You're not going to believe this one: A recent poll of 1500 women in Britain and five other countries found that 22 percent of them would consider having both breasts removed if they were at high risk for breast cancer. We're not talking about the removal of breasts that have cancer; we're talking about the removal of both breasts, a double mastectomy, as a prevention strategy -- even without a diagnosis of cancer. Amazingly, one out of five women said yes.
Now, wait a minute. Let's get a hold of our senses for a second here. If you went to a group of women and said, "Your mother died of breast cancer. Therefore, we are going to take a scalpel and physically slice off both of your breasts just on the off-chance that we might be able to prevent breast cancer in you" -- are you telling me that 22 percent of those women would say yes? How insane is that?
This is a case in which you can't just blame the medical community. Of course, they're evidently practicing medical insanity in suggesting such a drastic "preventative" measure, but you can't really blame the surgeons here -- you have to blame the 22 percent who said yes. What is wrong with these women that they would blindly say, "Yeah, sure, cut them off. I might have cancer some day, so just remove all the parts that could become cancerous." What do you do if you're a guy and you have a history of prostate cancer? What if you have a family history of colon cancer, lung cancer or liver cancer? Do you just take those organs out? Is this what conventional medicine has come down to? Let's remove the parts that might become diseased! Is this how far off the deep end modern medicine has gone?
What happened to true prevention? What happened to helping patients heal? What happened to conserving and supporting the health of one's organs? What happened to keeping one's breasts healthy so that you don't have to cut anything out for the sake of preventing cancer down the road? What happened to that kind of thinking? I mean, isn't medicine based on, "First, do no harm"? Isn't that the opening line of the Hippocratic Oath? Aren't doctorssupposed to be helping patients, not slicing them up? "Doctor, my arm hurts." "Don't worry, we can remove it." Is that what medicine has come to?

Women in the UK were even more likely to say yes

Here's another interesting fact to all of this -- this will be especially disconcerting to those of you in the UK. Thirty-one percent of women from the UK said yes in this survey, compared to 22 percent overall. Now, I know that in the UK you like to think of Americans as being mad, and you're 51% right. But in this case, it's the British who are crazy to the tune of one-third of their female population saying yes to this. "Sure, doc. Cut them off. I don't need these. I'm preventing breast cancer."Now, does all of this remind anybody else of Bush's war on Iraq and its so-called "preemptive defense?" Maybe medicine could call this "offensive prevention." They'll prevent a disease before it happens by removing the organs that it might affect. God forbid if you have a history of brain tumors in your family -- off with your head! That's their plan; that's where they're taking medicine. That's the level of insanity that seems to be pervading the thinking of medical authoritiesout there. Give a doctor a scalpel and he wants to cut off everything in sight.

Let's get real about breast cancer

Despite the insanity of conventional medicine, you nonetheless can deal with breast cancer in a rational way. You can treat it and overcome it. You can even reverse it with natural medicine. It's not that difficult to do, really. In all truthfulness, cancer is one of the easiest diseases to reverse with natural medicine. I'm talking about medicinal herbs, reishimushrooms, shiitake mushrooms, outstanding nutrition and avoidance of certain food ingredients and environmental toxins such as plastic cookware -- measures like that. It's not overly difficult to reverse this disease or even prevent it from happening in the first place, but what modern medicine wants to do is take away your organs.When they're not removing your organs, they're irradiating them: "Let's smash your breasts between this machine like a pancake and irradiate them to see if we can find some tumors in there." That's what they call a mammogram. They refer to it as prevention -- preventing cancer by irradiating your breast, which makes about as much sense as treatingdiabetes by giving you sugar. How is that prevention? How can that even be classified as medicine?
A mammogram is not a preventative technique; it is a diagnostic technique for detection, and it's not even very effective. Even worse, it causes cancer. That's right: the radiation emitted by these mammogram machines is, all by itself, a significant cause of breast cancer. (And many of these machines are not properly calibrated to begin with, so even the radiologist may not know how much radiation you're actually getting...) See the Mammograms cause breast cancerarticle to learn more.
So mammograms are touted as "prevention", and we now have all these celebrities running around urging everyone, "Go get screened for cancer! Come on, rush on in there! Put yourself in the machine, get irradiated and find out if you have a cancerous tumor in there."
So, let me pose a question: If the double mastectomy becomes an accepted prevention procedure, would celebrities recommend that women go in and have their breasts removed? Imagine this public service announcement: "Hi, I'm a famous actress. I have my breasts, but I don't think it's safe for you to have yours. Go in and get them removed. It's good medicine; it will prevent breast cancer." Is that what we're heading toward?

I'm not making this up

I sometimes receive emails from people who think that I'm making this stuff up. They say, "Mike, you've lost it this time. You're just making this up. Modern medicine couldn't be that crazy." Unfortunately, I can assure you I'm not making this up. You can verify for yourself: Go to Google News or any search engine you want and search for the keywords "double mastectomy breast cancer prevention." The Times of London did this report, so you can check it out yourself.I am not making this stuff up, folks. In fact, I couldn't possibly make this type of stuff up; it is much too bizarre to pop into my head. I'm busy thinking about other things, like "How are those tomato plants doing today in the back yard? I wonder if the soil is acidic enough to support the growth of this blueberry plant? I would sure like to have some fresh blueberries this year." Those are the thoughts that occur to me in the normal course of things. I certainly don't think, "Hmm, maybe we could prevent cancer in the world by removing all the organs that could be afflicted by cancer. Yes!" It's a mad scientist kind of thought: "Take the breasts off. Take the organs out of everybody." But that's what is going through the heads of the doctors, scientists and medical authorities who are suggesting this kind of thing. It's truly scary and downright insane; yet, it passes as organized medicine. Pretty soon, they'll start making women feel guilty for keeping their breasts. You know, in the same way they make parents feel guilty if they don't put their kids on Ritalin.

Defend your natural-born breasts

I know that most of the readers here are women and I just have some advice that I'd like to pass on to you. You can accept or refuse it, but my advice is that you should not remove your breasts. Keep them right where they are; don't let any surgeon near them. Who knows what they want to do?Keep your breasts, and adopt a healthy lifestyle instead -- a lifestyle that supports womens' health. For example, implement a lifestyle of eating fermented soy products and avoiding red meat, especially processed meats. Avoid hydrogenated oils and consume healthy oils instead -- olive oil, macadamia nut oil, salmon oil and flax oil, for example. Eat lots of nuts and seeds in their raw, unprocessed state. Avoid milk and dairy products, food additives, added sugars, artificial food coloring and artificial sweeteners. You know the drill. You know how to be healthy. You know how to prevent breast cancer. It's not that difficult to prevent.
Live your life in a healthy, happy way and stay away from these insane surgeons with scalpels and mad ideas about removing organs that might someday have cancer. I mean, think about it: They want to take a perfectly healthy piece of tissue off of your body. There's not even any disease in it, but they'd still like to take it.
That's insane! It's like saying, "You might have foot disease someday -- let's take the foot off." Wouldn't you normally wait for something to actually be diseased before you chop it off? There are a lot of amputations in this country for diabetics. They get gangrene because they have diabetic neuropathy and eventually they don't have active nerve endings in their limbs any more. In fact, the majority of amputations in this country are due to diabetes, but at least there's a point beyond which they can justify it. They can say, "This leg isn't going to make it. You can't feel it, you can't move it, and it's getting infected." In such a case, an amputation is medically justified. But let's say that they said, "You're diabetic? Hmm, I think we should take your legs now before they get infected as a preventative measure" -- that's what they're saying about breast cancer. "Take them off now to prevent breast cancer."
They're going to use fear, of course, saying, "We'll be saving your life by taking these off! You could very well save your life down the road. You want to save your life, don't you?" Then they say, "Don't listen to those internet people. They don't know what they're talking about; they don't have a medical degree. What do they know about breast cancer? We have to remove these now. You cannot wait! If you remove your breasts now, you might live six to twelve months; otherwise, you'll only live one to three months." They'll use that kind of language on you to scare you into submitting to theirsurgical procedures.

This is strange medicine. These are strange days, folks. And this, it appears, is just one of many strange (but true) stories I'll be bringing to your attention. So stay tuned for more.

About the author: Mike Adams is a holistic nutritionist with a passion for sharing empowering information to help improve personal and planetary health He has authored more than 1,500 articles and dozens of reports, guides and interviews on natural health topics, impacting the lives of millions of readers around the world who are experiencing phenomenal health benefits from reading his articles. Adams is an independent journalist with strong ethics who does not get paid to write articles about any product or company. In 2007, Adams launched EcoLEDs, a maker of energy efficient LED lights that greatly reduce CO2 emissions. He also founded an environmentally-friendly online retailer called BetterLifeGoods.com that uses retail profits to help support consumer advocacy programs. He's also the founder of a well known HTML email software company whose 'Email Marketing Director' software currently runs the NaturalNews subscription database. Adams also serves as the executive director of the Consumer Wellness Center, a non-profit consumer protection group, and practices nature photography, Capoeira, Pilates and organic gardening. Known as the 'Health Ranger,' Adams' personal health statistics and mission statements are located atwww.HealthRanger.org

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 Cancer systems biology: a network modeling perspective

Pamela K. Kreeger and Douglas A. Lauffenburger^1,* Department of Biomedical Engineering, University of Wisconsin-Madison, Madison, WI 53706, USA
¹ Department of Biological Engineering, Massachusetts Institute of Technology, Building 16, Room 343, 77 Massachusetts Avenue, Cambridge, MA 02139, USA
^* To whom correspondence should be addressed. Tel: ; Fax: +1 617 258 0204; Email: lauffen@mit.edu
Cancer is now appreciated as not only a highly heterogenous pathology with respect to cell type and tissue origin but also as a disease involving dysregulation of multiple pathways governing fundamental cell processes such as death, proliferation, differentiation and migration. Thus, the activities of molecular networks that execute metabolic or cytoskeletal processes, or regulate these by signal transduction, are altered in a complex manner by diverse genetic mutations in concert with the environmental context. A major challenge therefore is how to develop actionable understanding of this multivariate dysregulation, with respect both to how it arises from diverse genetic mutations and to how it may be ameliorated by prospective treatments. While high-throughput experimental platform technologies ranging from genomic sequencing to transcriptomic, proteomic and metabolomic profiling are now commonly used for molecular-level characterization of tumor cells and surrounding tissues, the resulting data sets defy straightforward intuitive interpretation with respect to potential therapeutic targets or the effects of perturbation. In this review article, we will discuss how significant advances can be obtained by applying computational modeling approaches to elucidate the pathways most critically involved in tumor formation and progression, impact of particular mutations on pathway operation, consequences of altered cell behavior in tissue environments and effects of molecular therapeutics.

Abbreviations: EGFR, epidermal growth factor receptor; ERK, extracellular signal-regulated kinase; TNF, tumor necrosis factor
Received August 19, 2009; revised October 17, 2009; accepted October 18, 2009.

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Telomeres and telomerase in cancer

Steven E. Artandi^* and Ronald A. DePinho^1,* Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
¹ Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
^* To whom correspondence should be addressed. Email: ronald_depinho@dfci.harvard.edu or sartandi@stanford.edu
Myriad genetic and epigenetic alterations are required to drive normal cells toward malignant transformation. These somatic events commandeer many signaling pathways that cooperate to endow aspiring cancer cells with a full range of biological capabilities needed to grow, disseminate and ultimately kill its host. Cancer genomes are highly rearranged and are characterized by complex translocations and regional copy number alterations that target loci harboring cancer-relevant genes. Efforts to uncover the underlying mechanisms driving genome instability in cancer have revealed a prominent role for telomeres. Telomeres are nucleoprotein structures that protect the ends of eukaryotic chromosomes and are particularly vulnerable due to progressive shortening during each round of DNA replication and, thus, a lifetime of tissue renewal places the organism at risk for increasing chromosomal instability. Indeed, telomere erosion has been documented in aging tissues and hyperproliferative disease states—conditions strongly associated with increased cancer risk. Telomere dysfunction can produce the opposing pathophysiological states of degenerative aging or cancer with the specific outcome dictated by the integrity of DNA damage checkpoint responses. In most advanced cancers, telomerase is reactivated and serves to maintain telomere length and emerging data have also documented the capacity of telomerase to directly regulate cancer-promoting pathways. This review covers the role of telomeres and telomerase in the biology of normal tissue stem/progenitor cells and in the development of cancer.

Abbreviations: acd, adrenocortical dysplasia; aCGH, array comparative genome hybridization; APC, adenomatous polyposis coli; ATM, ataxia telangiectasia mutated; CNA, copy number alterations; DC, dyskeratosis congenita; min, multiple intestinal neoplasia; POT1, protection of telomeres 1; scaRNA, small Cajal body-specific RNA; snoRNA, small nucleolar RNA; TCAB1, telomerase Cajal body protein 1; TERC, telomerase RNA component; TERT, telomerase reverse transcriptase; TRF1, telomeric repeat binding factor 1; TRF2, telomeric repeat binding factor 2
Received September 25, 2009; revised October 27, 2009; accepted October 27, 2009.

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Senescence: an antiviral defense that is tumor suppressive?

Roger R. Reddel^{1,2,* 1} Cancer Research Unit, Children's Medical Research Institute, 214 Hawkesbury Road, Westmead, New South Wales 2145, Australia
² Sydney Medical School, University of Sydney, New South Wales 2006, Australia
^* To whom correspondence should be addressed. Tel: +61 2 8865 2901; Fax: +61 2 8865 2860;Email: rreddel@cmri.usyd.edu.au
Normal mammalian somatic cells proliferate a finite number of times in vitro before permanently withdrawing from the cell cycle into a cellular state referred to as senescence. Senescence may be triggered by excessive mitogenic stimulation or by various forms of cellular damage including excessive telomere shortening. Over the past decade, there has been continuing accumulation of evidence that senescence occurs in vivo, that it is relevant to aging and that it has a tumor suppressor function. However, the phenotype of senescence has also been found to include a number of puzzling features, including the secretion of proinflammatory factors that may foster tumorigenesis as well as the senescence of neighboring cells. On the basis of these antagonistic pro- and antitumorigenic effects, and of the observation that many viruses have developed proteins that prevent senescence of the cells they infect, it is argued that the primary function of senescence may have been as an antiviral defense mechanism. Recent progress in understanding how tumor cells evade senescence is also reviewed here.

Abbreviations: ALT, alternative lengthening of telomeres; PML, promyelocytic leukemia; Rb, retinoblastoma; RNP, ribonucleoprotein; SA, senescence-associated; SAHF, senescence-associated heterochromatin foci; TERC, telomerase RNA Component; TERT, telomerase reverse transcriptase; TMM, telomere length maintenance mechanism
Received October 30, 2009; revised October 30, 2009; accepted October 30, 2009.

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Epigenetics in cancer

Shikhar Sharma^1,2, Theresa K. Kelly¹ and Peter A. Jones^{1,* 1} Department of Urology, Biochemistry and Molecular Biology
² Department of Genetics, Molecular and Cellular Biology, USC/Norris Comprehensive Cancer Center Keck School of Medicine, University of Southern California, Los Angeles, CA 90089-9181, USA
^* To whom correspondence should be addressed: Tel: +1 323 865 0816; Fax: +1 323 865 0102; Email: jones_p@ccnt.usc.edu
Epigenetic mechanisms are essential for normal development and maintenance of tissue-specific gene expression patterns in mammals. Disruption of epigenetic processes can lead to altered gene function and malignant cellular transformation. Global changes in the epigenetic landscape are a hallmark of cancer. The initiation and progression of cancer, traditionally seen as a genetic disease, is now realized to involve epigenetic abnormalities along with genetic alterations. Recent advancements in the rapidly evolving field of cancer epigenetics have shown extensive reprogramming of every component of the epigenetic machinery in cancer including DNA methylation, histone modifications, nucleosome positioning and non-coding RNAs, specifically microRNA expression. The reversible nature of epigenetic aberrations has led to the emergence of the promising field of epigenetic therapy, which is already making progress with the recent FDA approval of three epigenetic drugs for cancer treatment. In this review, we discuss the current understanding of alterations in the epigenetic landscape that occur in cancer compared with normal cells, the roles of these changes in cancer initiation and progression, including the cancer stem cell model, and the potential use of this knowledge in designing more effective treatment strategies.

Abbreviations: DNMT, DNA methyltransferase; ES, embryonic stem; HAT, histone acetyltransferase; HDAC, histone deacetylase; HDM, histone demethylase; HMT, histone methyltransferase; LOI, loss of imprinting; miRNA, microRNA; NFR, nucleosome-free region; NuRD, nucleosome remodeling and deacetylase
Received August 14, 2009; revised September 1, 2009; accepted September 3, 2009.

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Inflammation and cancer: interweaving microRNA, free radical, cytokine and p53 pathways

Aaron J. Schetter¹, Niels H. H. Heegaard^1,2 and Curtis C. Harris^{1,* 1} Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
² Department of Clinical Biochemistry and Immunology, Statens Serum Institute, Copenhagen, DK-2300, Denmark
^* To whom correspondence should be addressed. Tel: +1 301 496 2048; Fax: +1 301 496 0497; Email: harrisc@mail.nih.gov
Chronic inflammation and infection are major causes of cancer. There are continued improvements to our understanding of the molecular connections between inflammation and cancer. Key mediators of inflammation-induced cancer include nuclear factor kappa B, reactive oxygen and nitrogen species, inflammatory cytokines, prostaglandins and specific microRNAs. The collective activity of these mediators is largely responsible for either a pro-tumorigenic or anti-tumorigenic inflammatory response through changes in cell proliferation, cell death, cellular senescence, DNA mutation rates, DNA methylation and angiogenesis. As our understanding grows, inflammatory mediators will provide opportunities to develop novel diagnostic and therapeutic strategies. In this review, we provide a general overview of the connection between inflammation, microRNAs and cancer and highlight how our improved understanding of these connections may provide novel preventive, diagnostic and therapeutic strategies to reduce the health burden of cancer.

Abbreviations: CLL, chronic lymphocytic leukemia; COX-2, cyclooxygenase-2; IFN, interferon; IL, interleukin; KRAS, kirsten rat sarcoma oncogene; LPS, lipopolysaccharide; NFB, nuclear factor kappa B; NO, nitric oxide; NOS, nitric oxide synthase; NSAIDs, non-steroidal, anti-inflammatory drugs; p53, protein 53; PGs, prostaglandins; RAS, rat sarcoma oncogene; RISC, RNA-induced silencing complex; RONS, reactive oxygen and nitrogen species; TGFβ, transforming growth factor; TNF, tumor necrosis factor; UTR, untranslated region
Received September 22, 2009; revised October 29, 2009; accepted October 29, 2009.

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Chemical biology of mutagenesis and DNA repair: cellular responses to DNA alkylation

Nidhi Shrivastav^1,2, Deyu Li^1,2 and John M. Essigmann^{1,2,* 1} Department of Biological Engineering
² Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
^* To whom correspondence should be addressed. Tel: +1 6172536227; Fax: +1 6172535445; Email: jessig@mit.edu
The reaction of DNA-damaging agents with the genome results in a plethora of lesions, commonly referred to as adducts. Adducts may cause DNA to mutate, they may represent the chemical precursors of lethal events and they can disrupt expression of genes. Determination of which adduct is responsible for each of these biological endpoints is difficult, but this task has been accomplished for some carcinogenic DNA-damaging agents. Here, we describe the respective contributions of specific DNA lesions to the biological effects of low molecular weight alkylating agents.

Abbreviations: AAG, human 3-methyladenine-DNA glycosylase; AP site, apurinic site; BER, base excision repair; dAMP, deoxyadenosine monophosphate; dCMP, deoxycytidine monophosphate; dGMP, deoxyguanosine monophosphate; dNMP, deoxynucleoside monophosphate; dTTP, deoxythymidine triphosphate; EA, 1,N⁶-ethanoadenine; eA, 1,N⁶-ethenoadenine; eC, 3,N⁴-ethenocytosine; 1EtA, N1-ethyladenine; 3EtC, N3-ethylcytosine; Fapy, formamidopyrimidine; 1MeA, N1-methyladenine; 3MeA, N3-methyladenine; 7MeA, N7-methyladenine; 3MeC, N3-methylcytosine; 1MeG, N1-methylguanine; 3MeG, N3-methylguanine; 7MeG, N7-methylguanine; 8MeG, 8-methylguanine; MePT, methylphosphotriester; 3MeT, N3-methylthymine; MGMT, O⁶-methylguanine-DNA methyltransferase; MMR, mismatch repair; MMS, methylmethanesulfonate; MNNG, N-methyl-N'-nitro-N-nitrosoguanidine; MNU, N-methyl-N-nitrosourea; MGP, N-methylpurine-DNA glycosylase; NER, nucleotide excision repair; O⁶EtG, O⁶-ethylguanine; O⁶MeG, O⁶-methylguanine; O⁴MeT, O⁴-methylthymine; SAM, S-adenosylmethionine; TAG, 3-methyladenine-DNA glycosylase I
Received August 19, 2009; revised October 20, 2009; accepted October 21, 2009.

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Mycotoxins and human disease: a largely ignored global health issue

Christopher P. Wild^* and Yun Yun Gong¹ International Agency for Research on Cancer, 69372 Lyon Cedex 08, France
¹ Molecular Epidemiology Unit, LIGHT Laboratories, University of Leeds, Leeds, LS2 9JT, UK
^* To whom correspondence should be addressed. Tel: +33 (0) 4 72 73 84 85; Fax: +33 (0) 4 72 73 85 64; Email: director@iarc.fr
Aflatoxins and fumonisins (FB) are mycotoxins contaminating a large fraction of the world's food, including maize, cereals, groundnuts and tree nuts. The toxins frequently co-occur in maize. Where these commodities are dietary staples, for example, in parts of Africa, Asia and Latin America, the contamination translates to high-level chronic exposure. This is particularly true in subsistence farming communities where regulations to control exposure are either non-existent or practically unenforceable. Aflatoxins are hepatocarcinogenic in humans, particularly in conjunction with chronic hepatitis B virus infection, and cause aflatoxicosis in episodic poisoning outbreaks. In animals, these toxins also impair growth and are immunosuppressive; the latter effects are of increasing interest in human populations. FB have been reported to induce liver and kidney tumours in rodents and are classified as Group 2B ‘possibly carcinogenic to humans’, with ecological studies implying a possible link to increased oesophageal cancer. Recent studies also suggest that the FB may cause neural tube defects in some maize-consuming populations. There is a plausible mechanism for this effect via a disruption of ceramide synthase and sphingolipid biosynthesis. Notwithstanding the need for a better evidence-base on mycotoxins and human health, supported by better biomarkers of exposure and effect in epidemiological studies, the existing data are sufficient to prioritize exposure reduction in vulnerable populations. For both toxins, there are a number of practical primary and secondary prevention strategies which could be beneficial if the political will and financial investment can be applied to what remains a largely and rather shamefully ignored global health issue.

Abbreviations: AFB1-N7-Gua, 8,9-dihydro-8-(N7-guanyl)-9-hydroxy AFB1; CYP, cytochrome P450; FAPY, formamidopyrimidine; FB, fumonisins; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; HBx, hepatitis B x; HCC, hepatocellular carcinoma; LC-MS, liquid chromatography-mass spectrometry; NTD, neural tube defect; OC, oesophageal cancer; OR, odds ratio
Received October 13, 2009; revised October 18, 2009; accepted October 22, 2009.

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Calories and carcinogenesis: lessons learned from 30 years of calorie restriction research

Stephen D. Hursting^1,2,*, Sarah M. Smith¹, Laura M. Lashinger^1,2, Alison E. Harvey¹ and Susan N. Perkins^{1 1} Department of Nutritional Sciences, The University of Texas at Austin, 103 West 24th Street, Austin, TX 78712,USA
² Department of Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Smithville, TX 78957, USA
^* To whom correspondence should be addressed. Tel: +1 512 971 2809; Fax: +1 512 471 4661;Email: shursting@mail.utexas.edu
Calorie restriction (CR) is arguably the most potent, broadly acting dietary regimen for suppressing the carcinogenesis process, and many of the key studies in this field have been published in Carcinogenesis. Translation of the knowledge gained from CR research in animal models to cancer prevention strategies in humans is urgently needed given the worldwide obesity epidemic and the established link between obesity and increased risk of many cancers. This review synthesizes the evidence on key biological mechanisms underlying many of the beneficial effects of CR, with particular emphasis on the impact of CR on growth factor signaling pathways and inflammatory processes and on the emerging development of pharmacological mimetics of CR. These approaches will facilitate the translation of CR research into effective strategies for cancer prevention in humans.

Abbreviations: AMPK, adenosine monophosphate-activated kinase; ATP, adenosine triphosphate; CR, calorie restriction; IGF, insulin-like growth factor; IL, interleukin; mTOR, mammalian target of rapamycin; PI3K, phosphatidylinositol 3-kinase; PPAR, peroxisome proliferators-activated receptor; SIRT1, silent mating type information regulation homolog; TNF-, tumor necrosis factor-alpha; TSC, tuberous sclerosis complex
Received September 28, 2009; revised November 3, 2009; accepted November 3, 2009.

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Nrf2: friend or foe for chemoprevention?

Thomas W. Kensler^1,2,3,* and Nobunao Wakabayashi^{1,3 1} Department of Environmental Health Sciences, Bloomberg School of Public Health
² Department of Pharmacology and Molecular Sciences, School of Medicine, Johns Hopkins University, 615 North Wolfe Street, Baltimore, MD 21205, USA
³ Present address: Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA 15260, USA
^* To whom correspondence should be addressed. Tel: +410 955 1292; Fax: +410 955 0119; Email: tkensler@jhsph.edu
Health reflects the ability of an organism to adapt to stress. Stresses—metabolic, proteotoxic, mitotic, oxidative and DNA-damage stresses—not only contribute to the etiology of cancer and other chronic degenerative diseases but are also hallmarks of the cancer phenotype. Activation of the Kelch-like ECH-associated protein 1 (KEAP1)–NF-E2-related factor 2 (NRF2)-signaling pathway is an adaptive response to environmental and endogenous stresses and serves to render animals resistant to chemical carcinogenesis and other forms of toxicity, whilst disruption of the pathway exacerbates these outcomes. This pathway can be induced by thiol-reactive small molecules that demonstrate protective efficacy in preclinical chemoprevention models and in clinical trials. However, mutations and epigenetic modifications affecting the regulation and fate of NRF2 can lead to constitutive dominant hyperactivation of signaling that preserves rather than attenuates cancer phenotypes by providing selective resistance to stresses. This review provides a synopsis of KEAP1–NRF2 signaling, compares the impact of genetic versus pharmacologic activation and considers both the attributes and concerns of targeting the pathway in chemoprevention.

Abbreviations: ARE, antioxidant response element; BHT, butylated hydroxytoluene; CDDO-Im, 1-(2-cyano-3,12-dioxooleana-1,9[11]-dien-28-oyl)imidazole; GST, glutathione S-transferase; KEAP1, Kelch-like ECH-associated protein 1; NQO1, NAD(P)H: quinone oxidoreductase 1; NRF2, NF-E2-related factor 2; oltipraz, 5-(2-pyrazinyl)-4-methyl-1,2-dithiole-3-thione; sulforaphane, (-)-1-isothiocyanato-(4R)-methylsulfinyl)butane; ROS, reactive oxygen species
Received September 2, 2009; revised September 16, 2009; accepted September 18, 2009.

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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

The global burden of cancer: priorities for prevention

Michael J. Thun^*, John Oliver DeLancey, Melissa M. Center, Ahmedin Jemal and Elizabeth M. Ward American Cancer Society, Research Department, 250 Williams Street, Northwest, Atlanta, GA 30303-1002, USA
^* To whom correspondence should be addressed. Tel: +1 404 329 5747; Fax: +1 404 327 6450; Email: michael.thun@cancer.org
Despite decreases in the cancer death rates in high-resource countries, such as the USA, the number of cancer cases and deaths is projected to more than double worldwide over the next 20–40 years. Cancer is now the third leading cause of death, with >12 million new cases and 7.6 million cancer deaths estimated to have occurred globally in 2007 (1). By 2030, it is projected that there will be 26 million new cancer cases and 17 million cancer deaths per year. The projected increase will be driven largely by growth and aging of populations and will be largest in low- and medium-resource countries. Under current trends, increased longevity in developing countries will nearly triple the number of people who survive to age 65 by 2050. This demographic shift is compounded by the entrenchment of modifiable risk factors such as smoking and obesity in many low-and medium-resource countries and by the slower decline in cancers related to chronic infections (especially stomach, liver and uterine cervix) in economically developing than in industrialized countries. This paper identifies several preventive measures that offer the most feasible approach to mitigate the anticipated global increase in cancer in countries that can least afford it. Foremost among these are the need to strengthen efforts in international tobacco control and to increase the availability of vaccines against hepatitis B and human papilloma virus in countries where they are most needed.

Abbreviations: EBV, Epstein Barr virus; FCTC, Framework Convention on Tobacco Control; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; HAART, highly active antiretroviral therapy; HHV-8, human herpes virus 8; HIV, human immunodeficiency virus; HPV, human papilloma virus; KS, Kaposi’s sarcoma; NHL, non-Hodgkin’s lymphoma; WHO, World Health Organization
Received September 16, 2009; revised October 20, 2009; accepted October 20, 2009.

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Genome-wide association studies in cancer—current and future directions

Charles C. Chung¹, Wagner C. S. Magalhaes^1,2, Jesus Gonzalez-Bosquet¹ and Stephen J. Chanock^{1,* 1} Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892-4608, USA
² Departamento de Biologia Geral, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, CEP 31270-910, Belo Horizonte, MG, Brazil
^* To whom correspondence should be addressed. Tel: +1 301 435 7559; Fax: +1 301 402 3134; Email: chanocks@mail.nih.gov
Genome-wide association studies (GWAS) have emerged as an important tool for discovering regions of the genome that harbor genetic variants that confer risk for different types of cancers. The success of GWAS in the last 3 years is due to the convergence of new technologies that can genotype hundreds of thousands of single-nucleotide polymorphism markers together with comprehensive annotation of genetic variation. This approach has provided the opportunity to scan across the genome in a sufficiently large set of cases and controls without a set of prior hypotheses in search of susceptibility alleles with low effect sizes. Generally, the susceptibility alleles discovered thus far are common, namely, with a frequency in one or more population of >10% and each allele confers a small contribution to the overall risk for the disease. For nearly all regions conclusively identified by GWAS, the per allele effect sizes estimated are <1.3. Consequently, the findings of GWAS underscore the complex nature of cancer and have focused attention on a subset of the genetic variants that comprise the genomic architecture of each type of cancer, which already can differ substantially by the number of regions associated with specific types of cancer. For instance, in prostate cancer, there could be >30 distinct regions harboring common susceptibility alleles identified by GWAS, whereas in lung cancer, a disease strongly driven by exposure to tobacco products, so far, only three regions have been conclusively established. To date, >85 regions have been conclusively associated in over a dozen different cancers, yet no more than five regions have been associated with more than one distinct cancer type. GWAS are an important discovery tool that require extensive follow-up to map each region, investigate the biological mechanism underpinning the association and eventually test the optimal markers for assessing risk for a disease or its outcome, such as in pharmacogenomics, the study of the effect of genetic variation on pharmacological interventions. The success of GWAS has opened new horizons for exploration and highlighted the complex genomic architecture of disease susceptibility.

Abbreviations: CNV, copy number variation; GWAS, genome-wide association studies; LD, linkage disequilibrium; MAF, minor allele frequency; PSA, prostate serum antigen; SNP, single-nucleotide polymorphism
Received October 30, 2009; revised October 30, 2009; accepted October 30, 2009.

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Biomarkers in cancer epidemiology: an integrative approach

Paolo Boffetta^* International Prevention Research Institute, 95 cours Lafayette, 69006 Lyon, France
^* To whom correspondence should be addressed. Tel: +33 658386724; Fax: +33 472387126; Email: paolo.boffetta@i-pri.org
There are different reasons for the increase in the use of biomarkers in cancer epidemiology which is as follows: (i) the fact that the identification of new carcinogens, characterized by complex exposure circumstances and weak effects, has become increasingly difficult with traditional epidemiological approaches; (ii) the increasing understanding of mechanisms of carcinogenesis and (iii) technical developments in molecular biology and genetics. While a distinction is made between biomarkers of exposure, intermediate events, disease, outcome and susceptibility, their integration in a unique conceptual model is needed. The use of exposure biomarkers in cancer epidemiology aims at measuring the biologically relevant exposure more validly and precisely. In some instances, there is an obvious improvement in using an exposure biomarker, as in the case of urinary markers of aflatoxin and tobacco-specific nitrosamines. Intermediate (effect) biomarkers measure early—in general non-persistent—biological events that take place in the continuum between exposure and cancer development. These include cellular or tissue toxicity, chromosomal alterations, changes in DNA, RNA and protein expression and alterations in functions relevant to carcinogenesis (e.g. DNA repair, immunological response, etc.). The analysis of acquired TP53 mutations is an example of the potentially important. Biomarkers should be validated and consideration of sources of bias and confounding in molecular epidemiology studies should be no less stringent than in other types of epidemiological studies. The overarching goal is the integration of different types of biomarkers to derive risk and outcome profiles for healthy individuals as well as patients.
Received October 7, 2009; revised October 24, 2009; accepted October 27, 2009.

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The evolving discipline of molecular epidemiology of cancer

Margaret R. Spitz and Melissa L. Bondy Department of Epidemiology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA
^* To whom correspondence should be addressed. Tel: +1 713 792 3020; Fax: +1 713 745 1165. Email: mspitz@mdanderson.org
Classical epidemiologic studies have made seminal contributions to identifying the etiology of most common cancers. Molecular epidemiology was conceived of as an extension of traditional epidemiology to incorporate biomarkers with questionnaire data to further our understanding of the mechanisms of carcinogenesis. Early molecular epidemiologic studies employed functional assays. These studies were hampered by the need for sequential and/or prediagnostic samples, viable lymphocytes and the uncertainty of how well these functional data (derived from surrogate lymphocytic tissue) reflected events in the target tissue. The completion of the Human Genome Project and Hapmap Project, together with the unparalleled advances in high-throughput genotyping revolutionized the practice of molecular epidemiology. Early studies had been constrained by existing technology to use the hypothesis-driven candidate gene approach, with disappointing results. Pathway analysis addressed some of the concerns, although the study of interacting and overlapping gene networks remained a challenge. Whole-genome scanning approaches were designed as agnostic studies using a dense set of markers to capture much of the common genome variation to study germ-line genetic variation as risk factors for common complex diseases. It should be possible to exploit the wealth of these data for pharmacogenetic studies to realize the promise of personalized therapy. Going forward, the temptation for epidemiologists to be lured by high-tech ‘omics’ will be immense. Systems Epidemiology, the observational prototype of systems biology, is an extension of classical epidemiology to include powerful new platforms such as the transcriptome, proteome and metabolome. However, there will always be the need for impeccably designed and well-powered epidemiologic studies with rigorous quality control of data, specimen acquisition and statistical analysis.

Abbreviations: CBMN, cytokinesis-block micronucleus; DRC, DNA repair capacity; GWA, genome-wide association; IARC, International Agency for Research on Cancer; LD, linkage disequilibrium; miRNA, microRNA; MN, micronuclei; NPB, nucleoplasmic bridge; SNP, single-nucleotide polymorphism
Received August 24, 2009; revised October 2, 2009; accepted October 3, 2009.

What if there was one nutrient which?

1. Desensitized estrogen receptors in the breast.

2. Reduced estrogen production in overactive ovaries.

3. Reduced fibrocystic breast disease which often precedes breast cancer. 4. Caused more cell death than the chemo drug, Fluorouracil .

5. Prevented rats from getting cancer when they were fed the breast cancer  causing toxin DMBA.

Research suggests that some breast cancers may be an iodine deficiency disease. As iodine consumption has gone down, breast cancer rates have gone up. But the research goes far deeper, exploring the effects of iodine supplementation on breast disease and breast cancer. This important breakthrough has been in the research pipeline for years but only recently found momentum.  After sifting through 50 years of iodine research and corresponding with researchers around the world, the editors report that abnormal iodine metabolism, due either to bromide dominance in the environment or a dietary deficiency of iodine, must be addressed as part of a preventive and or a therapeutic strategy.  

                                  Iodine Deficiency Growing Worse

• Iodine consumption by Americans has dropped 50% since the 1970s as breast cancer rates have risen (1).  In the US Goiter Belt,  where iodine in the soil is
  

lower, breast  cancer is higher (2).

• By contrast, the incidence and severity of breast cancer are less in Japan than
  

in Europe and the US, attributable to the diet (3).  Japanese women consume 25 times more dietary iodine than North American women and have lower breast cancer rates (4).

• Meanwhile, since the 1970s, in the US and several other countries, iodine-blocking bromides have been added to flour,  some sodas, and medications, exacerbating the iodine deficiency.
  

• Fluoridated drinking water also depletes iodine absorption. Thus, as women
  

consume less iodine and excrete more due to toxic elements, our risk for breast cancer grows(5).

                   Iodine and Benign Breast Disease

• Blocking iodine in rats' food supply led to progressive human-like fibrocystic
  

disease (atypia, sclerosing, calcifications, dysplastic changes) as the rats aged (6). Supplementing patients with fibrocystic disease with iodine helped to resolve fibrosis and reduced breast size (7).

• For women with painful breasts accompanying fibrocystic disease, iodine  
  

improved symptoms in more than 50% of the women who took 6.0 mg. of iodine for 6 months (8), and brown sea alga improved pain and nodularity in 94% of the women (9).  From the editors' observations of the Iodine Investigation Project participants, depending on the kind of iodine agent used, painful breast symptoms have resolved in from 24 hours to two months.

• Since benign breast disease increases the risk of breast cancer (10), and iodine improves fibrocystic disease, we at Breast Cancer Choices propose studies to see if iodine supplementation decreases the risk of getting breast cancer and the risk of recurrence.
  

                                           Iodine and Breast Cancer        

• For breast patients, iodine's therapeutic mechanisms of action may be at least
  

three-pronged:  Hormonal (11),  Biochemical (12-18), Genetic (19). That is, iodine desensitizes the estrogen receptors, alters the chemical pathways as well effects on the genes, resulting in less cell growth, and causing anti-tumor effect by causing apoptosis (programmed cell death) of malignant cells.

• Iodine-rich seaweed exhibits an anti-cancer effect in rats and in the lab on human breast cancer cells.
  

Adding seaweed to rats' food delays the onset and number of rat mammary tumors (20,21). And in the lab, mekabu seaweed plant induced cell death in three kinds of human breast cancer cells. Mekabu had a stronger effect on the cells than the chemo drug, 5-fluorouracil (22).

• Adding  iodine to chemically-induced (DMBA) rat breast tumors stops the
  

growth of the tumors.  Adding iodine plus medroxyprogesterone gave the highestlevel of response: the growth-suppressed tumors showed 100% times the iodine content than the full blown (nonsuppressed) tumors. The researchers suggest that the uptake of iodine was enhanced by medroxyprogesterone. (23).  As David Brownstein, MD, phrased it, "You cannot give breast cancer to rats that have sufficient iodine."

• In small, preliminary patient studies, using the screening iodine-loading test, breast cancer patients excreted less urinary iodine than healthy people, implying iodine-deficiency (24,25).
  

          What to do about iodine deficiency?

• The editors at Breast Cancer Choices recommend patients read as much as they
  

can from the Iodine Related Links on the top left side of this page.

• Secondly,  we recommend taking the Iodine Loading Test  which will provide a guideline to your current iodine sufficiency status. Then join the Iodine Investigation Project and participate in our confidential database so we can follow your progress. Next, consider finding an iodine-literate practioner (ILP)  from our directory or one willing to consider this non-toxic therapy.
  

• Iodine Protocol. Depending upon the results of your screening iodine-loading test,  most doctors we are familiar with currently recommend 50 mg or more of iodine daily in the form of Iodoral tablets (a combined iodine-iodide formula), but others recommend an iodine-only formulation or Lugol's iodine solution.
  

• Where to Get Iodoral:  Iodoral tablets may be available from your health practitioner. The Breast Cancer Choices charity fund-raises for the Iodine investigation Project through sales of Iodoral. If we have provided information to you, please consider buying from a charity rather than a for-profit company.
  

• Iodine Companion Nutrients. Many Iodine Literate Doctors suggest selenium(26),  vitamin C (27), and magnesium(28) enhance the therapeutic value of iodine. Niacin was also recommended at the February 07 Iodine Conference. Thyroid function should be closely monitored and may require an adjustment of thyroid medications.
  

• For those experiencing uncommon detox side effects such as constipation, acne or rash,the Yahoo Iodine Group has used 1/2 teaspoon Celtic salt dissolved in a large glass of water, taken twice a day. Drinking additional water and taking extra vitamin C may help even more.  
  

                              What to Expect The Breast Cancer Choices Iodine Investigation Project is currently following patients taking iodine to prevent recurrence. Most patients report no side effects.  Some report a range of non-breast improvements such as change in thyroid status, need for less thyroid medication, weight loss, ovarian cysts resolving, fibroids shrinking, improved energy, mood and mental clarity. But be aware  some iodine takers report what we believe to be iodine detoxing bromide into the bloodstream causing symptoms of bromism. According to a Department of Defense commissioned report, , bromism symptoms can manifest as lethargy, depression, "dark" thoughts, "brain fog," constipation, leg and hip pain, acne, rashes and other symptoms. These side effects are usually reversible in 24-48 hours by discontinuing the iodine and allowing a short period of washout before restarting at a lower dose. Again, as stated above, Celtic salt in water has relieved detox symptoms quickly by speeding up bromide detox through the kidneys. See Iodine Protocol. CAUTION:  DO NOT TAKE IODINE IF YOU ARE ALLERGIC TO IODIZED SALT

		Since bromide excretion seems to be higher in breast cancer patients than
		undiagnosed persons (29), it is important that each patient develop a strategy with her physician to clear the bromide. Ways of eliminating bromide detox symptoms by taking 1/2 teaspoon of Celtic salt in water are currently being used.

References: 1. NHANES.  National Health and Nutrition Survey showed iodine levels have declined 50% in the US. CDC National Center for Health Statistics.  CDC. gov 2000. 2. Eskin BA., Iodine and Mammary Cancer, Tans NY, Academy of Sciences 1970. 3. Kurihara M., "Cancer Statistics in the World," Nagoya Univ. Press, Nagoya, pp. 80-81 1984. 4. Aceves C., et al., Is Iodine a Gatekeeper of the Integrity of the Mammary Gland?, Journal of Mammary Gland Biology and Neoplasia, 2005.   5. Brownstein D., Iodine.  Why You Need It.  Why You Can't Live Without It, 2nd Edition, Medical Alternative Press 2006. 6. Krouse TB et al., Age-Related Changes Resembling Fibrocystic Disease in Iodine-Blocked Rat Breasts, Arch Pathol Lab Med, 1979 7. Ghent WR et al., Iodine Replacement in Fibrocystic Disease of the Breast, Can J Surg 1993. 8.  Kessler J, The Effect of Supraphysiologic Levels of Iodine in Patients with Cyclic Mastalgia, The Breast Journal 2004. 9. Bezpalov VG et al., Investigation of the Drug "Mamoclam" for the Treatment of Patients with Fibroadenomatosis of the Breast, Vopr Onkol, 2005. 10. Hartmann LC et al., Benign Breast Disease and the Risk of Breast Cancer, N Engl J Med 2005. 11. Shah NM et al., Iodoprotein Formation by Rat Mammary Glands During Pregnancy and Early Postpartum Period, Proc Soc Exp 1986 12.Venturi S., Is There a Role for Iodine in Breast Disease?, The Breast  2001. 13.Cann SA., et al., Hypothesis:  Iodine, Selenium, and the Development of Breast Cancer, Cancer Causes control 2000. 14.Smyth PP., Role of Iodine in Antioxidant Defence in Thyroid and Breast Disease, Biofactors 2003. 15.Coochi M. et al., A New Hypothesis of Bio-Chemical Cooperation?, Prog Nutr 2000. 16.Thrall KD., Differences in the Distribution of Iodine and Iodide in the Sprague-Dawley Rats, J Toxicol Environ Health 1992. 17. Eskin BA.,et al., Different Tissue Responses for Iodine and Iodide in Rat Thyroid and Mammary Glands, Biol Trace Elem Res 1995. 18.Ghent WR. et al., IBID. 19. Eskin BA. et al., Microarray Characterization of Iodine Metabolic Pathways in Breast Cancer, p. 379 2006. 20. Teas J. et al., Dietary Seaweed (Laminaria) and Mammary Carcinogens in Rats, Cancer Res 1984. 21. Funahashi H. et al., Wakame Seaweed Suppresses the Proliferation of 7,12-Dimethybenz(a)- Anthracene-Induced Mammary Tumors in Rats, Jpn J Cancer Res 1999. 22. Funahashi H. et al., Seaweed Preventing Breast Cancer?, Jpn J Cancer Res 2001. 23. Funahashi H. et al., Suppressive Effect of Iodine on DMBA-Induced Breast Tumor Growth in the Rat, J Surg Oncol 1996. 24. Eskin BA. et al., Identification of Breast Cancer by Differences in Urinary Iodine, Abstract Number 2150, Presentation AACR Conference 2005. 25. Brownstein D., IBID 26. Cann SA. et al.,  IBID. 27. Abraham GE., et al., Evidence that the Administration of Vitamin C Improves a Defective Cellular Transport Mechanism for Iodine:  A Case Report, The Original Internist 2005. 28. Abraham GE., The Safe and Effective Implementation of Orthoiodosupplementation in Medical Practice, The Orginal Internist 2004. 29. Brownstein D., IBID. The statements above have not been evaluated by the U.S. Food & Drug Administration.  The supplements discussed are not intended to diagnose, treat, cure, or prevent any disease.  Do not take iodine without the supervision of an Iodine-Literate Doctor who is qualified to interpret lab work in the context of supplementation. This website is intended as information only. The editors of this site are not medically-trained. Please consult your licensed health care practitioner before implementing any health strategy. The information provided on this site is designed to support, not replace, the relationship that exists between a patient/site visitor and his/her existing physician. This site accepts no advertising. The contents of this site are copyrighted 2004-2010 by Breast Cancer Choices, Inc. Contact us with comments or for reprint permission at admin@breastcancerchoices.org Web page updated January 18,  2010.