Editing Malignant transformation (section)

==Examples of diet-related malignant transformation==

===Diet and colon cancer===

Colon cancer provides one example of the mechanisms by which diet, the top factor listed in the table, is an external factor in cancer.  The Western diet of African Americans in the United States is associated with a yearly colon cancer rate of 65 per 100,000 individuals, while the high fiber/low fat diet of rural Native Africans in South Africa is associated with a yearly colon cancer rate of <5 per 100,000.<ref name="O'Keefe2015">{{cite journal |vauthors=O'Keefe SJ, Li JV, Lahti L, Ou J, Carbonero F, Mohammed K, Posma JM, Kinross J, Wahl E, Ruder E, Vipperla K, Naidoo V, Mtshali L, Tims S, Puylaert PG, DeLany J, Krasinskas A, Benefiel AC, Kaseb HO, Newton K, Nicholson JK, de Vos WM, Gaskins HR, Zoetendal EG |title=Fat, fibre and cancer risk in African Americans and rural Africans |journal=Nat Commun |volume=6 |pages=6342 |year=2015 |pmid=25919227 |pmc=4415091 |doi=10.1038/ncomms7342 |bibcode=2015NatCo...6.6342O }}</ref>  Feeding the Western diet for two weeks to Native Africans increased their secondary bile acids, including carcinogenic [[deoxycholic acid]],<ref name=Bernstein2011>{{cite journal |vauthors=Bernstein C, Holubec H, Bhattacharyya AK, Nguyen H, Payne CM, Zaitlin B, Bernstein H |title=Carcinogenicity of deoxycholate, a secondary bile acid |journal=Arch. Toxicol. |volume=85 |issue=8 |pages=863–71 |year=2011 |pmid=21267546 |pmc=3149672 |doi=10.1007/s00204-011-0648-7 }}</ref> by 400%, and also changed the colonic microbiota.<ref name="O'Keefe2015" />  Evidence reviewed by Sun and Kato<ref name=SunKato>{{cite journal |vauthors=Sun J, Kato I |title=Gut microbiota, inflammation and colorectal cancer |journal=Genes & Diseases|volume=3 |issue=2 |pages=130–143 |year=2016 |pmid=28078319 |doi=10.1016/j.gendis.2016.03.004 |pmc=5221561}}</ref> indicates that differences in human colonic microbiota play an important role in the progression of colon cancer.

===Diet and lung cancer===

A second example, relating a dietary component to a cancer, is illustrated by lung cancer.  Two large population-based studies were performed, one in Italy and one in the United States.<ref name="pmid28077426">{{cite journal |vauthors=Lee JT, Lai GY, Liao LM, Subar AF, Bertazzi PA, Pesatori AC, Freedman ND, Landi MT, Lam TK |title=Nut consumption and lung cancer risk: Results from two large observational studies |journal=Cancer Epidemiol. Biomarkers Prev. |volume= 26|issue= 6|pages= 826–836|year=2017 |pmid=28077426 |pmc=6020049 |doi=10.1158/1055-9965.EPI-16-0806 }}</ref>  In Italy, the study population consisted of two cohorts:  the first, 1721 individuals diagnosed with lung cancer and no severe disease, and the second, 1918 control individuals with absence of lung cancer history or any advanced diseases.  All individuals filled out a food frequency questionnaire including consumption of walnuts, hazelnuts, almonds, and peanuts, and indicating smoking status.  In the United States, 495,785 members of [[AARP]] were questioned on consumption of peanuts, walnuts, seeds, or other nuts in addition to other foods and smoking status.  In this U.S. study 18,533 incident lung cancer cases were identified during up to 16 years of follow-up.  Overall, individuals in the highest quintile of frequency of nut consumption had a 26% lower risk of lung cancer in the Italian study and a 14% lower risk of lung cancer in the U.S. study.  Similar results were obtained among individuals who were smokers.