Life Extension Magazine®

Nuclear power plant where radiation adds risk for cancer

Environmental Toxins and Cancer Risk

We are surrounded by environmental toxins that lead to DNA damage and cancer. Compelling studies show how specific nutrients can protect and help counteract these harmful chemicals.

Scientifically reviewed by: Dr. Shaylind Benson, ND, in October 2024. Written by: Stephanie Westfall.

The chemicals in our water, air, and food, the materials in our home, and non ionizing radiation present cancer risks.1-5

But that doesn’t mean that we are defenseless. Researchers have identified several mechanisms by which most cancer-producing toxins disrupt our body’s defense systems. Compelling evidence reveals how we can defend against these carcinogenic mechanisms.

After reading this article, you’ll be able to select protective approaches that best fit your individual exposure to help counteract some of the highest risks in your own environment.

How Toxins Produce Cancer

While we once thought of “cancer” as a single devastating disease, we now recognize that a range of cells, in various tissues, can undergo “malignant transformation” to become cancer.6

In fact, the body’s natural defenses are repeatedly inhibiting processes involved in cancer development through a series of targeted responses, much like a nation’s security forces.

On occasion, however, a precancerous or malignant cell slips through all of those defenses and may proceed to start a tumor.

In the worst case, the tumor can release tiny clumps of malignant cells that spread cancer to distant parts of the body. Metastatic cancer is almost always a predictor of death as a result of the disease.7

Despite the vast number and diversity of cancer types, there are a relatively small number of events that typically occur in the progression from healthy cell to malignancy. Toxic environmental chemicals, electromagnetic fields,8,9 and ionizing radiation may initiate and/or promote malignancy, operating along a number of mechanisms. Some of these mechanisms include:10-22

  • DNA damage,
  • Liver detoxification impairment,
  • Immune impairment,
  • Endocrine disruptors, and
  • Loss of apoptosis.

Powerful Cancer Prevention from Mother Nature

It is easy to become fearful about the vast numbers of toxic chemicals and other influences all around us, lurking to produce catastrophic cancers. Fortunately, there are solutions in the form of specific nutrients with powerful cancer-preventing effects.

Compelling scientific studies show that specific nutrients counteract major processes by which toxic compounds and radiation promote malignancies.

By discussing the five major pathways through which toxins initiate cancer, and the nutrients that specifically counteract each of those cancer-promoting processes, we can put together a rigorous cancer chemoprevention regimen.

TABLE 1: Nutrients That Reduce DNA Damage

Nutrient

Cancers Affected*

Carotenoids (lutein, astaxanthin, lycopene)38-43

Prostate, colon

Coenzyme Q1044-46

Colon, head-and-neck

Fish oil (omega-3 fats)47,48

Colon, skin

Genistein (from soy)49

Leukemia

Plant polyphenols28,50,51

Multiple

Probiotics (Lacto-bacillus rhamnosus)34

Colon

Quercetin45

Head-and-neck

Selenium29,30

Colon, breast

Vitamin C32,33,52-56

Breast, colon, skin

Vitamin D36,57

Colon, skin

Vitamin E31,58-63

Liver, breast

*These are only a few of the types of cancers affected by these nutrients.

DNA Damage

The first way toxins may lead to cancer is by breaking DNA strands. Damage to DNA is a major initiating factor in cellular transformation to cancer. DNA damage can be caused by toxins that break DNA strands (such as pro-oxidant chemicals or ionizing radiation).10,23 Such damage can induce mutations in the DNA that trigger cancer.24-27 That is why nutrients that prevent DNA damage, or ones that promote its repair, are so potent in protecting against cancer.

Given the role of oxidative stress in causing such damage, nutrients that reduce DNA damage (i.e. vitamins C and E and the trace mineral selenium), are often considered as a first line of defense.28-33

Surprisingly, probiotics, which are normally associated with improved gastrointestinal function, have been found to be effective at reducing DNA damage specifically in the colon. This may help to prevent colon cancer, the third cause of cancer-related deaths in the US.34,35

And, while sunlight exposure can boost vitamin D levels, such exposure also raises DNA skin damage, but vitamin D supplementation can protect against DNA damage throughout the body.36,37

Nearly a dozen nutrients have been found to prevent DNA damage, resulting in a positive impact on cancers of the prostate, colon, breast, skin, liver, and more.

Table 1 above lists just a few of the nutrients known for their DNA-protective effects.

What You Need to Know
Environmental Toxinsand Cancer

Environmental Toxins and Cancer

  • The heavily industrialized nature of our modern world constantly exposes us to toxic, cancer inducing, and cancer promoting influences.
  • Chemical toxins as well as various sources of radiation can initiate cancer through DNA damage and promote tumor development through mechanisms involving liver enzyme systems, suppressed immunity, disruption of your hormones, and hijacking of cells’ normal death-inducing programs.
  • You can’t realistically evade all of the factors that can cause cancer in your life, but you can leverage modern scientific knowledge to your benefit.
  • Many nutrients are available with known cancer-fighting benefits, including those that directly counteract the major processes by which toxic compounds and radiation promote malignancies.
  • Choose one or more nutrients from each category to provide yourself with the best possible natural protection against toxic, cancer-inducing forces in your environment.

Liver Detoxification Systems

The second way environmental toxins cause cancer is through their detrimental impact on liver detoxification systems. Liver detoxification systems play a major role in managing ingested toxins because blood from the digestive tract goes to the liver before being pumped around to the remainder of the body.

The liver has two major detoxification pathways: Phase I and Phase II. Phase I enzymes convert toxic chemicals into compounds that may be more toxic than the parent compound.64 Unfortunately, if the toxic load is too heavy, it can cause overactivity of Phase I enzymes, which can have the reverse effect of converting relatively harmless substances into potential DNA-damaging carcinogens.11,12,65

Making matters worse, the worst offenders of overactive Phase I enzymes are substances some people encounter on a daily basis, including alcohol, saturated fats, and exhaust fumes, among others.64,66

In Phase II detoxification, the liver adds another substance to the toxic chemical in order to make it more water soluble. This allows your body to excrete the toxin through bile or urine, helping remove the potentially carcinogenic substance from the body.11,12,64,67,68

For these reasons, cancer-preventive nutrients that influence liver metabolism are generally those that regulate toxin-enhancing Phase I reactions, promote toxin-neutralizing Phase II reactions, or, in many cases, do both.69-71 Nutrients that regulate these liver detoxification systems come largely from dietary plants and their extracts.

Several nutrients have this dual action on liver enzymes, including curcumin, folic acid, and garlic, among others. Research suggests this may have a positive impact on preventing some of the most common and deadly cancers.50,51

See Table 2 for a list of nutrients that prevent cancer by regulating the liver’s detoxification enzymes.

TABLE 2: Nutrients That Regulate Liver Detoxification Enzymes
TABLE 2: Nutrients That Regulate Liver Detoxification Enzymes

Nutrient

Impact on Liver Enzymes

Cancers Affected*

Chlorophyllin72,

Inhibit Phase I;

boost Phase II

Liver, colon, prostate

Curcumin73-78

Inhibit Phase I; boost Phase II

Breast, colon, prostate, pancreas

Folic acid79-81

Inhibit Phase I;

boost Phase II

Breast, pancreas

Garlic82-86

Inhibit Phase I;

boost Phase II

Breast, liver, prostate

Genistein87

Boost Phase II

Colon

Isothiocyanates (sulforaphane, PEITC) from cruciferous vegetables 69,72,88

Inhibit Phase I;

boost Phase II

Liver, colon, breast, prostate

Plant flavonoids (i.e. chrysin, genistein, quercetin) 89,90

Inhibit Phase I;

boost Phase II

Multiple

Silymarin (milk thistle)91

Boost Phase II

Liver

*These are only a few of the types of cancers affected by these nutrients.

Immune Surveillance

The third way environmental toxins can cause cancer is through their impact on immune surveillance. Immune surveillance refers to the immune system’s continual search for cells bearing signs that they have become cancerous.92 A number of environmental toxins can suppress immune surveillance, raising the risk that a malignant cell will slip under the radar, form a tumor, and successfully spread to other parts of the body.13-17,93

Nutrients that enhance immune surveillance are only now being recognized as powerful contributors to the body’s lifelong fight against cancer. These nutrients boost those components of the immune system that are responsible for recognizing the unique tumor “markers” displayed on the surface of malignant cells, and then destroying those cells.

Nutrients that enhance immune surveillance may stimulate growth and proliferation of tumor-detecting lymphocytes, promote a vigorous attack on tumor cells by so-called “natural killer cells,” and/or stimulate antibody production, which aids in immobilization and destruction of malignant cells.

Table 3 lists nutrients capable of activating one or more components of the immune system in order to destroy developing cancers.

TABLE 3: Nutrients That Boost Immune Surveillance

Nutrient

Immune Mechanism

Cancers Affected*

Enzymatically modified rice bran94-97

Increases natural killer cell activity

Leukemia, Multiple Myeloma, Liver

Cistanche extracts98-101

Increases naïve T-cells, increased expression of transforming growth factor beta, decreases inflammation

Colon

Grape seed proanthocyanidins102

Induction of immunoregulatory cytokines; stimulation of tumor-destroying T cells

Skin

Green tea polyphenols (EGCG) 102-107

Activation of tumor-killing T-lymphocytes and natural killer cells; induction of immuno-regulatory cytokines

Colon, skin, lung, prostate, breast

Probiotics (lactic acid bacteria)108-110

Decrease inflammation; increase immunoregulatory cytokines; increased interferon-gamma production

Colon, skin

Reishi mushroom (Ganoderma lucidum)111-114

Enhanced proliferation of tumor-killing T-lymphocytes, antibody-producing B-lymphocytes, and natural killer cells

Liver, lymphoma, lung

Resveratrol115,116

Sensitizes tumor cells to killing by cytokine-induced killer cells; enhances cytokine-induced killer cell activity

Leukemia

Silymarin102

Induction of immunoregulatory cytokines; stimulation of tumor-destroying T cells

Skin

Vitamin D117

Reduced inflammation

Colon

*These are only a few of the types of cancers affected by these nutrients.

Endocrine Disruptors

The fourth way environmental toxins can cause cancer is through their impact on endocrine disruptors. Endocrine disruptors are chemicals that interact with sex hormones and/or their receptors to promote cancer development.17-19,118

Not surprisingly, nutrients that inhibit endocrine disruptors show promise in preventing hormone-dependent cancers such as those of the breast, uterus, and prostate. Although scientists don’t yet fully know how these nutrients work to inhibit endocrine disruptors, it may involve enhanced excretion or reduced absorption of toxins from the intestinal tract.119,120

Table 4 lists nutrients capable of inhibiting endocrine-disrupting pollutants. In addition, there are also a number of plant flavonoids (i.e. chrysin, genistein, quercetin) that are effective against endocrine disrupting toxins.

They appear to reduce the activity of estrogen-producing enzymes such as aromatase, thereby reducing overall sex hormone predominance and starving hormone-dependent tumors of their vital growth factors.89

TABLE 4: Nutrients That Inhibit Endocrine Disruptors

Nutrient

Toxin Inhibited

Cancers Affected*

Chlorella pyrenoidosa 120-124

(More efficiently obtained as chlorophyllin)

Dioxin (a polychlorinated biphenyl [PCB]), perfluorinated compounds (PFCs)

Breast, prostate

Folic acid125-127

Bisphenol A (BPA), phthalates

Breast, prostate

Genistein125,126

BPA, phthalates

Breast, prostate

Probiotics (Lactobacillus, Bifidobacterium) 119,128,129

BPA

Breast, prostate

Vitamin C52

Heavy metals (lead, copper, iron)

Liver, lung, prostate

Vitamin E52

Heavy metals (lead, copper, iron)

Liver, lung, prostate

*These are only a few of the types of cancers affected by these nutrients.

Loss of Apoptosis

Another way environmental toxins are associated with cancer is through inducing a loss of apoptosis, or programmed cell death. Loss of apoptosis refers to the “immortality” typical of cancer cells. Normal body cells are programmed to die off when appropriate.130 Cancer cells have lost this ability (often as a result of DNA damage), which allows them to reproduce essentially without limit.131 A number of chemical toxins, particularly aflatoxin, a potent inducer of liver damage, can switch off the gene responsible for producing apoptosis,132 which results in cancer promotion.20-22

Nutrients that restore cells’ natural ability to die by apoptosis represent the final category in our listing of nutrients that help fight against cancers caused by environmental toxins. These nutrients typically act by modifying various signaling pathways. This means that they can activate genes that become suppressed when cells become cancerous, including genes that normally support the graceful death of a cell that is no longer useful or poses a threat.133

By restoring the natural self-destruction program initiated by apoptosis genes, these nutrients put a sharp roadblock in the way of a developing tumor. This allows other anticancer mechanisms such as immune surveillance to clear the remainder of the battlefield.133

Nutrients known to promote apoptosis include coffee extract, quercetin, pine bark extract, and selenium. Research shows they have a positive impact on bladder, colon, and ovarian cancers, among others.

See Table 5 for a more detailed list of nutrients that promote or restore apoptosis capabilities in malignant cells.

Table 5: Nutrients That Promote Apoptosis

Nutrient

Cancers Affected*

Chlorophyllin134,135

Bladder

Coffee extract136

Colon

Curcumin25,137,138

Leukemia, colon

Emblica officinalis (amla; Indian gooseberry)139

Ovary

Green tea extract (EGCG)140-144

Leukemia, lymphoma, head-and-neck

Lycopene38

Prostate

Phenyl isothiocyanate (PEITC) from cruciferous vegetables67

Bladder, lung

Pine bark extract (Enzogenol)145,146

Leukemia

Prebiotics (fermentable fiber, which produces butyrate, induces apoptosis)136

Colon

Probiotics (Lactobacillus salivarius)147

Oral

Propolis136,148

Colon

Quercetin139

Ovary

Red clover isoflavones149

Prostate

Rosemary (carnosol)150, 151

Prostate, colon, skin, breast, kidney, liver

Sarsaparilla (Smilax glabra)152

Multiple

Selenium153

Colon, lung, prostate

Soy isoflavones (genistein, daidzein)38,154

Prostate

*These are only a few of the types of cancers affected by these nutrients.

Sources of Cancer-Inducing and Cancer-Promoting Toxins

While it is impossible to avoid all cancer-causing environmental toxins, it is important to be aware of some of the most prominent sources. We have compiled a list of common toxins broken down by their environmental sources. As you’ll see from this list, these can be found in sources we interact with on a daily basis, including our food, water, plastic, cell phones, and even sunlight.

  • Aflatoxins are toxic chemicals produced by Aspergillus fungi growing on grains and peanuts, particularly those stored improperly. Chronic exposure induces cancer by multiple mechanisms.155,156
  • Polycyclic aromatic hydrocarbons are chemical structures composed of carbon, hydrogen, and occasionally other atoms. They are products of fossil fuel combustion, particularly petrochemicals, and are a major source of cancer-causing chemicals in polluted air.157,158
  • Bisphenol A (BPA) is one of the highest-volume toxic chemicals found worldwide.159 It is used in making all kinds of plastics and resins, including water bottles and food containers.
  • Heavy metals (including cadmium, arsenic, nickel, lead, and mercury) are naturally occurring components of the earth’s crust.160 Human exposure results from mining,161 smelting,162 and petroleum manufacturing,163 all of which release heavy metals into the air, water, and soil.
  • Pesticides and herbicides,164 especially those containing organic chemicals bonded to chlorine or bromine, are found in agricultural settings, where they make their way into the food chain. Sadly, even after the highly toxic dichlorodiphenyltrichloroethane (DDT) was banned, risks still abound, both because of persistent DDT in the environment and because newer compounds intended to replace DDT (such as methoxychlor) are turning out to have their own cancer-inducing properties.18
  • Dioxins and dioxin-like chemicals such as polychlorinated biphenyls (PCBs) are commonly found in foods of animal origin (meat, dairy, and fish,165,166 depending on the country of origin).167
  • Heterocyclic amines are chemicals that form when meat is cooked at high temperatures (e.g., grilled or broiled).72
  • Ultraviolet radiation is a natural component of sunlight, but serves as a powerful source of many of the changes that lead to cancer.168
  • Electromagnetic field radiation, especially the kind produced by cellular phones and their transmitting stations,169 are only now emerging as potential environmental threats. Such radiation is associated with DNA damage,170-172 potentially leading to cancer.173,174

This is by no means an exhaustive listing of cancer-related environmental toxins. Toxins are ubiquitous, particularly in our highly industrialized society. They are, therefore, nearly impossible to avoid, but as we have read, we know that we are not helpless. We can arm ourselves with knowledge about natural products capable of offsetting much of the increased cancer risk posed by environmental toxins.

Toxins That Induce or Promote Cancer*

Basic Mechanism

Toxins

Increased DNA damage

  • Aflatoxin A1175
  • Air pollutants (polycyclic aromatic hydrocarbons, tobacco smoke)157, 158,176-181
  • Arsenic182
  • Bisphenol A (BPA)183
  • Cadmium chloride175
  • Microwave radiation184
  • Mobile phone radiation169,185
  • Nickel salts186
  • Paraquat (an herbicide)175
  • Pesticides187-189
  • Ultraviolet light36,102

Activation by liver enzymes

  • Aflatoxin B1190,191
  • Dioxin192
  • Heterocyclic amines (from cooking meat)190,193
  • Nicotine194
  • Paraquat194
  • Polycyclic aromatic hydrocarbons (e.g., benzo[a]pyrene)192,194

Suppress immune surveillance

  • Dioxin16
  • Mercury195
  • Mycotoxins (e.g., aflatoxins, fumonisins, and deoxynivalenol)155,196
  • Perfluorinated hydrocarbons195
  • Tobacco smoke197
  • Ultraviolet light108

Endocrine disruption

  • BPA198-200
  • Cyprodinil (a fungicide related to polycyclic aromatic hydrocarbons)201
  • DDT202
  • Dioxin17, 203
  • Heavy metals (arsenic, cadmium, lead, mercury)198
  • Methoxychlor18
  • Phthalates198,204,205
  • Polychlorinated/polybrominated organic compounds (e.g., PCBs)167,204,206
  • Polycyclic aromatic hydrocarbons 198,204
  • Triclosan18

Loss of apoptosis

  • Aflatoxins207-209
  • Heavy metals 210-213
  • Pesticides/herbicides214
  • UV light215,216

*These are only a few of the types of cancers affected by these nutrients.

Summary

We are awash in a sea of toxins and invisible radiation that constantly promotes malignant transformation of our cells, leading to persistently high rates of cancer.

Despite the seemingly immeasurable amount of environmental toxins, there are five mechanisms through which they typically work to promote cancer. This allows us to identify nutrients that have cancer-fighting properties that work specifically against these mechanisms.

Just as the chemicals that cause cancer do so by multiple mechanisms, natural products offer multiple, overlapping, and complementary approaches to cancer prevention.

By becoming familiar with the major cancer-inducing and cancer-promoting toxic influences in your world, you can then develop a supplement regimen that covers all five mechanisms by which we know that toxins and radiation induce cancerous changes.

By choosing carefully from among the nutrients listed in this article, you can establish a solid cancer-fighting base in your own body—one that works with your natural defenses to defeat cancers before they get established.

If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.

References

  1. Abnet CC. Carcinogenic food contaminants. Cancer Invest. 2007 Apr-May;25(3):189-96.
  2. Wogan GN, Hecht SS, Felton JS, Conney AH, Loeb LA. Environmental and chemical carcinogenesis. Semin Cancer Biol. 2004 Dec;14(6):473-86.
  3. Hardell L, Sage C. Biological effects from electromagnetic field exposure and public exposure standards. Biomed Pharmacother. 2008 Feb;62(2):104-9.
  4. Morgan LL, Miller AB, Sasco A, Davis DL. Mobile phone radiation causes brain tumors and should be classified as a probable human carcinogen (2A) (Review). Int J Oncol. 2015 May;46(5):1865-71.
  5. Sugimura T. Nutrition and dietary carcinogens. Carcinogenesis. 2000 Mar;21(3):387-95.
  6. National Institutes of Health (US) Biological Sciences Curriculum Study. NIH Curriculum Supplement Series. Bethesda (MD): National Institutes of Health (US); 2007.
  7. Spano D, Heck C, De Antonellis P, Christofori G, Zollo M. Molecular networks that regulate cancer metastasis. Semin Cancer Biol. 2012 Jun;22(3):234-49.
  8. Mihai CT, Rotinberg P, Brinza F, Vochita G. Extremely low-frequency electromagnetic fields cause DNA strand breaks in normal cells. Journal of Environmental Health Science and Engineering. 2014;12:15.
  9. Yakymenko I, Sidorik E. Risks of carcinogenesis from electromagnetic radiation of mobile telephony devices. Exp Oncol. 2010 Jul;32(2):54-60.
  10. Ames BN, Shigenaga MK, Hagen TM. Oxidants, antioxidants, and the degenerative diseases of aging. Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):7915-22.
  11. Hawas UW, Gamal-Eldeen AM, El-Toumy SA, Meyer JJ, Hussein AA. Inhibition of the initiation stage of carcinogenesis by Salvia disermas constituents. Z Naturforsch C. 2009 Nov-Dec;64(11-12):831-9.
  12. Srivastava DS, Mandhani A, Mittal RD. Genetic polymorphisms of cytochrome P450 CYP1A1 (*2A) and microsomal epoxide hydrolase gene, interactions with tobacco-users, and susceptibility to bladder cancer: a study from North India. Arch Toxicol. 2008 Sep;82(9):633-9.
  13. Liu S, Li S, Du Y. Polychlorinated biphenyls (PCBs) enhance metastatic properties of breast cancer cells by activating Rho-associated kinase (ROCK). PLoS One. 2010;5(6):e11272.
  14. Larsen JC. Risk assessments of polychlorinated dibenzo- p-dioxins, polychlorinated dibenzofurans, and dioxin-like polychlorinated biphenyls in food. Mol Nutr Food Res. 2006 Oct;50(10):885-96.
  15. Hosnijeh FS, Heederik D, Vermeulen R. A review of the role of lymphoma markers and occupational and environmental exposures. Vet Q. 2012 Jun;32(2):61-73.
  16. Platten M, Wick W, Van den Eynde BJ. Tryptophan catabolism in cancer: beyond IDO and tryptophan depletion. Cancer Res. 2012 Nov 1;72(21):5435-40.
  17. Chu XT, de la Cruz J, Hwang SG, Hong H. Tumorigenic effects of endocrine-disrupting chemicals are alleviated by licorice (Glycyrrhiza glabra) root extract through suppression of AhR expression in mammalian cells. Asian Pac J Cancer Prev. 2014;15(12):4809-13.
  18. Kim JY, Yi BR, Go RE, Hwang KA, Nam KH, Choi KC. Methoxychlor and triclosan stimulates ovarian cancer growth by regulating cell cycle- and apoptosis-related genes via an estrogen receptor-dependent pathway. Environ Toxicol Pharmacol. 2014 May;37(3):1264-74.
  19. Wong RL, Walker CL. Molecular pathways: environmental estrogens activate nongenomic signaling to developmentally reprogram the epigenome. Clin Cancer Res. 2013 Jul 15;19(14):3732-7.
  20. Ghebranious N, Sell S. The mouse equivalent of the human p53ser249 mutation p53ser246 enhances aflatoxin hepatocarcinogenesis in hepatitis B surface antigen transgenic and p53 heterozygous null mice. Hepatology. 1998 Apr;27(4):967-73.
  21. Lee CC, Liu JY, Lin JK, Chu JS, Shew JY. p53 point mutation enhanced by hepatic regeneration in aflatoxin B1-induced rat liver tumors and preneoplastic lesions. Cancer Lett. 1998 Mar 13; 125(1-2):1-7.
  22. Farazi PA, Glickman J, Horner J, Depinho RA. Cooperative interactions of p53 mutation, telomere dysfunction, and chronic liver damage in hepatocellular carcinoma progression. Cancer Res. 2006 May 1;66(9):4766-73.
  23. Helbock HJ, Beckman KB, Shigenaga MK, et al. DNA oxidation matters: the HPLC-electrochemical detection assay of 8-oxo-deoxyguanosine and 8-oxo-guanine. Proc Natl Acad Sci U S A. 1998 Jan 6;95(1):288-93.
  24. Chen JH, Zhang P, Chen WD, et al. ATM-mediated PTEN phosphorylation promotes PTEN nuclear translocation and autophagy in response to DNA-damaging agents in cancer cells. Autophagy. 2015 Feb 20:0.
  25. Rana C, Piplani H, Vaish V, Nehru B, Sanyal SN. Downregulation of telomerase activity by diclofenac and curcumin is associated with cell cycle arrest and induction of apoptosis in colon cancer. Tumour Biol. 2015 Mar 6.
  26. Tran UM, Rajarajacholan U, Soh J, et al. LincRNA-p21 acts as a mediator of ING1b-induced apoptosis. Cell Death Dis. 2015;6:e1668.
  27. Chen Y, Williams V, Filippova M, Filippov V, Duerksen-Hughes P. Viral carcinogenesis: factors inducing DNA damage and virus integration. Cancers (Basel). 2014;6(4):2155-86.
  28. Weisel T, Baum M, Eisenbrand G, et al. An anthocyanin/polyphenolic-rich fruit juice reduces oxidative DNA damage and increases glutathione level in healthy probands. Biotechnol J. 2006 Apr;1(4):388-97.
  29. Al-Taie OH, Seufert J, Karvar S, et al. Selenium supplementation enhances low selenium levels and stimulates glutathione peroxidase activity in peripheral blood and distal colon mucosa in past and present carriers of colon adenomas. Nutr Cancer. 2003;46(2):125-30.
  30. Dziaman T, Huzarski T, Gackowski D, et al. Selenium supplementation reduced oxidative DNA damage in adnexectomized BRCA1 mutations carriers. Cancer Epidemiol Biomarkers Prev. 2009 Nov;18(11):2923-8.
  31. Hu JJ, Chi CX, Frenkel K, et al. Alpha-tocopherol dietary supplement decreases titers of antibody against 5-hydroxymethyl-2’-deoxyuridine (HMdU). Cancer Epidemiol Biomarkers Prev. 1999 Aug;8(8):693-8.
  32. Konopacka M. Role of vitamin C in oxidative DNA damage. Postepy Hig Med Dosw (Online). 2004;58:343-8.
  33. Lutsenko EA, Cárcamo JM, Golde DW. Vitamin C prevents DNA mutation induced by oxidative stress. J Biol Chem. 2002 May 10;277(19):16895-9.
  34. Dominici L, Villarini M, Trotta F, Federici E, et al. Protective effects of probiotic Lactobacillus rhamnosus IMC501 in mice treated with PhIP. J Microbiol Biotechnol. 2014 Mar 28;24(3):371-8.
  35. Li H, Liu K, Boardman LA, et al. Circulating Prostaglandin Biosynthesis in Colorectal Cancer and Potential Clinical Significance. EBioMedicine. 2015 Feb 1;2(2):165-71.
  36. Petersen B, Wulf HC, Triguero-Mas M, et al. Sun and ski holidays improve vitamin D status, but are associated with high levels of DNA damage. J Invest Dermatol. 2014 Nov;134(11):2806-13.
  37. Nair-Shalliker V, Armstrong BK, Fenech M. Does vitamin D protect against DNA damage? Mutat Res. 2012 May 1;733(1-2):50-7.
  38. Vaishampayan U, Hussain M, Banerjee M, et al. Lycopene and soy isoflavones in the treatment of prostate cancer. Nutr Cancer. 2007;59(1):1-7.
  39. Zhao X, Aldini G, Johnson EJ, et al. Modification of lymphocyte DNA damage by carotenoid supplementation in postmenopausal women. Am J Clin Nutr. 2006 Jan;83(1):163-9.
  40. Nagendraprabhu P, Sudhandiran G. Astaxanthin inhibits tumor invasion by decreasing extracellular matrix production and induces apoptosis in experimental rat colon carcinogenesis by modulating the expressions of ERK-2, NFkB and COX-2. Invest New Drugs. 2011 Apr;29(2):207-24.
  41. Park JS, Chyun JH, Kim YK, Line LL, Chew BP. Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans. Nutr Metab (Lond). 2010;7:18.
  42. Gao S, Qin T, Liu Z, Caceres MA, Ronchi CF, Chen CY, Yeum KJ, Taylor A, Blumberg JB, Liu Y, Shang F. Lutein and zeaxanthin supplementation reduces H2O2-induced oxidative damage in human lens epithelial cells. Mol Vis. 2011;17:3180-90.
  43. Serpeloni JM, Barcelos GR, Friedmann Angeli JP, Mercadante AZ, Lourdes Pires Bianchi M, Antunes LM. Dietary carotenoid lutein protects against DNA damage and alterations of the redox status induced by cisplatin in human derived HepG2 cells. Toxicol In Vitro. 2012 Mar;26(2):288-94.
  44. Kim JM, Park E. Coenzyme Q10 attenuated DMH-induced precancerous lesions in SD rats. J Nutr Sci Vitaminol (Tokyo). 2010;56(2):139-44.
  45. Reiter M, Rupp K, Baumeister P, Zieger S, Harreus U. Antioxidant effects of quercetin and coenzyme Q10 in mini organ cultures of human nasal mucosa cells. Anticancer Res. 2009 Jan;29(1):33-9.
  46. Sakano K, Takahashi M, Kitano M, Sugimura T, Wakabayashi K. Suppression of azoxymethane-induced colonic premalignant lesion formation by coenzyme Q10 in rats. Asian Pac J Cancer Prev. 2006 Oct-Dec;7(4):599-603.
  47. Kansal S, Bhatnagar A, Agnihotri N. Fish oil suppresses cell growth and metastatic potential by regulating PTEN and NF-kappaB signaling in colorectal cancer. PLoS One. 2014;9(1):e84627.
  48. Rhodes LE, Shahbakhti H, Azurdia RM, et al. Effect of eicosapentaenoic acid, an omega-3 polyunsaturated fatty acid, on UVR-related cancer risk in humans. An assessment of early genotoxic markers. Carcinogenesis. 2003 May;24(5):919-25.
  49. Souza LR, Silva E, Calloway E, Kucuk O, Rossi M, McLemore ML. Genistein protects hematopoietic stem cells against G-CSF-induced DNA damage. Cancer Prev Res (Phila). 2014 May;7(5):534-44.
  50. Scalbert A, Johnson IT, Saltmarsh M. Polyphenols: antioxidants and beyond. Am J Clin Nutr. 2005 Jan;81(1 Suppl):215S-217S.
  51. Stoner GD, Mukhtar H. Polyphenols as cancer chemopreventive agents. J Cell Biochem Suppl. 1995;22:169-80.
  52. Wilhelm Filho D, Avila S, Jr., Possamai FP, et al. Antioxidant therapy attenuates oxidative stress in the blood of subjects exposed to occupational airborne contamination from coal mining extraction and incineration of hospital residues. Ecotoxicology. 2010 Oct;19(7):1193-200.
  53. Hu F, Wu Z, Li G, et al. The plasma level of retinol, vitamins A, C and alpha-tocopherol could reduce breast cancer risk? A meta-analysis and meta-regression. J Cancer Res Clin Oncol. 2015 Apr;141(4):601-14.
  54. Liu Y, Yu Q, Zhu Z, et al. Vitamin and multiple-vitamin supplement intake and incidence of colorectal cancer: a meta-analysis of cohort studies. Med Oncol. 2015 Jan;32(1):434.
  55. Venturelli S, Sinnberg TW, Berger A, et al. Epigenetic impacts of ascorbate on human metastatic melanoma cells. Front Oncol. 2014;4:227.
  56. Kim JE, Kang JS, Lee WJ. Vitamin C Induces Apoptosis in Human Colon Cancer Cell Line, HCT-8 Via the Modulation of Calcium Influx in Endoplasmic Reticulum and the Dissociation of Bad from 14-3-3β. Immune Netw. 2012 Oct;12(5):189-95.
  57. Fedirko V, Bostick RM, Long Q, et al. Effects of supplemental vitamin D and calcium on oxidative DNA damage marker in normal colorectal mucosa: a randomized clinical trial. Cancer Epidemiol Biomarkers Prev. 2010 Jan;19(1):280-91.
  58. Pappachan JM, Antonio FA, Edavalath M, Mukherjee A. Non-alcoholic fatty liver disease: a diabetologist’s perspective. Endocrine. 2014 Apr;45(3):344-53.
  59. Pearlman M, Loomba R. State of the art: treatment of nonalcoholic steatohepatitis. Curr Opin Gastroenterol. 2014 May;30(3):223-37.
  60. Singh S, Singh PP, Roberts LR, Sanchez W. Chemopreventive strategies in hepatocellular carcinoma. Nat Rev Gastroenterol Hepatol. 2014 Jan;11(1):45-54.
  61. Sylvester PW, Akl MR, Malaviya A, et al. Potential role of tocotrienols in the treatment and prevention of breast cancer. Biofactors. 2014 Jan-Feb;40(1):49-58.
  62. Hartmann A, Niess AM, Grünert-Fuchs M, Poch B, Speit G. Vitamin E prevents exercise-induced DNA damage. Mutat Res. 1995 Apr;346(4):195-202.
  63. Kline K, Yu W, Sanders BG. Vitamin E and breast cancer. J Nutr. 2004 Dec;134(12 Suppl):3458S-62S.
  64. Liska DJ. The detoxification enzyme systems. Altern Med Rev. 1998 Jun;3(3):187-98. Review.
  65. Talalay P, Prochaska HJ, Spencer SR. Regulation of enzymes that detoxify the electrophilic forms of chemical carcinogens. Princess Takamatsu Symp. 1990;21:177-87.
  66. Sweeney BP, Bromilow J. Liver enzyme induction and inhibition: implications for anaesthesia. Anaesthesia. 2006 Feb;61(2):159-77.
  67. Pullar JM, Thomson SJ, King MJ, Turnbull CI, Midwinter RG, Hampton MB. The chemopreventive agent phenethyl isothiocyanate sensitizes cells to fas-mediated apoptosis. Carcinogenesis. 2004 May;25(5):765-72.
  68. Wen X, Donepudi AC, Thomas PE, Slitt AL, King RS, Aleksunes LM. Regulation of hepatic Phase II metabolism in pregnant mice. J Pharmacol Exper Ther . 2013;344(1):244-52.
  69. De Figueiredo SM, Filho SA, Nogueira-Machado JA, Caligiorne RB. The anti-oxidant properties of isothiocyanates: a review. Recent Pat Endocr Metab Immune Drug Discov. 2013 Sep;7(3):213-25.
  70. Tortorella SM, Royce SG, Licciardi PV, Karagiannis TC. Dietary sulforaphane in cancer chemoprevention: the role of epigenetic regulation and HDAC inhibition. Antioxid Redox Signal. 2014 Nov 3.
  71. Rose P, Faulkner K, Williamson G, Mithen R. 7-Methylsulfinylheptyl and 8-methylsulfinyloctyl isothiocyanates from watercress are potent inducers of phase II enzymes. Carcinogenesis. 2000 Nov;21(11):1983-8.
  72. Dingley KH, Ubick EA, Chiarappa-Zucca ML, et al. Effect of dietary constituents with chemopreventive potential on adduct formation of a low dose of the heterocyclic amines PhIP and IQ and phase II hepatic enzymes. Nutr Cancer. 2003;46(2):212-21.
  73. Iqbal M, Sharma SD, Okazaki Y, Fujisawa M, Okada S. Dietary supplementation of curcumin enhances antioxidant and phase II metabolizing enzymes in ddY male mice: possible role in protection against chemical carcinogenesis and toxicity. Pharmacol Toxicol. 2003 Jan;92(1):33-8.
  74. Carroll CE, Benakanakere I, Besch-Williford C, Ellersieck MR, Hyder SM. Curcumin delays development of medroxyprogesterone acetate-accelerated 7,12-dimethylbenz[a]anthracene-induced mammary tumors. Menopause. 2010 Jan-Feb;17(1):178-84.
  75. Hull MA. Nutritional agents with anti-inflammatory properties in chemoprevention of colorectal neoplasia. Recent Results Cancer Res. 2013;191:143-56.
  76. Li Y, Ahmad A, Kong D, Bao B, Sarkar FH. Recent progress on nutraceutical research in prostate cancer. Cancer Metastasis Rev. 2014 Sep;33(2-3):629-40.
  77. Pericleous M, Rossi RE, Mandair D, Whyand T, Caplin ME. Nutrition and pancreatic cancer. Anticancer Res. 2014 Jan;34(1):9-21.
  78. Garg R, Gupta S, Maru GB. Dietary curcumin modulates transcriptional regulators of phase I and phase II enzymes in benzo[a]pyrene-treated mice: mechanism of its anti-initiating action. Carcinogenesis. 2008 May;29(5):1022-32.
  79. Canistro D, Pozzetti L, Sapone A, et al. Perturbation of rat hepatic metabolising enzymes by folic acid supplementation. Mutat Res. 2008 Jan 1;637(1-2):16-22.
  80. Chen P, Li C, Li X, Li J, Chu R, Wang H. Higher dietary folate intake reduces the breast cancer risk: a systematic review and meta-analysis. Br J Cancer. 2014 Apr 29;110(9):2327-38.
  81. Lin HL, An QZ, Wang QZ, Liu CX. Folate intake and pancreatic cancer risk: an overall and dose-response meta-analysis. Public Health. 2013 Jul;127(7):607-13.
  82. Butt MS, Sultan MT, Butt MS, Iqbal J. Garlic: nature’s protection against physiological threats. Crit Rev Food Sci Nutr. 2009 Jun;49(6):538-51.
  83. De Martino A, Filomeni G, Aquilano K, Ciriolo MR, Rotilio G. Effects of water garlic extracts on cell cycle and viability of HepG2 hepatoma cells. J Nutr Biochem. 2006 Nov;17(11):742-9.
  84. Liu Z, Li M, Chen K, et al. S-allylcysteine induces cell cycle arrest and apoptosis in androgen-independent human prostate cancer cells. Mol Med Rep. 2012 Feb;5(2):439-43.
  85. Modem S, Dicarlo SE, Reddy TR. Fresh Garlic Extract Induces Growth Arrest and Morphological Differentiation of MCF7 Breast Cancer Cells. Genes Cancer. 2012 Feb;3(2):177-86.
  86. Zhang CL, Zeng T, Zhao XL, Xie KQ. Garlic oil attenuated nitrosodiethylamine-induced hepatocarcinogenesis by modulating the metabolic activation and detoxification enzymes. Int J Biol Sci. 2013;9(3):237-45
  87. Chen Y, Huang C, Zhou T, Chen G. Genistein induction of human sulfotransferases in HepG2 and Caco-2 cells. Basic Clin Pharmacol Toxicol. 2008 Dec;103(6):553-9.
  88. Morris ME, Dave RA. Pharmacokinetics and pharmacodynamics of phenethyl isothiocyanate: implications in breast cancer prevention. Aaps J. 2014 Jul;16(4):705-13.
  89. Moon YJ, Wang X, Morris ME. Dietary flavonoids: effects on xenobiotic and carcinogen metabolism. Toxicol In Vitro. 2006 Mar;20(2):187-210.
  90. Nishiumi S, Miyamoto S, Kawabata K, et al. Dietary flavonoids as cancer-preventive and therapeutic biofactors. Front Biosci (Schol Ed). 2011;3:1332-62.
  91. Gopalakrishnan R, Sundaram J, Sattu K, Pandi A, Thiruvengadam D. Dietary supplementation of silymarin is associated with decreased cell proliferation, increased apoptosis, and activation of detoxification system in hepatocellular carcinoma. Mol Cell Biochem. 2013 May;377(1-2):163-76.
  92. Hamaï A, Benlalam H, Meslin F, Hasmim M, Carré T, Akalay I, Janji B, Berchem G, Noman MZ, Chouaib S. Immune surveillance of human cancer: if the cytotoxic T-lymphocytes play the music, does the tumoral system call the tune? Tissue Antigens. 2010 Jan;75(1):1-8.
  93. Bryden WL. Mycotoxins in the food chain: human health implications. Asia Pac J Clin Nutr. 2007;16 Suppl 1:95-101.
  94. Cholujova D, Jakubikova J, Czako B, et al. MGN-3 arabinoxylan rice bran modulates innate immunity in multiple myeloma patients. Cancer Immunol Immunother. 2013 Mar;62(3):437-45.
  95. Ali KH, Melillo AB, Leonard SM, et al. An open-label, randomized clinical trial to assess the immunomodulatory activity of a novel oligosaccharide compound in healthy adults. FFHD. 2012;2(7):265-79.
  96. Bang MH, Van Riep T, Thinh NT, et al. Arabinoxylan rice bran (MGN-3) enhances the effects of interventional therapies for the treatment of hepatocellular carcinoma: a three-year randomized clinical trial. Anticancer Res. 2010 Dec;30(12):5145-51.
  97. Revilla E, Santa-Maria C, Miramontes E, et al. Antiproliferative and immunoactivatory ability of an enzymatic extract from rice bran. Food Chem. 2013 Jan 15;136(2):526-31.
  98. Zhang K, Ma X, He W, et al. Extracts of Cistanche deserticola can antagonize immunosenescence and extend life span in senescence-accelerated mouse prone 8 (SAM-P8) mice. Evid Based Complement Alternat Med. 2014;2014:601383.
  99. Zhai Z, Liu Y, Wu L, et al. Enhancement of innate and adaptive immune functions by multiple Echinacea species. J Med Food. 2007 Sep;10(3):423-34.
  100. Jia Y, Guan Q, Guo Y, Du C. Echinacoside stimulates cell proliferation and prevents cell apoptosis in intestinal epithelial MODE-K cells by up-regulation of transforming growth factor-beta1 expression. J Pharmacol Sci. 2012;118(1):99-108.
  101. Jia Y, Guan Q, Guo Y, Du C. Reduction of inflammatory hyperplasia in the intestine in colon cancer prone mice by water-extract of Cistanche deserticola. Phytother Res. 2012 Jun;26(6):812-9.
  102. Katiyar SK. UV-induced immune suppression and photocarcinogenesis: chemoprevention by dietary botanical agents. Cancer Lett. 2007 Sep 18;255(1):1-11.
  103. Mantena SK, Meeran SM, Elmets CA, Katiyar SK. Orally administered green tea polyphenols prevent ultraviolet radiation-induced skin cancer in mice through activation of cytotoxic T cells and inhibition of angiogenesis in tumors. J Nutr. 2005 Dec;135(12):2871-7.
  104. Mantena SK, Roy AM, Katiyar SK. Epigallocatechin-3-gallate inhibits photocarcinogenesis through inhibition of angiogenic factors and activation of CD8+ T cells in tumors. Photochem Photobiol. 2005 Sep-Oct;81(5):1174-9.
  105. Katiyar S, Elmets CA, Katiyar SK. Green tea and skin cancer: photoimmunology, angiogenesis and DNA repair. J Nutr Biochem. 2007 May;18(5):287-96.
  106. Butt MS, Sultan MT. Green tea: nature’s defense against malignancies. Crit Rev Food Sci Nutr. 2009 May;49(5):463-73.
  107. Shimizu K, Kinouchi Shimizu N, Hakamata W, Unno K, Asai T, Oku N. Preventive effect of green tea catechins on experimental tumor metastasis in senescence-accelerated mice. Biol Pharm Bull. 2010;33(1):117-21.
  108. Weill FS, Cela EM, Paz ML, Ferrari A, Leoni J, Gonzalez Maglio DH. Lipoteichoic acid from Lactobacillus rhamnosus GG as an oral photoprotective agent against UV-induced carcinogenesis. Br J Nutr. 2013 Feb 14;109(3):457-66.
  109. De Moreno de Leblanc A, Perdigon G. The application of probiotic fermented milks in cancer and intestinal inflammation. Proc Nutr Soc. 2010 Aug;69(3):421-8.
  110. Zuccotti GV, Meneghin F, Raimondi C, et al. Probiotics in clinical practice: an overview. J Int Med Res. 2008;36 Suppl 1:1a-53a.
  111. Cheuk W, Chan JK, Nuovo G, Chan MK, Fok M. Regression of gastric large B-Cell lymphoma accompanied by a florid lymphoma-like T-cell reaction: immunomodulatory effect of Ganoderma lucidum (Lingzhi)? Int J Surg Pathol. 2007 Apr;15(2):180-6.
  112. Xu Z, Chen X, Zhong Z, Chen L, Wang Y. Ganoderma lucidum polysaccharides: immunomodulation and potential anti-tumor activities. Am J Chin Med. 2011;39(1):15-27.
  113. Sun LX, Li WD, Lin ZB, et al. Protection against lung cancer patient plasma-induced lymphocyte suppression by Ganoderma lucidum polysaccharides. Cell Physiol Biochem. 2014;33(2):289-99.
  114. Liu YJ, Shen J, Xia YM, Zhang J, Park HS. The polysaccharides from Ganoderma lucidum: Are they always inhibitors on human hepatocarcinoma cells? Carbohydr Polym. 2012 Oct 15;90(3):1210-5.
  115. Hu L, Cao D, Li Y, He Y, Guo K. Resveratrol sensitized leukemia stem cell-like KG-1a cells to cytokine-induced killer cells-mediated cytolysis through NKG2D ligands and TRAIL receptors. Cancer Biol Ther. 2012 May;13(7):516-26.
  116. Noh KT, Chae SH, Chun SH, Jung ID, Kang HK, Park YM. Resveratrol suppresses tumor progression via the regulation of indoleamine 2,3-dioxygenase. Biochem Biophys Res Commun. 2013 Feb 8;431(2):348-53.
  117. Hopkins MH, Owen J, Ahearn T, et al. Effects of supplemental vitamin D and calcium on biomarkers of inflammation in colorectal adenoma patients: a randomized, controlled clinical trial. Cancer Prev Res (Phila). 2011 Oct;4(10):1645-54.
  118. Jeng HA. Exposure to endocrine disrupting chemicals and male reproductive health. Front Public Health. 2014 Jun 5;2:55.
  119. Oishi K, Sato T, Yokoi W, Yoshida Y, Ito M, Sawada H. Effect of probiotics, Bifidobacterium breve and Lactobacillus casei, on bisphenol A exposure in rats. Biosci Biotechnol Biochem. 2008 Jun;72(6):1409-15.
  120. Takekoshi H, Suzuki G, Chubachi H, Nakano M. Effect of Chlorella pyrenoidosa on fecal excretion and liver accumulation of polychlorinated dibenzo-p-dioxin in mice. Chemosphere. 2005 Apr;59(2):297-304.
  121. Nakano S, Noguchi T, Takekoshi H, Suzuki G, Nakano M. Maternal-fetal distribution and transfer of dioxins in pregnant women in Japan, and attempts to reduce maternal transfer with Chlorella (Chlorella pyrenoidosa) supplements. Chemosphere. 2005 Dec;61(9):1244-55.
  122. Nakano S, Takekoshi H, Nakano M. Chlorella (Chlorella pyrenoidosa) supplementation decreases dioxin and increases immunoglobulin a concentrations in breast milk. J Med Food. 2007 Mar;10(1):134-42.
  123. Kubatka P, Kapinová A, Kružliak P, et al. Antineoplastic effects of Chlorella pyrenoidosa in the breast cancer model. Nutrition. 2015 Apr;31(4):560-9.
  124. Genuis SJ, Curtis L, Birkholz D. Gastrointestinal elimination of perfluorinated compounds using cholestyramine and chlorella pyrenoidosa. ISRN Toxicol. 2013 Sep 9;2013:657849.
  125. Dolinoy DC, Huang D, Jirtle RL. Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. Proc Natl Acad Sci U S A. 2007 Aug 7;104(32):13056-61.
  126. Singh S, Li SS. Epigenetic effects of environmental chemicals bisphenol a and phthalates. Int J Mol Sci. 2012;13(8):10143-53.
  127. Ormond G, Nieuwenhuijsen MJ, Nelson P, et al. Endocrine disruptors in the workplace, hair spray, folate supplementation, and risk of hypospadias: case–control study. Environ Health Perspect. 2009;117(2):303-7.
  128. Maroof H, Hassan ZM, Mobarez AM, Mohamadabadi MA. Lactobacillus acidophilus could modulate the immune response against breast cancer in murine model. J Clin Immunol. 2012 Dec;32(6):1353-9.
  129. Horinaka M, Yoshida T, Kishi A, et al. Lactobacillus strains induce TRAIL production and facilitate natural killer activity against cancer cells. FEBS Lett. 2010 Feb 5;584(3):577-82.
  130. Elmore S. Apoptosis: a review of programmed cell death. Toxicol Pathol. 2007 Jun;35(4):495-516.
  131. Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000.
  132. Hamid AS, Tesfamariam IG, Zhang Y, Zhang ZG. Aflatoxin B1-induced hepatocellular carcinoma in developing countries: Geographical distribution, mechanism of action and prevention. Oncology Letters. 2013;5(4):1087-92.
  133. Prasad S, Kim JH, Gupta SC, Aggarwal BB. Targeting death receptors for TRAIL by agents designed by Mother Nature. Trends Pharmacol Sci. 2014 Oct;35(10):520-36.
  134. Du L, Jiang N, Wang G, et al. Autophagy inhibition sensitizes bladder cancer cells to the photodynamic effects of the novel photosensitizer chlorophyllin e4. J Photochem Photobiol B. 2014 Apr 5;133:1-10.
  135. Lihuan D, Jingcun Z, Ning J, et al. Photodynamic therapy with the novel photosensitizer chlorophyllin f induces apoptosis and autophagy in human bladder cancer cells. Lasers Surg Med. 2014 Apr;46(4):319-34.
  136. Bordonaro M, Drago E, Atamna W, Lazarova DL. Comprehensive suppression of all apoptosis-induced proliferation pathways as a proposed approach to colorectal cancer prevention and therapy. PLoS One. 2014;9(12):e115068.
  137. Yu J, Peng Y, Wu LC, et al. Curcumin down-regulates DNA methyltransferase 1 and plays an anti-leukemic role in acute myeloid leukemia. PLoS One. 2013;8(2):e55934.
  138. Su CC, Lin JG, Li TM, et al. Curcumin-induced apoptosis of human colon cancer colo 205 cells through the production of ROS, Ca2+ and the activation of caspase-3. Anticancer Res. 2006 Nov-Dec;26(6B):4379-89.
  139. De A, De A, Papasian C, et al. Emblica officinalis extract induces autophagy and inhibits human ovarian cancer cell proliferation, angiogenesis, growth of mouse xenograft tumors. PLoS One. 2013;8(8):e72748.
  140. O’Callaghan YC, Drummond E, O’Gorman DM, O’Brien NM. Antioxidant and pro-apoptotic effects of marine-derived, multi-mineral aquamin supplemented with a pine bark extract, Enzogenol, and a green tea extract, Sunphenon. J Med Food. 2013 Oct;16(10):920-6.
  141. Fang CY, Wu CC, Hsu HY, et al. EGCG inhibits proliferation, invasiveness and tumor growth by up-regulation of adhesion molecules, suppression of gelatinases activity, and induction of apoptosis in nasopharyngeal carcinoma cells. Int J Mol Sci. 2015;16(2):2530-58.
  142. Irimie AI, Braicu C, Zanoaga O, et al. Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis and autophagy in oral cancer SSC-4 cells. Onco Targets Ther. 2015;8:461-70.
  143. Harakeh S, Diab-Assaf M, Azar R, et al. Epigallocatechin-3-gallate inhibits tax-dependent activation of nuclear factor kappa B and of matrix metalloproteinase 9 in human T-cell lymphotropic virus-1 positive leukemia cells. Asian Pac J Cancer Prev. 2014;15(3):1219-25.
  144. Yu AF, Shen JZ, Chen ZZ, Fan LP, Lin FA. Demethylation and transcription of p16 gene in malignant lymphoma cell line CA46 induced by EGCG. Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2008 Oct;16(5):1073-8.
  145. Iravani S, Zolfaghari B. Pharmaceutical and nutraceutical effects of Pinus pinaster bark extract. Res Pharm Sci. 2011;6(1):1-11.
  146. O’Callaghan YC, Drummond E, O’Gorman DM, O’Brien NM. Antioxidant and pro-apoptotic effects of marine-derived, multi-mineral aquamin supplemented with a pine bark extract, enzogenol, and a green tea extract, sunphenon. J Med Food. 2013 Oct;16(10):920-6.
  147. Zhang M, Wang F, Jiang L, et al. Lactobacillus salivarius REN inhibits rat oral cancer induced by 4-nitroquioline 1-oxide. Cancer Prev Res (Phila). 2013 Jul;6(7):686-94.
  148. Drago E, Bordonaro M, Lee S, Atamna W, Lazarova DL. Propolis augments apoptosis induced by butyrate via targeting cell survival pathways. PLoS One. 2013;8(9):e73151.
  149. Jarred RA, Keikha M, Dowling C, et al. Induction of apoptosis in low to moderate-grade human prostate carcinoma by red clover-derived dietary isoflavones. Cancer Epidemiol Biomarkers Prev. 2002 Dec;11(12):1689-96.
  150. Chun KS, Kundu J, Chae IG, Kundu JK. Carnosol: a phenolic diterpene with cancer chemopreventive potential. J Cancer Prev. 2014 Jun;19(2):103-10.
  151. Min KJ, Jung KJ, Kwon TK. Carnosic acid induces apoptosis through reactive oxygen species-mediated endoplasmic reticulum stress induction in human renal carcinoma caki cells. J Cancer Prev. 2014 Sep;19(3):170-8.
  152. She T, Qu L, Wang L, et al. Sarsaparilla (Smilax Glabra Rhizome) extract inhibits cancer cell growth by S phase arrest, apoptosis and autophagy via redox-dependent ERK1/2 pathway. Cancer Prev Res (Phila). 2015 Mar 2.
  153. Sun LH, Li JG, Zhao H, et al. Porcine serum can be biofortified with selenium to inhibit proliferation of three types of human cancer cells. J Nutr. 2013 Jul;143(7):1115-22.
  154. Dong X, Xu W, Sikes RA, Wu C. Combination of low dose of genistein and daidzein has synergistic preventive effects on isogenic human prostate cancer cells when compared with individual soy isoflavone. Food Chem. 2013 Dec 1;141(3):1923-33.
  155. Wild CP, Gong YY. Mycotoxins and human disease: a largely ignored global health issue. Carcinogenesis. 2010 Jan;31(1):71-82.
  156. Magnussen A, Parsi MA. Aflatoxins, hepatocellular carcinoma and public health. World J Gastro. 2013;19(10):1508-12.
  157. Belpomme D, Irigaray P, Hardell L, et al. The multitude and diversity of environmental carcinogens. Environ Res. 2007 Nov;105(3):414-29.
  158. Hung LJ, Chan TF, Wu CH, Chiu HF, Yang CY. Traffic air pollution and risk of death from ovarian cancer in Taiwan: fine particulate matter (PM2.5) as a proxy marker. J Toxicol Environ Health A. 2012;75(3):174-82.
  159. Rezg R, El-Fazaa S, Gharbi N, Mornagui B. Bisphenol A and human chronic diseases: current evidences, possible mechanisms, and future perspectives. Environ Int. 2014 Mar;64:83-90.
  160. Singh R, Gautam N, Mishra A, Gupta R. Heavy metals and living systems: An overview. Indian J Pharmacol. 2011 May;43(3):246-53.
  161. Murgueytio AM, Evans RG, Roberts D. Relationship between soil and dust lead in a lead mining area and blood lead levels. J Expo Anal Environ Epidemiol. 1998 Apr-Jun;8(2):173-86.
  162. Selevan SG, Landrigan PJ, Stern FB, Jones JH. Mortality of lead smelter workers. Am J Epidemiol. 1985 Oct;122(4):673-83.
  163. Edwards VC, Coppock RW, Zinn LL. Toxicoses related to the petroleum industry. Vet Hum Toxicol. 1979 Oct;21(5):328-37.
  164. Aktar MW, Sengupta D, Chowdhury A. Impact of pesticides use in agriculture: their benefits and hazards. Interdiscip Toxicol. 2009 Mar;2(1):1-12.
  165. Schecter A, Startin J, Wright C, et al. Dioxins in U.S. food and estimated daily intake. Chemosphere. 1994 Nov-Dec;29(9-11):2261-5.
  166. Rauscher-Gabernig E, Mischek D, Moche W, Prean M. Dietary intake of dioxins, furans and dioxin-like PCBs in Austria. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2013;30(10):1770-9.
  167. Paoli D, Giannandrea F, Gallo M, et al. Exposure to polychlorinated biphenyls and hexachlorobenzene, semen quality and testicular cancer risk. J Endocrinol Invest. 2015 Mar 15.
  168. Ananthaswamy HN, Pierceall WE. Molecular mechanisms of ultraviolet radiation carcinogenesis. Photochem Photobiol. 1990 Dec;52(6):1119-36.
  169. Gandhi G, Kaur G, Nisar U. A cross-sectional case control study on genetic damage in individuals residing in the vicinity of a mobile phone base station. Electromagn Biol Med. 2014 Jul 9:1-11.
  170. Hou Q, Wang M, Wu S, et al. Oxidative changes and apoptosis induced by 1800-MHz electromagnetic radiation in NIH/3T3 cells. Electromagn Biol Med. 2015 Mar;34(1):85-92.
  171. Liu C, Duan W, Xu S, et al. Exposure to 1800 MHz radiofrequency electromagnetic radiation induces oxidative DNA base damage in a mouse spermatocyte-derived cell line. Toxicol Lett. 2013 Mar 27;218(1):2-9.
  172. Liu C, Gao P, Xu SC, et al. Mobile phone radiation induces mode-dependent DNA damage in a mouse spermatocyte-derived cell line: a protective role of melatonin. Int J Radiat Biol. 2013 Nov;89(11):993-1001.
  173. Volkow ND, Tomasi D, Wang GJ, et al. Effects of cell phone radiofrequency signal exposure on brain glucose metabolism. Jama. 2011 Feb 23;305(8):808-13.
  174. Hardell L, Carlberg M, Hansson Mild K. Pooled analysis of two case-control studies on the use of cellular and cordless telephones and the risk of benign brain tumours diagnosed during 1997-2003. Int J Oncol. 2006 Feb;28(2):509-18.
  175. Gonzalez-Hunt CP, Leung MC, Bodhicharla RK, et al. Exposure to mitochondrial genotoxins and dopaminergic neurodegeneration in Caenorhabditis elegans. PLoS One. 2014;9(12):e114459.
  176. Jarvis IW, Dreij K, Mattsson A, Jernstrom B, Stenius U. Interactions between polycyclic aromatic hydrocarbons in complex mixtures and implications for cancer risk assessment. Toxicology. 2014 Jul 3;321:27-39.
  177. Deziel NC, Rull RP, Colt JS, et al. Polycyclic aromatic hydrocarbons in residential dust and risk of childhood acute lymphoblastic leukemia. Environ Res. 2014 Aug;133:388-95.
  178. Hew KM, Walker AI, Kohli A, et al. Childhood exposure to ambient polycyclic aromatic hydrocarbons is linked to epigenetic modifications and impaired systemic immunity in T cells. Clin Exp Allergy. 2015 Jan;45(1):238-48.
  179. Rota M, Bosetti C, Boccia S, Boffetta P, La Vecchia C. Occupational exposures to polycyclic aromatic hydrocarbons and respiratory and urinary tract cancers: an updated systematic review and a meta-analysis to 2014. Arch Toxicol. 2014 Aug;88(8):1479-90.
  180. Safe SH. Environmental and dietary estrogens and human health: is there a problem? Environ Health Perspect. 1995 Apr;103(4): 346-51.
  181. Schaal C, Chellappan SP. Nicotine-mediated cell proliferation and tumor progression in smoking-related cancers. Mol Cancer Res. 2014 Jan;12(1):14-23.
  182. Graham B, Stevens J, Wells P, et al. Enhancement of arsenic trioxide-mediated changes in human induced pluripotent stem cells (IPS). Int J Environ Res Public Health. 2014 Jul;11(7):7524-36.
  183. Xin F, Jiang L, Liu X, et al. Bisphenol A induces oxidative stress-associated DNA damage in INS-1 cells. Mutat Res Genet Toxicol Environ Mutagen. 2014 Jul 15;769:29-33.
  184. Belyaev IY, Hillert L, Protopopova M, et al. 915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci in human lymphocytes from hypersensitive and healthy persons. Bioelectromagnetics. 2005 Apr;26(3):173-84.
  185. De Iuliis GN, Newey RJ, King BV, Aitken RJ. Mobile phone radiation induces reactive oxygen species production and DNA damage in human spermatozoa in vitro. PLoS One. 2009;4(7):e6446.
  186. Huffnagle IM, Joyner A, Rumble B, Hysa S, Rudel D, Hvastkovs EG. Dual electrochemical and physiological apoptosis assay detection of in vivo generated nickel chloride induced DNA damage in Caenorhabditis elegans. Anal Chem. 2014 Aug 19;86(16):8418-24.
  187. Ames BN, Gold LS. Natural chemicals, synthetic chemicals, risk assessment, and cancer. Princess Takamatsu Symp. 1990;21:303-14.
  188. Gomez-Martin A, Altakroni B, Lozano-Paniagua D, et al. Increased N7-methyldeoxyguanosine DNA adducts after occupational exposure to pesticides and influence of genetic polymorphisms of paraoxonase-1 and glutathione S-transferase M1 and T1. Environ Mol Mutagen. 2014 Nov 26.
  189. How V, Hashim Z, Ismail P, Md Said S, Omar D, Bahri Mohd Tamrin S. Exploring cancer development in adulthood: cholinesterase depression and genotoxic effect from chronic exposure to organophosphate pesticides among rural farm children. J Agromedicine. 2014;19(1):35-43.
  190. Waters MD, Stack HF, Jackson MA, Brockman HE, De Flora S. Activity profiles of antimutagens: in vitro and in vivo data. Mutat Res. 1996 Feb 19;350(1):109-29.
  191. He XY, Tang L, Wang SL, Cai QS, Wang JS, Hong JY. Efficient activation of aflatoxin B1 by cytochrome P450 2A13, an enzyme predominantly expressed in human respiratory tract. Int J Cancer. 2006 Jun 1;118(11):2665-71.
  192. Barouki R, Morel Y. Repression of cytochrome P450 1A1 gene expression by oxidative stress: mechanisms and biological implications. Biochem Pharmacol. 2001 Mar 1;61(5):511-6.
  193. Kleman MI, Overvik E, Poellinger L, Gustafsson JA. Induction of cytochrome P4501A isozymes by heterocyclic amines and other food-derived compounds. Princess Takamatsu Symp. 1995;23:163-71.
  194. Foth H. Role of the lung in accumulation and metabolism of xenobiotic compounds--implications for chemically induced toxicity. Crit Rev Toxicol. 1995;25(2):165-205.
  195. Vetvicka V, Vetvickova J. Glucan-resveratrol-vitamin C combination offers protection against toxic agents. Toxins (Basel). 2012 Nov;4(11):1301-8.
  196. Turner PC, Flannery B, Isitt C, Ali M, Pestka J. The role of biomarkers in evaluating human health concerns from fungal contaminants in food. Nutr Res Rev. 2012 Jun;25(1):162-79.
  197. Mehta H, Nazzal K, Sadikot RT. Cigarette smoking and innate immunity. Inflamm Res. 2008 Nov;57(11):497-503.
  198. Balabanic D, Rupnik M, Klemencic AK. Negative impact of endocrine-disrupting compounds on human reproductive health. Reprod Fertil Dev. 2011;23(3):403-16.
  199. Ferreira LL, Couto R, Oliveira PJ. Bisphenol A as epigenetic modulator: setting the stage for carcinogenesis? Eur J Clin Invest. 2015 Jan;45 Suppl 1:32-6.
  200. Hussain I, Bhan A, Ansari KI, et al. Bisphenol-A induces expression of HOXC6, an estrogen-regulated homeobox-containing gene associated with breast cancer. Biochim Biophys Acta. 2015 Feb 25.
  201. Fang CC, Chen FY, Chen CR, et al. Cyprodinil as an activator of aryl hydrocarbon receptor. Toxicology. 2013 Feb 8;304:32-40.
  202. Pestana D, Teixeira D, Faria A, Domingues V, Monteiro R, Calhau C. Effects of environmental organochlorine pesticides on human breast cancer: putative involvement on invasive cell ability. Environ Toxicol. 2015 Feb;30(2):168-76.
  203. Villeneuve S, Cyr D, Lynge E, et al. Occupation and occupational exposure to endocrine disrupting chemicals in male breast cancer: a case-control study in Europe. Occup Environ Med. 2010 Dec;67(12):837-44.
  204. De Coster S, van Larebeke N. Endocrine-disrupting chemicals: associated disorders and mechanisms of action. J Environ Public Health. 2012;2012:713696.
  205. Erkekoglu P, Kocer-Gumusel B. Genotoxicity of phthalates. Toxicol Mech Methods. 2014 Dec;24(9):616-26.
  206. Tremoen NH, Fowler PA, Ropstad E, Verhaegen S, Krogenaes A. Exposure to the three structurally different PCB congeners (PCB 118, 153, and 126) results in decreased protein expression and altered steroidogenesis in the human adrenocortical carcinoma cell line H295R. J Toxicol Environ Health A. 2014;77(9-11):516-34.
  207. Van Vleet TR, Watterson TL, Klein PJ, Coulombe RA, Jr. Aflatoxin B1 alters the expression of p53 in cytochrome P450-expressing human lung cells. Toxicol Sci. 2006 Feb;89(2):399-407.
  208. Villar S, Le Roux-Goglin E, Gouas DA, et al. Seasonal variation in TP53 R249S-mutated serum DNA with aflatoxin exposure and hepatitis B virus infection. Environ Health Perspect. 2011 Nov;119(11):1635-40.
  209. Zhang YJ, Rossner P, Jr., Chen Y, et al. Aflatoxin B1 and polycyclic aromatic hydrocarbon adducts, p53 mutations and p16 methylation in liver tissue and plasma of hepatocellular carcinoma patients. Int J Cancer. 2006 Sep 1;119(5):985-91.
  210. Sandoval M, Morales M, Tapia R, et al. p53 response to arsenic exposure in epithelial cells: protein kinase B/Akt involvement. Toxicol Sci. 2007 Sep;99(1):126-40.
  211. Golovine K, Makhov P, Uzzo RG, et al. Cadmium down-regulates expression of XIAP at the post-transcriptional level in prostate cancer cells through an NF-kappaB-independent, proteasome-mediated mechanism. Mol Cancer. 2010;9:183.
  212. Yang YX, Li XL, Wang L, et al. Anti-apoptotic proteins and catalase-dependent apoptosis resistance in nickel chloride-transformed human lung epithelial cells. Int J Oncol. 2013 Sep;43(3):936-46.
  213. Son YO, Pratheeshkumar P, Roy RV, et al. Nrf2/p62 signaling in apoptosis resistance and its role in cadmium-induced carcinogenesis. J Biol Chem. 2014 Oct 10;289(41):28660-75.
  214. Yadava N, Schneider SS, Jerry DJ, Kim C. Impaired mitochondrial metabolism and mammary carcinogenesis. J Mammary Gland Biol Neoplasia. 2013 Mar;18(1):75-87.
  215. Gichuhi S, Ohnuma S, Sagoo MS, Burton MJ. Pathophysiology of ocular surface squamous neoplasia. Exp Eye Res. 2014 Dec;129:172-82.
  216. Reichrath J, Rass K. Ultraviolet damage, DNA repair and vitamin D in nonmelanoma skin cancer and in malignant melanoma: an update. Adv Exp Med Biol. 2014;810:208-33.