Eicosapentaenoic acid free fatty acid prevents and suppresses colonic neoplasia in colitis‐associated colorectal cancer acting on Notch signaling and gut microbiota
Inflammatory bowel diseases are associated with increased risk of developing colitis‐associated colorectal cancer (CAC). Epidemiological data show that the consumption of ω‐3 polyunsaturated fatty acids (ω‐3 PUFAs) decreases the risk of sporadic colorectal cancer (CRC). Importantly, recent data have...
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| Published in | International journal of cancer Vol. 135; no. 9; pp. 2004 - 2013 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Hoboken, NJ
Wiley-Blackwell
01.11.2014
Wiley Subscription Services, Inc |
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| Online Access | Get full text |
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| Abstract | Inflammatory bowel diseases are associated with increased risk of developing colitis‐associated colorectal cancer (CAC). Epidemiological data show that the consumption of ω‐3 polyunsaturated fatty acids (ω‐3 PUFAs) decreases the risk of sporadic colorectal cancer (CRC). Importantly, recent data have shown that eicosapentaenoic acid‐free fatty acid (EPA‐FFA) reduces polyp formation and growth in models of familial adenomatous polyposis. However, the effects of dietary EPA‐FFA are unknown in CAC. We tested the effectiveness of substituting EPA‐FFA, for other dietary fats, in preventing inflammation and cancer in the AOM‐DSS model of CAC. The AOM‐DSS protocols were designed to evaluate the effect of EPA‐FFA on both initiation and promotion of carcinogenesis. We found that EPA‐FFA diet strongly decreased tumor multiplicity, incidence and maximum tumor size in the promotion and initiation arms. Moreover EPA–FFA, in particular in the initiation arm, led to reduced cell proliferation and nuclear β‐catenin expression, whilst it increased apoptosis. In both arms, EPA‐FFA treatment led to increased membrane switch from ω‐6 to ω‐3 PUFAs and a concomitant reduction in PGE2 production. We observed no significant changes in intestinal inflammation between EPA‐FFA treated arms and AOM‐DSS controls. Importantly, we found that EPA‐FFA treatment restored the loss of Notch signaling found in the AOM‐DSS control and resulted in the enrichment of Lactobacillus species in the gut microbiota. Taken together, our data suggest that EPA‐FFA is an excellent candidate for CRC chemoprevention in CAC.
What's new?
Recent clinical data show that, as yet, there is no agent clearly protecting against colorectal cancer (CRC) development in long‐standing inflammatory bowel diseases. This study tests the effect of dietary supplementation with eicosapentaenoic acid, as free fatty acid (EPA‐FFA), in a mouse model of colitis‐associated CRC. The results demonstrate for the first time that EPA‐FFA is an effective chemopreventive agent during both initiation and promotion of colitis‐associated colorectal cancer in mice, with changes in Notch1 signaling and gut microbiota composition. Early EPA‐FFA supplementation could thus be a good strategy for CRC prevention in subjects affected by inflammatory bowel diseases. |
|---|---|
| AbstractList | Inflammatory bowel diseases are associated with increased risk of developing colitis-associated colorectal cancer (CAC). Epidemiological data show that the consumption of ¿-3 polyunsaturated fatty acids (¿-3 PUFAs) decreases the risk of sporadic colorectal cancer (CRC). Importantly, recent data have shown that eicosapentaenoic acid-free fatty acid (EPA-FFA) reduces polyp formation and growth in models of familial adenomatous polyposis. However, the effects of dietary EPA-FFA are unknown in CAC. We tested the effectiveness of substituting EPA-FFA, for other dietary fats, in preventing inflammation and cancer in the AOM-DSS model of CAC. The AOM-DSS protocols were designed to evaluate the effect of EPA-FFA on both initiation and promotion of carcinogenesis. We found that EPA-FFA diet strongly decreased tumor multiplicity, incidence and maximum tumor size in the promotion and initiation arms. Moreover EPA–FFA, in particular in the initiation arm, led to reduced cell proliferation and nuclear ß-catenin expression, whilst it increased apoptosis. In both arms, EPA-FFA treatment led to increased membrane switch from ¿-6 to ¿-3 PUFAs and a concomitant reduction in PGE2 production. We observed no significant changes in intestinal inflammation between EPA-FFA treated arms and AOM-DSS controls. Importantly, we found that EPA-FFA treatment restored the loss of Notch signaling found in the AOM-DSS control and resulted in the enrichment of Lactobacillus species in the gut microbiota. Taken together, our data suggest that EPA-FFA is an excellent candidate for CRC chemoprevention in CAC. Inflammatory bowel diseases are associated with increased risk of developing colitis-associated colorectal cancer (CAC). Epidemiological data show that the consumption of [omega]-3 polyunsaturated fatty acids ([omega]-3 PUFAs) decreases the risk of sporadic colorectal cancer (CRC). Importantly, recent data have shown that eicosapentaenoic acid-free fatty acid (EPA-FFA) reduces polyp formation and growth in models of familial adenomatous polyposis. However, the effects of dietary EPA-FFA are unknown in CAC. We tested the effectiveness of substituting EPA-FFA, for other dietary fats, in preventing inflammation and cancer in the AOM-DSS model of CAC. The AOM-DSS protocols were designed to evaluate the effect of EPA-FFA on both initiation and promotion of carcinogenesis. We found that EPA-FFA diet strongly decreased tumor multiplicity, incidence and maximum tumor size in the promotion and initiation arms. Moreover EPA-FFA, in particular in the initiation arm, led to reduced cell proliferation and nuclear [beta]-catenin expression, whilst it increased apoptosis. In both arms, EPA-FFA treatment led to increased membrane switch from [omega]-6 to [omega]-3 PUFAs and a concomitant reduction in PGE2 production. We observed no significant changes in intestinal inflammation between EPA-FFA treated arms and AOM-DSS controls. Importantly, we found that EPA-FFA treatment restored the loss of Notch signaling found in the AOM-DSS control and resulted in the enrichment of Lactobacillus species in the gut microbiota. Taken together, our data suggest that EPA-FFA is an excellent candidate for CRC chemoprevention in CAC. What's new? Recent clinical data show that, as yet, there is no agent clearly protecting against colorectal cancer (CRC) development in long-standing inflammatory bowel diseases. This study tests the effect of dietary supplementation with eicosapentaenoic acid, as free fatty acid (EPA-FFA), in a mouse model of colitis-associated CRC. The results demonstrate for the first time that EPA-FFA is an effective chemopreventive agent during both initiation and promotion of colitis-associated colorectal cancer in mice, with changes in Notch1 signaling and gut microbiota composition. Early EPA-FFA supplementation could thus be a good strategy for CRC prevention in subjects affected by inflammatory bowel diseases. Inflammatory bowel diseases are associated with increased risk of developing colitis-associated colorectal cancer (CAC). Epidemiological data show that the consumption of omega -3 polyunsaturated fatty acids ( omega -3 PUFAs) decreases the risk of sporadic colorectal cancer (CRC). Importantly, recent data have shown that eicosapentaenoic acid-free fatty acid (EPA-FFA) reduces polyp formation and growth in models of familial adenomatous polyposis. However, the effects of dietary EPA-FFA are unknown in CAC. We tested the effectiveness of substituting EPA-FFA, for other dietary fats, in preventing inflammation and cancer in the AOM-DSS model of CAC. The AOM-DSS protocols were designed to evaluate the effect of EPA-FFA on both initiation and promotion of carcinogenesis. We found that EPA-FFA diet strongly decreased tumor multiplicity, incidence and maximum tumor size in the promotion and initiation arms. Moreover EPA-FFA, in particular in the initiation arm, led to reduced cell proliferation and nuclear beta -catenin expression, whilst it increased apoptosis. In both arms, EPA-FFA treatment led to increased membrane switch from omega -6 to omega -3 PUFAs and a concomitant reduction in PGE sub(2) production. We observed no significant changes in intestinal inflammation between EPA-FFA treated arms and AOM-DSS controls. Importantly, we found that EPA-FFA treatment restored the loss of Notch signaling found in the AOM-DSS control and resulted in the enrichment of Lactobacillus species in the gut microbiota. Taken together, our data suggest that EPA-FFA is an excellent candidate for CRC chemoprevention in CAC. What's new? Recent clinical data show that, as yet, there is no agent clearly protecting against colorectal cancer (CRC) development in long-standing inflammatory bowel diseases. This study tests the effect of dietary supplementation with eicosapentaenoic acid, as free fatty acid (EPA-FFA), in a mouse model of colitis-associated CRC. The results demonstrate for the first time that EPA-FFA is an effective chemopreventive agent during both initiation and promotion of colitis-associated colorectal cancer in mice, with changes in Notch1 signaling and gut microbiota composition. Early EPA-FFA supplementation could thus be a good strategy for CRC prevention in subjects affected by inflammatory bowel diseases. Inflammatory bowel diseases are associated with increased risk of developing colitis-associated colorectal cancer (CAC). Epidemiological data show that the consumption of ω-3 polyunsaturated fatty acids (ω-3 PUFAs) decreases the risk of sporadic colorectal cancer (CRC). Importantly, recent data have shown that eicosapentaenoic acid-free fatty acid (EPA-FFA) reduces polyp formation and growth in models of familial adenomatous polyposis. However, the effects of dietary EPA-FFA are unknown in CAC. We tested the effectiveness of substituting EPA-FFA, for other dietary fats, in preventing inflammation and cancer in the AOM-DSS model of CAC. The AOM-DSS protocols were designed to evaluate the effect of EPA-FFA on both initiation and promotion of carcinogenesis. We found that EPA-FFA diet strongly decreased tumor multiplicity, incidence and maximum tumor size in the promotion and initiation arms. Moreover EPA-FFA, in particular in the initiation arm, led to reduced cell proliferation and nuclear β-catenin expression, whilst it increased apoptosis. In both arms, EPA-FFA treatment led to increased membrane switch from ω-6 to ω-3 PUFAs and a concomitant reduction in PGE2 production. We observed no significant changes in intestinal inflammation between EPA-FFA treated arms and AOM-DSS controls. Importantly, we found that EPA-FFA treatment restored the loss of Notch signaling found in the AOM-DSS control and resulted in the enrichment of Lactobacillus species in the gut microbiota. Taken together, our data suggest that EPA-FFA is an excellent candidate for CRC chemoprevention in CAC.Inflammatory bowel diseases are associated with increased risk of developing colitis-associated colorectal cancer (CAC). Epidemiological data show that the consumption of ω-3 polyunsaturated fatty acids (ω-3 PUFAs) decreases the risk of sporadic colorectal cancer (CRC). Importantly, recent data have shown that eicosapentaenoic acid-free fatty acid (EPA-FFA) reduces polyp formation and growth in models of familial adenomatous polyposis. However, the effects of dietary EPA-FFA are unknown in CAC. We tested the effectiveness of substituting EPA-FFA, for other dietary fats, in preventing inflammation and cancer in the AOM-DSS model of CAC. The AOM-DSS protocols were designed to evaluate the effect of EPA-FFA on both initiation and promotion of carcinogenesis. We found that EPA-FFA diet strongly decreased tumor multiplicity, incidence and maximum tumor size in the promotion and initiation arms. Moreover EPA-FFA, in particular in the initiation arm, led to reduced cell proliferation and nuclear β-catenin expression, whilst it increased apoptosis. In both arms, EPA-FFA treatment led to increased membrane switch from ω-6 to ω-3 PUFAs and a concomitant reduction in PGE2 production. We observed no significant changes in intestinal inflammation between EPA-FFA treated arms and AOM-DSS controls. Importantly, we found that EPA-FFA treatment restored the loss of Notch signaling found in the AOM-DSS control and resulted in the enrichment of Lactobacillus species in the gut microbiota. Taken together, our data suggest that EPA-FFA is an excellent candidate for CRC chemoprevention in CAC. Inflammatory bowel diseases are associated with increased risk of developing colitis‐associated colorectal cancer (CAC). Epidemiological data show that the consumption of ω‐3 polyunsaturated fatty acids (ω‐3 PUFAs) decreases the risk of sporadic colorectal cancer (CRC). Importantly, recent data have shown that eicosapentaenoic acid‐free fatty acid (EPA‐FFA) reduces polyp formation and growth in models of familial adenomatous polyposis. However, the effects of dietary EPA‐FFA are unknown in CAC. We tested the effectiveness of substituting EPA‐FFA, for other dietary fats, in preventing inflammation and cancer in the AOM‐DSS model of CAC. The AOM‐DSS protocols were designed to evaluate the effect of EPA‐FFA on both initiation and promotion of carcinogenesis. We found that EPA‐FFA diet strongly decreased tumor multiplicity, incidence and maximum tumor size in the promotion and initiation arms. Moreover EPA–FFA, in particular in the initiation arm, led to reduced cell proliferation and nuclear β‐catenin expression, whilst it increased apoptosis. In both arms, EPA‐FFA treatment led to increased membrane switch from ω‐6 to ω‐3 PUFAs and a concomitant reduction in PGE2 production. We observed no significant changes in intestinal inflammation between EPA‐FFA treated arms and AOM‐DSS controls. Importantly, we found that EPA‐FFA treatment restored the loss of Notch signaling found in the AOM‐DSS control and resulted in the enrichment of Lactobacillus species in the gut microbiota. Taken together, our data suggest that EPA‐FFA is an excellent candidate for CRC chemoprevention in CAC. What's new? Recent clinical data show that, as yet, there is no agent clearly protecting against colorectal cancer (CRC) development in long‐standing inflammatory bowel diseases. This study tests the effect of dietary supplementation with eicosapentaenoic acid, as free fatty acid (EPA‐FFA), in a mouse model of colitis‐associated CRC. The results demonstrate for the first time that EPA‐FFA is an effective chemopreventive agent during both initiation and promotion of colitis‐associated colorectal cancer in mice, with changes in Notch1 signaling and gut microbiota composition. Early EPA‐FFA supplementation could thus be a good strategy for CRC prevention in subjects affected by inflammatory bowel diseases. Inflammatory bowel diseases are associated with increased risk of developing colitis‐associated colorectal cancer (CAC). Epidemiological data show that the consumption of ω‐3 polyunsaturated fatty acids (ω‐3 PUFAs) decreases the risk of sporadic colorectal cancer (CRC). Importantly, recent data have shown that eicosapentaenoic acid‐free fatty acid (EPA‐FFA) reduces polyp formation and growth in models of familial adenomatous polyposis. However, the effects of dietary EPA‐FFA are unknown in CAC. We tested the effectiveness of substituting EPA‐FFA, for other dietary fats, in preventing inflammation and cancer in the AOM‐DSS model of CAC. The AOM‐DSS protocols were designed to evaluate the effect of EPA‐FFA on both initiation and promotion of carcinogenesis. We found that EPA‐FFA diet strongly decreased tumor multiplicity, incidence and maximum tumor size in the promotion and initiation arms. Moreover EPA–FFA, in particular in the initiation arm, led to reduced cell proliferation and nuclear β‐catenin expression, whilst it increased apoptosis. In both arms, EPA‐FFA treatment led to increased membrane switch from ω‐6 to ω‐3 PUFAs and a concomitant reduction in PGE 2 production. We observed no significant changes in intestinal inflammation between EPA‐FFA treated arms and AOM‐DSS controls. Importantly, we found that EPA‐FFA treatment restored the loss of Notch signaling found in the AOM‐DSS control and resulted in the enrichment of Lactobacillus species in the gut microbiota. Taken together, our data suggest that EPA‐FFA is an excellent candidate for CRC chemoprevention in CAC. What's new? Recent clinical data show that, as yet, there is no agent clearly protecting against colorectal cancer (CRC) development in long‐standing inflammatory bowel diseases. This study tests the effect of dietary supplementation with eicosapentaenoic acid, as free fatty acid (EPA‐FFA), in a mouse model of colitis‐associated CRC. The results demonstrate for the first time that EPA‐FFA is an effective chemopreventive agent during both initiation and promotion of colitis‐associated colorectal cancer in mice, with changes in Notch1 signaling and gut microbiota composition. Early EPA‐FFA supplementation could thus be a good strategy for CRC prevention in subjects affected by inflammatory bowel diseases. Inflammatory bowel diseases are associated with increased risk of developing colitis-associated colorectal cancer (CAC). Epidemiological data show that the consumption of ω-3 polyunsaturated fatty acids (ω-3 PUFAs) decreases the risk of sporadic colorectal cancer (CRC). Importantly, recent data have shown that eicosapentaenoic acid-free fatty acid (EPA-FFA) reduces polyp formation and growth in models of familial adenomatous polyposis. However, the effects of dietary EPA-FFA are unknown in CAC. We tested the effectiveness of substituting EPA-FFA, for other dietary fats, in preventing inflammation and cancer in the AOM-DSS model of CAC. The AOM-DSS protocols were designed to evaluate the effect of EPA-FFA on both initiation and promotion of carcinogenesis. We found that EPA-FFA diet strongly decreased tumor multiplicity, incidence and maximum tumor size in the promotion and initiation arms. Moreover EPA-FFA, in particular in the initiation arm, led to reduced cell proliferation and nuclear β-catenin expression, whilst it increased apoptosis. In both arms, EPA-FFA treatment led to increased membrane switch from ω-6 to ω-3 PUFAs and a concomitant reduction in PGE2 production. We observed no significant changes in intestinal inflammation between EPA-FFA treated arms and AOM-DSS controls. Importantly, we found that EPA-FFA treatment restored the loss of Notch signaling found in the AOM-DSS control and resulted in the enrichment of Lactobacillus species in the gut microbiota. Taken together, our data suggest that EPA-FFA is an excellent candidate for CRC chemoprevention in CAC. |
| Author | Fogliano, Vincenzo Fazio, Chiara Belluzzi, Andrea Ceccarelli, Claudio Bazzoli, Franco Munarini, Alessandra Piazzi, Giulia Lembo, Vincenzo Mazzone, Giovanna Prossomariti, Anna Candela, Marco Brigidi, Patrizia D'Argenio, Giuseppe Romano, Marco Balbi, Tiziana Vitaglione, Paola D'Angelo, Leonarda Loadman, Paul M. Hull, Mark A. Ricciardiello, Luigi Biagi, Elena Chieco, Pasquale |
| Author_xml | – sequence: 1 givenname: Giulia surname: Piazzi fullname: Piazzi, Giulia organization: S. Orsola‐Malpighi Hospital, University of Bologna – sequence: 2 givenname: Giuseppe surname: D'Argenio fullname: D'Argenio, Giuseppe organization: University of Naples Federico II and Institute of Protein Biochemistry, CNR – sequence: 3 givenname: Anna surname: Prossomariti fullname: Prossomariti, Anna organization: S. Orsola‐Malpighi Hospital, University of Bologna – sequence: 4 givenname: Vincenzo surname: Lembo fullname: Lembo, Vincenzo organization: University of Naples Federico II and Institute of Protein Biochemistry, CNR – sequence: 5 givenname: Giovanna surname: Mazzone fullname: Mazzone, Giovanna organization: University of Naples Federico II and Institute of Protein Biochemistry, CNR – sequence: 6 givenname: Marco surname: Candela fullname: Candela, Marco organization: University of Bologna – sequence: 7 givenname: Elena surname: Biagi fullname: Biagi, Elena organization: University of Bologna – sequence: 8 givenname: Patrizia surname: Brigidi fullname: Brigidi, Patrizia organization: University of Bologna – sequence: 9 givenname: Paola surname: Vitaglione fullname: Vitaglione, Paola organization: University of Naples – sequence: 10 givenname: Vincenzo surname: Fogliano fullname: Fogliano, Vincenzo organization: Wageningen University & Research Centre – sequence: 11 givenname: Leonarda surname: D'Angelo fullname: D'Angelo, Leonarda organization: S. Orsola‐Malpighi Hospital, University of Bologna – sequence: 12 givenname: Chiara surname: Fazio fullname: Fazio, Chiara organization: S. Orsola‐Malpighi Hospital, University of Bologna – sequence: 13 givenname: Alessandra surname: Munarini fullname: Munarini, Alessandra organization: S. Orsola‐Malpighi Hospital, University of Bologna – sequence: 14 givenname: Andrea surname: Belluzzi fullname: Belluzzi, Andrea organization: S. Orsola‐Malpighi Hospital, University of Bologna – sequence: 15 givenname: Claudio surname: Ceccarelli fullname: Ceccarelli, Claudio organization: Diagnostic and Specialty Medicine, University of Bologna – sequence: 16 givenname: Pasquale surname: Chieco fullname: Chieco, Pasquale organization: S. Orsola‐Malpighi Hospital, University of Bologna – sequence: 17 givenname: Tiziana surname: Balbi fullname: Balbi, Tiziana organization: S. Orsola‐Malpighi Hospital, University of Bologna – sequence: 18 givenname: Paul M. surname: Loadman fullname: Loadman, Paul M. organization: Institute of Cancer Therapeutics, University of Bradford – sequence: 19 givenname: Mark A. surname: Hull fullname: Hull, Mark A. organization: Leeds Institute of Biomedical & Clinical Sciences, St James's University Hospital – sequence: 20 givenname: Marco surname: Romano fullname: Romano, Marco organization: Gastroenterology Unit, Second University of Naples – sequence: 21 givenname: Franco surname: Bazzoli fullname: Bazzoli, Franco organization: University of Bologna – sequence: 22 givenname: Luigi surname: Ricciardiello fullname: Ricciardiello, Luigi organization: S. Orsola‐Malpighi Hospital, University of Bologna |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28734015$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/24676631$$D View this record in MEDLINE/PubMed |
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| Copyright | 2014 UICC 2015 INIST-CNRS 2014 UICC. Wageningen University & Research |
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| Keywords | microbiota Notch receptor Rectal disease Digestive system Colorectal cancer Gut Notch omega 3 Lipids Inflammation Free fatty acid Malignant tumor n-3 fatty acid Colonic disease Prevention Signal transduction Colon cancer Cancerology Digestive diseases Intestinal disease Colitis Colon Eicosapentaenoic acid Cancer inflammation colon cancer |
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| Notes | Luigi Ricciardiello has received an unrestricted scientific grant from SLA Pharma AG. Mark Hull has received a travel grant and an unrestricted scientific grant from SLA Pharma AG. Conflct of Interest ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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| PublicationDate | 01 November 2014 |
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| SubjectTerms | Animals Apoptosis Biological and medical sciences Cancer Cell Proliferation cells chemoprevention Colitis - chemically induced Colitis - complications Colitis - pathology Colon - microbiology Colon - pathology colon cancer Colorectal cancer Colorectal Neoplasms - etiology Colorectal Neoplasms - pathology Colorectal Neoplasms - prevention & control dietary fish-oil differentiation docosahexaenoic acid Eicosapentaenoic Acid - administration & dosage Fatty acids Fatty Acids, Nonesterified - administration & dosage Gastroenterology. Liver. Pancreas. Abdomen Gastrointestinal Tract - drug effects Gastrointestinal Tract - metabolism Gastrointestinal Tract - microbiology Immunoenzyme Techniques inflammation Inflammation - etiology Inflammation - pathology Inflammation - prevention & control Inflammatory bowel disease intestinal microbiota Lactobacillus Male Medical research Medical sciences Mice Mice, Inbred C57BL microbiota Microbiota - drug effects Microbiota - physiology mouse model Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Notch omega 3 Real-Time Polymerase Chain Reaction Receptors, Notch - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Rodents sodium Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors |
| Title | Eicosapentaenoic acid free fatty acid prevents and suppresses colonic neoplasia in colitis‐associated colorectal cancer acting on Notch signaling and gut microbiota |
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