD  - Department of Cell, Development & Integrative Biology, University of Alabama at
      Birmingham, Birmingham, Alabama, United States of America.
FAU - Tollefsbol, Trygve O
AU  - Tollefsbol TO
AUID- ORCID: 0000-0002-0284-1511
AD  - Department of Biology, University of Alabama at Birmingham, Birmingham, Alabama, 
      United States of America.
AD  - Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham,
      Alabama, United States of America.
AD  - Comprehensive Center for Healthy Aging, University of Alabama at Birmingham,
      Birmingham, Alabama, United States of America.
AD  - Nutrition Obesity Research Center, University of Alabama at Birmingham,
      Birmingham, Alabama, United States of America.
AD  - Comprehensive Diabetes Center, University of Alabama at Birmingham, Birmingham,
      Alabama, United States of America.
LA  - eng
GR  - R01 CA178441 /NH/NIH HHS/United States
GR  - R01 CA2044346/NH/NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20171221
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
EDAT- 2017/12/22 06:00
MHDA- 2017/12/22 06:00
CRDT- 2017/12/22 06:00
PHST- 2017/09/01 00:00 [received]
PHST- 2017/12/03 00:00 [accepted]
PHST- 2017/12/22 06:00 [entrez]
PHST- 2017/12/22 06:00 [pubmed]
PHST- 2017/12/22 06:00 [medline]
AID - 10.1371/journal.pone.0189756 [doi]
AID - PONE-D-17-32177 [pii]
PST - epublish
SO  - PLoS One. 2017 Dec 21;12(12):e0189756. doi: 10.1371/journal.pone.0189756.
      eCollection 2017.