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Diet & Cancer

Diet & Cancer

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Published by Newdeersci
A review of numerous studies which have attempted to unravel the complex effects of diet on the induction and progression of cancer suggests that pro- and anti- cancer chemical agents may exist or be formed during cooking in most diets; these agents are difficult to properly identify but may promote or retard the formation of reactive nitrants which can damage biopolymers
A review of numerous studies which have attempted to unravel the complex effects of diet on the induction and progression of cancer suggests that pro- and anti- cancer chemical agents may exist or be formed during cooking in most diets; these agents are difficult to properly identify but may promote or retard the formation of reactive nitrants which can damage biopolymers

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Published by: Newdeersci on Jul 16, 2010
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10/25/2012

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 Diet & Cancer 
 Notes byD. Grant (BSc Msc PhD) New Deer, Scotland, UK AB53 6SXIt is commonly believed that the origin of cancer is entirely due to defective genes i.e. the existence insusceptible individuals of defective DNA sequences.Perhaps a useful concept is that cancer is caused by an alteration of DNA caused by the effects of acumulative effect of damage caused by environmental agents (carcinogens) such as those which areknown to be present in cigarette smoke or atmospheric pollution, acting in concert with inherited pro-cancer genes [1].Alteration of DNA may of course dramatically change in a harmful manner the activities of expressed proteins.A good diet contains antioxidants which can protect DNA against the mutagenic effects of toxicenvironmental pollutants, so a good diet is expected also to protect against pro-cancer effects of such pollutants (cf. e.g. S.P. Hussain, Nature Rev. Cancer, 2003, 3, 276-85).This sort of argument was behind the recent UK government’s publicity which advised subjects to eatfive portions of vegetables per day.A contrary message regarding the potentially anti-cancer role of good diet has, however, recently beengiven by the results of a large (5000,000: 142605M, 335873F)) epidemiological population survey(EPIC). While early indications from this survey seemed initially to strongly support the anti-cancer effects of fruit and vegetable dietary advice (cf. BBC News 27 May 2002) the final report (P. Boffettaet al., J.Natl. Cancer Inst., 2010, doi:10.1093/jnci/djq072) indicated that eating fruit and vegetables hadonly a relatively minor effect on cancer death rates in the surveyed population (as indicated by pressreports). This conclusion was however suggested to be misleading by a Cancer Research UK ScienceUpdate blog which pointed out that in the final EPIC study had actually shown that eating 2.5 portionsof fruit and vegetables /day had been associated with a 3% lower risk of cancer compared to peoplewho eat less than this amount, and those who eat 5 portions of fruit and vegetables/day had a 9% lower risk of cancer; furthermore those who eat more than 8 portions/day had a 11% lower risk. Neverthelessthe statistical overall benefit of fruit and vegetables in diet to anti-cancer health benefit had beenreduced considerably with the larger 500,000 sample compared the results of numerous smaller earlier surveys. This could indicate that regional differences between subgroups of the populations surveyedin the 500,000 sample which had not been identified might also contribute to the tendency for humansto die of cancer. [It should also be noted that the large survey however had successfully identified asub-group of cancers victims who were put more at risk of this disease by being heavy alcohol drinkersand who benefited to a greater degree than others from the ingestion of fruit and vegetables].Perhaps part of the reason for the apparent lack of a dramatic effect on the rate of deaths attributable tocancer of fruit and vegetables dietary intake in the majority of people in the large study, was the factthat toxic DNA-damaging substances can also inhibit cancer. An example of this is provided by the prominent anti-cancer drug cisplatin which is known to seriously damage DNA, but in an anti-cancer manner. The precise anti-cancer mechanism is however unknown but cisplatin was found in recentgene profiling studies to both up and down –regulate a consistent subset of genes (A.M. Galea & V.Murray, Cancer Informatics, 6, 1-41. Many scientifically sound studies had seemed to strongly suggest that dietary factors can have fairlydirect both pro and anti cancer effects. E.g. eating fruit and vegetables everyday had been thought tohave been well-established to considerably reduces the risk of cancer. But nitrite used as a preservativein some foods is pro cancer. Such pro-cancer factors had been estimated in 1984 (cf., I. Stipala, NewScientist,104 ,8) to cause a third of cancers worldwide but this proportion was greater in Japan whichhad the highest rates of death from cancers of the mouth pharynx, esophagus, stomach, lung and bladder. Other later surveys also showed pro-cancer effects of eating red meat (e.g. T. Norat et al., Int.J. Cancer 2002, 98, 241-256).It seems likely that
β
carotene, vitamin C and fibers in fruit and vegetable rich diets can inhibit cancer.However the pro-oxidant and pro-nitrant effects of excess iron ions e.g. under iron overload situations promoted by excessive consumption of red meat are able to create pro-cancer free radicals.Dietary meat can also putatively causes accumulation of a sugar (N-glycolylneuramic acid) which doesnot occur in adult humans (but its presence in tumours could suggest uptake from dietary sources such
 
as red meat and milk products and involvement of this sugar in the etiology of cancer, e.g. by theinduction of a chronic pro-oxidant immune response) [cf., BBC News 29 Sept 2003, “red meat cancer threat”; cf. also A. Varki, Yearbook. Phys. Anthropol., 2002, 44, 54-69; Glycoconjugate J., 2009, 26(3) 231-245; M. Hedlund et al., PNAS USA, 2008, 105 (48) 18936-18941] .Heparin, a drug which has been used for some seventy years was discovered many years ago tostimulate nuclear and chromatin transcription processes (S. Seki & T. Oda, Biochim..Biophys..Acta1977,479, 391; B.E. Coupar & C.J. Chesterton et al., Eur. J.Biochem., 1977, 79, 525-33 (this actionwas attributed to the interaction of this polyanion with the histones which removes DNA templaterestriction and allows RNA synthesis). Heparin signalling is representative of the larger high systemmanager system of animal biology afforded by heparan sulphates, a system of different polysaccharidemicrostructures which occur a linear alternating copolymer of glucosamine with iduronic/ glucuronicacid. This information storage and processing system, which is somewhat analogous to, but, of course,highly distinct from DNA, contains (heparin-like) signals which are known to be centrally implicatedin cellular control activities of putative central relevance to a fuller understanding of howenvironmental inputs which can promote or inhibit cancer. Indeed natural heparin-like moleculeswhich circulate in the bloodstream may provide a natural anti-cancer (and anti-other degenerativedisease) protection system (cf., H. Engleberg, Cancer (New York) 1999, 85, (23) 257-272 cf.,Circulation, 1961, 23, 573-577; D.L. Ornstein & L.R. Zacharski, Haemostasis, 1999, 29, 48-60. [Theamounts of these anti-cancer heparin like molecules are expected to vary with diet, and be higher witha high fruit and vegetable diet].Platinum and other inorganic elements which have been used for anti-cancer therapy also bind toheparin. (cf., D.Grant et al.,Biochem. Soc. Trans., 1996, 24 (2) 204S). Indeed natural heparin containsminute amounts of Pt and Ga. The anti-cancer effect of heparin may therefore derive at least in partfrom this phenomenon. Further studies are needed to probe this possibility.Glycosaminoglycans in general also exhibit antioxidant capacity being able to prevent DNAfragmentation under oxidative stress (cf. GM Campo et al., Free Rad. Res. 2004, 38 (6) 601-611.
Some other ‘diet & cancer’ studies
A study 884 of human subjects and controls by J Lin et al. of the University of Texas reported atthe101st annual meeting in 2010 of the American Association for Cancer Research.(cf., PressAssociation e.g. the Guardian 19 April 2010, p15) reported from that cooking meat or fish at hightemperatures increases the risk of cancer; this being attributed to the formation of heterocyclic aminecarcinogens under these cooking conditions. There was a 48% greater risk of bladder cancer betweenthe greatest and the least meat eaters in the survey. The occurrence of bladder cancer has also beentraditionally associated with occupational exposure to heterocylic amines. A survey of recent studiesof how such amines promote cancer is given by the National Cancer Institute Fact Sheet –“Heterocyclic amines in cooked meat” available at htttp://www.cancer.gov/cancertopics/factsheet/…/heterocyclic-aminesSir D. King et al., in a UK government study The Foresight Report written by 250 leading scientistshighlighted the danger to health of the global epidemic of obesity. 10% of all cancers in non-smokers is believed to be linked to obesity which is further believed to be related to diet.Obesity has also been linked to intoxication by globally distributed persistent organic pollutants (POPs)which become bio-concentrated in some fatty animal and some fish tissues as well as in some milk  products.A vegetarian or vegan diet is commonly believed to be associated with a major decrease in cancer risk.This is well illustrated by historical comparisons between data from countries ranging between fullEastern and full Western-lifestyles cf. the graphics presented by William Harris M.D. in 1999 atwww.vegsource.com/harris/cancer_vegdiet.htm, which shows how the incidence of cancers can bestatistically associated with situations where meat and dairy food intake differ markedly. The
 
incidence of breast cancer might be assumed on the basis of these data, to have been boosted by theconsumption in the Western lifestyle of some dairy products.The consumption of dairy products might then be assumed to be highly pro-cancer. Full fat dairy products are however sources of (anti-cancer) Vitamin D as well as of Vitamin A.Although there seemed to be little evidence of benefit to humans, it was indicated that Vitamin A prevented squamous cell cancers in laboratory animals (G. Kolata, Science, 1984, 223, 1161).[1]The traditional view that genetic alterations are involved in many cancers.Oncogenes are homologous to normal genes; in viruses they are known to be able to cause animalcancers.Cultured animal cancer cells often carry transforming genes that can cause normal cells to acquirecancerous characteristics.Faulty control of normal cellular genes may underlie pro-cancer genetic transformation.Mutagenic chemicals and radiation damage DNA which is believed to be why they are carcinogenic.Simian sarcoma virus v-sis was found to show homology with platelet derived growth factor (PDGF)and c-sis transcripts and synthesis of PDGF-like proteins were detected in human osteosarcoma.It seemed that a general principle was emerging that cancer was the result of aberrant growth factor activities (cf., e.g. , D.G. Graves et al., Science, 1984, 226, 972-974).PDGF activities are also affected by heparan sulphate suggesting that this polysaccharide, e.g. if defective, could affect oncogene activities.Proto-oncogenes. pp60
c src
(protein tyrosine kinase encoded by c-src is abundant in brain etc. and notconcerned with mitosis. This protein, however, undergoes a post-translational modification (not phosphyorylation) which greatly increases its activity. The modified form of pp60c-src found inneurons could be a functional analogue of v-src. v-src can meddle with differentiation (either blockingor reversing it). It is believed that phenotypes elicited by v-src and NGF are similar.L.A.MacMillan-Crow et al. reported (Arch. Biochem. Biophys., 2000, 377 (2) 350-6) that tyrosinenitration of c-src kinase occurs in human pancreatic ductal adenocarcinoma and that such nitrationcould likely boost tyrosine kinase signalling. This finding implicates the
nitration of oncogene products as a possible key factor in the progression of cancer.
It has often been assumed thattyrosine nitration is always a harmful effect, being a hallmark of any degenerative disease processes but S.W. Park et al., Mol. Cell. Proteomics, 2005, 4, 300-9, have indicated that tyrosine nitration of the p65 subunit of NF kappaB can rapidly inactivate nuclear factor kappa B associated pro-inflammatory(pro-cancer) processes.It is possible, however, that key roles may be played by certain dietary constituents which can act asanti-nitrants. These have not as yet been identified.Some clues about possible antinitrant chemical structures can be suggested by studies of selenium-containing molecules (e.g. ebselen (2-phenyl 1-2benzisoselenazol-3[2H]one}which may demonstratetherapeutic effectiveness against cancer (cf., V. Sharma et al., Int. J. Cancer, 2008, 123 (9) 2204-12;

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