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This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.
Prevention is defined as the reduction of cancer mortality via reduction in the incidence of cancer. This can be accomplished by avoiding a carcinogen or altering its metabolism; pursuing lifestyle or dietary practices that modify cancer-causing factors or genetic predispositions; medical intervention (e.g., chemoprevention); or early detection strategies that can result in removal of precancerous lesions, such as colonoscopy for colorectal polyps.
About the PDQ Cancer Prevention Summaries
The PDQ cancer prevention summaries are primarily organized by specific anatomic cancer site to facilitate consideration of the unique characteristics of specific malignancies. In this section, an overview of cancer prevention strategies is provided, including a summary of evidence for selected preventive strategies used in the prevention of a broad spectrum of malignancies. The strength of evidence and magnitude of effects of these strategies, however, may vary by cancer site. Other PDQ cancer prevention summaries address the prevention of specific types of cancer and provide more detailed descriptions of the evidence.
There are many common beliefs or speculations about causes of cancer. However, putative causes of cancer for which there exist very little scientific evidence, positive or negative, are not considered in these summaries. Therefore, absence of an environmental, dietary, or lifestyle factor from these summaries implies insufficient evidence for detailed consideration and not necessarily absence of effect. Many such factors are deserving of research regarding their potential roles in cancer, but if that research does not exist, has not been published, or the Editorial Board judges the research to be of poor quality, then they are not addressed in these summaries.
Carcinogenesis refers to an underlying etiologic pathway that leads to cancer. Several models of carcinogenesis have been proposed. Knudson proposed a "two-hit" model requiring a mutation in both copies of a gene resulting in cancer. Expansion of this concept has resulted in other widely cited models of carcinogenesis including those of Vogelstein and Kinzler [1] and Hanahan and Weinberg.[2] The model of Vogelstein and Kinzler emphasizes that cancer is ultimately a disease of damaged DNA, comprised of a series of genetic mutations that can transform normal cells to cancerous cells. The genetic mutations include inactivation of tumor suppressor genes and activation of oncogenes. Compared with cancers arising in the general population, individuals with a major inherited predisposition to cancer are born with inherited (i.e., germline) mutations in genes involved in cancer causation, giving them a head start on the pathway to cancer. Similar mutations would be expected to result in cancer progression among all individuals; however, in those without a major inherited cancer predisposition, the mutation would occur as a somatic mutation later during their lifetime.
The model of Hanahan and Weinberg focuses on the hallmark events at the cellular level that lead to a malignant tumor. In this model, the hallmarks of cancer include sustained angiogenesis, limitless replicative potential, evading apoptosis, self-sufficiency in growth signals, and insensitivity to antigrowth signals, leading to the defining characteristics of malignant tumors by giving them the ability to invade and metastasize. This model highlights the fact that malignant tumors arise and flourish within the environment of a whole organism. The tissue organizational field theory,[3] posits that carcinogenesis is better conceptualized at the level of tissues rather than cells. This theory is based on the dual premise that carcinogenesis is driven by defects in tissue organization and that all cells are inherently in a proliferative state.
Models of carcinogenesis such as these are purposefully simplistic but, nevertheless, illustrate that carcinogenesis requires a constellation of steps that often take place for decades.
The complexity of carcinogenesis is magnified when one considers that the specific details of the carcinogenic pathway described by these models would be expected to have unique characteristics for each anatomic site. Under these circumstances, the risk factors and clinical characteristics of malignancies exhibit considerable variation by anatomic site and by different tumor types within the same anatomic site. For these reasons, human cancer is really not a single disease but is a family of different diseases.
Risk Factors
The promise for cancer prevention is derived from observational epidemiologic studies that show associations between modifiable lifestyle factors or environmental exposures and specific cancers. For a few exposures, randomized controlled trials have tested whether interventions suggested by epidemiologic studies and leads based on laboratory research result in reduced cancer incidence and mortality.
Risk factors causally associated with cancer
Cigarette smoking/tobacco use
Decades of research have consistently established the strong association between tobacco use and cancers of many sites. Specifically, cigarette smoking has been established as a cause of cancers of the lung, oral cavity, esophagus, bladder, kidney, pancreas, stomach, cervix, and acute myelogenous leukemia. The body of epidemiologic evidence confirming these associations is substantial. Further support is demonstrated by the lung cancer death rates in the United States, which have mirrored smoking patterns, with increases in smoking followed by dramatic increases in lung cancer death rates and, more recently, decreases in smoking followed by decreases in lung cancer death rates in men. As a single exposure that is relatively easy to measure accurately, this extensive body of evidence has led to the estimation that cigarette smoking causes 30% of all cancer deaths in the United States. Smoking avoidance and smoking cessation result in decreased incidence and mortality from cancer. (Refer to the PDQ summaries on Lung Cancer Prevention; Lung Cancer Screening; and Cigarette Smoking: Health Risks and How to Quit for more information.)
Globally, infectious agents have been estimated to cause 18% of all cancer cases.[4] The burden of cancers caused by infections is much greater in developing nations (26%) than in developed nations (8%). Infection with an oncogenic strain of human papillomavirus (HPV) is considered a necessary event for subsequent cervical cancer, and vaccine-conferred immunity results in a marked decrease in precancerous lesions. Oncogenic strains of HPV are also linked with cancers of the penis, vagina, anus, and oropharynx. Other examples of infectious agents that cause cancer are hepatitis B and hepatitis C viruses (liver cancer), Epstein-Barr virus (Burkitt lymphoma), and Helicobacter pylori (gastric cancer). If an infectious agent is truly a cause of cancer, then efficacious anti-infective interventions would be expected in most instances to be effective cancer prevention interventions. This is the expectation with vaccines that protect against infection with oncogenic strains of HPV. An example in which this principle would not hold true is that in the setting of antibiotic resistance, the use of antibiotics may not prevent carcinogenesis from cancer-causing bacteria. (Refer to the PDQ summaries on Cervical Cancer Prevention; Cervical Cancer Screening; Liver (Hepatocellular) Cancer Prevention; and Liver (Hepatocellular) Cancer Screening for more information.)
Radiation is energy in the form of high-speed particles or electromagnetic waves. Exposure to radiation, primarily ultraviolet radiation and ionizing radiation, is a clearly established cause of cancer. Exposure to solar ultraviolet radiation is the major cause of nonmelanoma skin cancers, which are by far the most common malignancies in human populations.[5]
Ionizing radiation is radiation with enough energy to remove tightly bound electrons from their orbits, causing atoms to become charged or ionized. Ions formed in the molecules of living cells can go on to react with and potentially damage other atoms in the cell. At low doses (e.g., those associated with background radiation), the cells repair the damage rapidly. At moderate doses, the cells may be changed permanently or die from their inability to repair the damage. Cells changed permanently may go on to produce abnormal cells when they divide, and in some circumstances, these altered cells may become cancerous or lead to other abnormalities (e.g., birth defects). Defects in ability to repair damage caused by ionizing radiation may influence the impact of radiation exposure on cancer risk.
There is extensive epidemiologic and biologic evidence that links exposure to ionizing radiation with the development of cancer, and in particular, cancer that involves the hematological system, breast, lungs, and thyroid. The National Research Council of the National Academies, Committee to Assess the Health Risks from Exposure to Low Levels of Ionizing Radiation, the Biologic Effects of Ionizing Radiation VII report,[6] the most widely cited source on the topic, concluded after a comprehensive review of the medical literature that no dose of radiation should be considered completely safe, and attempts should be made to keep radiation doses as low as possible. In this report, three lines of evidence were cited documenting the association between ionizing radiation exposure and cancer. The first line of evidence comes from studies of the development of cancer among Japanese atomic-bomb survivors. Even at low doses of radiation, atomic-bomb survivors were at a significantly increased risk of developing cancer.[6] The second line of evidence comes from epidemiological studies of medically irradiated populations who were irradiated for both malignant and benign diseases. Following high-dose radiation therapy for malignant disease, the risk of secondary malignancy is high. The relatively common use of radiation for benign disease between 1940 and 1960 resulted in a substantial relative risk (RR) of developing cancer. The third line of evidence comes from an increased risk of cancer-specific mortality associated with exposure to medical ionizing radiation, for both the recipients of diagnostic x-rays and x-ray personnel.
The major sources of population exposure to ionizing radiation are medical radiation (including x-rays, computed tomography [CT], fluoroscopy, and nuclear medicine) and naturally occurring radon gas in the basements of homes. Limiting unnecessary CT scans and other diagnostic studies, as well as reducing radiation exposure doses, are important prevention strategies.[7,8] (Refer to the PDQ summaries on Breast Cancer Prevention; Breast Cancer Screening; Skin Cancer Prevention; and Lung Cancer Prevention for more information.)
Exposure to ionizing radiation has increased during the last 2 decades as a result of the dramatic increase in the use of CT. Exposure to ionizing radiation associated with CT is in the range where carcinogenesis has been demonstrated.[9]
The radiation doses associated with CT scans are in the range where an increased risk of cancer has been directly observed.[10] Exposure doses also varied as much as 20-fold across institutions for each study type. The risk of a future cancer depended on the age at exposure and sex of the patient, with risks decreasing with increasing age at exposure and women having a higher risk than men at each age group. For example, one radiation-induced cancer would occur among 270 women exposed to coronary angiography at age 40 years compared with one cancer in 595 exposed men. Among those aged 20 years having an abdomen-pelvis CT scan, 1 of 470 women and 1 of 620 men would develop a future radiation-associated cancer.[10] It has been estimated that the CT scans performed in the United States in 2007 could result in 29,000 (95% uncertainty limits of 15,000–45,000) cancers in the future. One-third of the cancers projected were caused by CT scans among individuals aged 35 to 54 years. This estimate was derived from risk models based on organ-specific radiation doses from national surveys, frequency of CT scans in 2007 by age and sex from survey and insurance claim data, and the National Research Council's "Biological Effects of Ionizing Radiation" report.[9] Repeat exposure to radiation from medical imaging will further increase cancer risk, as risk is proportional to exposure. One study found that half the subjects who were exposed to radiation from medical imaging underwent repeat imaging within 3 years. Overall, 0.2% of the nearly 1 million subjects followed up for 3 years received doses above 50 mSv.[11]
Medications that suppress the immune system, commonly used, for example, in patients undergoing organ transplantation, are associated with an increased cancer risk.[12]
Risk/protective factors with uncertain associations with cancer
Estimates concerning the potential contribution of diet to the population burden of cancer have varied widely. In contrast to the epidemiologic evidence on cigarette smoking and cancer, evidence for the influence of dietary factors and cancer is uncertain. An assessment of the potential role of diet entails measuring the net contribution of diets, comprising factors that may protect against cancer and other factors that may increase cancer risk. Measuring an individual's usual diet and its direct relevance to cancer risk also poses challenges.
An assessment of the overall evidence of diet in relation to cancer prevention published by the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) [13] was based on systematic reviews of the epidemiologic evidence. With respect to dietary factors that may protect against cancer, the greatest consistency was seen for fruits and nonstarchy vegetables. In the WCRF/AICR report, conclusions were reached that both fruits and nonstarchy vegetables were associated with "probable decreased risk" for cancers of the mouth, esophagus, and stomach. Fruits, but not nonstarchy vegetables, were also judged to be associated with "probable decreased risk" of lung cancer. Thus, even for the two dietary exposure classes that the current evidence suggests may have the greatest cancer prevention potential, the evidence was judged to be less than convincing and was applicable to only a few malignancies.
Examples in which the type of study design led to substantively different results further illustrate the complexities of the relationship between food and nutrient intake and human cancer risk. Observational epidemiologic studies (case-control and cohort studies) have suggested associations between diet and cancer development, but randomized trials of interventions provided little or no support. For example, on the basis of population-based epidemiologic data, high-fiber diets were recommended to prevent colon neoplasms. However, a randomized controlled trial of supplemental wheat bran fiber did not reduce the risk of subsequent adenomatous polyps in individuals with previously resected polyps. Ecologic, cohort, and case-control studies found an association between fat and red meat intake and colon cancer risk, but a randomized controlled trial of a low-fat diet in postmenopausal women showed no reduction in colon cancer. The low-fat diet did not affect all-cancer mortality, overall mortality, or cardiovascular disease.
Life-long dietary patterns or dietary intake during specific life stages may be important in inducing or preventing cancer but would not be detected by relatively short-term randomized clinical trials.
With respect to dietary factors that may increase cancer risk, the strongest evidence in the WCRF/AICR report was for drinking alcohol. The evidence was judged to be "convincing" that drinking alcohol increased the risk of cancers of the mouth, esophagus, breast, and colorectum (the latter in men). Further, the evidence was judged to be "probable" that drinking alcohol increased the risk of liver cancer and colorectal cancer (CRC) (the latter in women).
In relation to human cancer, diets reflect the sum total of a complex mixture of exposures, as demonstrated by the examples of fruit/vegetable intake and alcohol consumption. No dietary factors appear to be uniformly relevant to all forms of cancer. (Refer to the PDQ summaries on Breast Cancer Prevention; Breast Cancer Screening; Colorectal Cancer Prevention; and Lung Cancer Prevention for more information.)
Physical activity
A growing body of epidemiologic evidence suggests that people who are more physically active have a lower risk of certain malignancies than those who are more sedentary. In the WCRF/AICR report, the evidence was judged to be "convincing" that increased physical activity protects against CRC. The evidence was also judged to be "probable" that physical activity was associated with lower risk of postmenopausal breast cancer and endometrial cancer. As with the dietary factors described above, physical activity seems to play a more prominent role in selected malignancies. The inverse associations observed for selected malignancies make this a promising area for cancer prevention research, particularly since causal associations have not been established. The excess risk of many cancers seen with obesity, in combination with evidence to suggest that physical activity is inversely associated with at least a few cancers, raises the hypothesis that energy balance may influence cancer risk. (Refer to the PDQ summaries on Breast Cancer Prevention; Colorectal Cancer Prevention; and Endometrial Cancer Prevention for more information.)
Obesity is being increasingly recognized as an important cancer risk factor. The WCRF/AICR report concluded that obesity is convincingly linked to postmenopausal breast cancer and cancers of the esophagus, pancreas, colorectum, endometrium, and kidney. Furthermore, the WCRF/AICR report judged body fatness to be a probable risk factor for cancer of the gallbladder. A prospective study of nationally representative cohorts that examined obesity in relation to cancer mortality emphasizes that factors associated with cancer do not uniformly apply to all human malignancies. The study results revealed that obesity was associated with an increased risk of dying from obesity-associated malignancies, but obesity was not associated with overall cancer mortality.[14] If the associations between obesity and the cancers mentioned above are causal, which has yet to be established, the current increase in the prevalence of obesity in the United States and elsewhere poses a severe challenge to cancer prevention efforts. Furthermore, weight loss has yet to be shown to reduce risk of obesity-associated malignancies.[15] (Refer to the PDQ summaries on Breast Cancer Prevention; Colorectal Cancer Prevention; Endometrial Cancer Prevention; and Lung Cancer Prevention for more information.)
Interventions With Proven Benefits
Chemoprevention refers to the use of natural or synthetic compounds to interfere with early stages of carcinogenesis, before invasive cancer appears.[16] Chemoprevention trials have had some positive results. Daily use of selective estrogen receptor modulators (tamoxifen or raloxifene) for up to 5 years reduces the incidence of breast cancer by about 50% in high-risk women. Finasteride (an alpha-reductase inhibitor) lowers the incidence of prostate cancer; this finding was complicated by a greater cumulative incidence of high-grade cancers in the finasteride-versus-placebo-group. Further analysis suggests this was due to finasteride's shrinking the prostate but not the cancer, thereby increasing the ability to diagnose high-grade cancer without contributing to progression of prostate carcinogenesis. Dutasteride has also been shown to reduce the incidence of prostate cancer.[17] The impact of finasteride on prostate cancer mortality is uncertain.
Other chemoprevention candidates include COX-2 inhibitors and aspirin. COX-2 inhibitors inhibit the cyclooxygenase enzymes involved in the synthesis of proinflammatory prostaglandins. There is evidence to suggest that COX-2 inhibitors prevent colon and breast cancer, but the possibility of increased cardiovascular events may preclude their usefulness. In secondary analyses of pooled data from seven randomized placebo-controlled trials whose primary endpoints were vascular events, aspirin taken daily for 4 or more years was associated with an 18% reduction in overall cancer deaths (odds ratio, 0.82; 95% confidence interval [CI], 0.70–0.95).[18] Whether or not aspirin would have the same impact in reducing cancer incidence remains an open question, but the evidence for colon cancer suggests it may. Also, assessment of the risk-benefit profile needs to account for the effect of aspirin on the risk of bleeding. (Refer to the PDQ summaries on Breast Cancer Prevention; Colorectal Cancer Prevention; and Prostate Cancer Prevention for more information.)
Interventions With No Proven Benefit
Vitamin and dietary supplement use
Some have advocated vitamin and mineral supplements for cancer prevention. Many different mechanistic pathways for anticancer effects have been invoked. A commonly tested hypothesis is that antioxidant vitamins may protect against cancer, based on the premise that oxidative damage to DNA leads to cancer progression. Hence preventing oxidative DNA damage would prevent progression to cancer. However, the evidence is insufficient to support the use of multivitamin and mineral supplements or single vitamins or minerals to prevent cancer.[19] Beta carotene is an antioxidant that was thought to prevent or reverse smoking-related changes leading to lung cancer based on the results of several observational epidemiologic studies examining either dietary intake of beta carotene from food sources or blood levels as a marker of dietary intake.[13] However, two prospective placebo-controlled trials found that smokers and former smokers who received beta carotene supplements had increased lung cancer incidence and mortality.[20]
Other unanticipated adverse events have been documented for dietary supplement use. A meta-analysis of 11 randomized, double-blind, placebo-controlled trials of daily doses of calcium greater than or equal to 500 mg/day versus placebo documented that calcium supplements were associated with a significantly elevated risk of myocardial infarction (RR, 1.27; 95% CI, 1.01–1.59).[21] Dietary calcium intake has not been observed to be associated with an increased risk of myocardial infarction.[22] The discrepancy in findings between calcium in the diet versus high-dose supplementation raises questions about the value of dietary supplements compared with dietary intake. The Iowa Women's Health Study, an observational study that enrolled over 40,000 women aged 55 to 69 years in 1986, examined the association between dietary supplement use and mortality.[23] Statistically significant excess mortality risk was observed with the use of multivitamins, B6, folic acid, iron, magnesium, zinc, and copper. Only calcium users were associated with a statistically significant reduction in mortality rates compared with nonusers.
Research into the potential anticancer properties of vitamin and mineral supplements is ongoing, and the results continue to reinforce the lack of efficacy of vitamin supplements in preventing cancer. The extended follow-up results of the Selenium and Vitamin E Cancer Prevention Trial (SELECT) found a statistically significant excess risk of prostate cancer associated with vitamin E supplementation (400 IU/day of all rac-α-tocopherol acetate) compared with placebo (hazard ratio [HR], 1.17; 99% CI, 1.0004–1.36; P = .008). The absolute increase in risk of prostate cancer with vitamin E use was 1.6 per 1000 person-years. Selenium did not reduce the risk of prostate cancer (HR, 1.09; 99% CI, 0.93–1.27).[24]
The results of the Physicians' Health Study II demonstrated that supplementation with vitamin E and/or vitamin C had no benefit compared with placebo in preventing either prostate cancer incidence or total cancer incidence.[25]
The results of the Women's Antioxidant Cardiovascular Study indicated that, compared with placebo, supplementation with vitamin C, vitamin E, or beta carotene was not efficacious in reducing total cancer incidence.[26] In this same study, daily supplements containing folic acid, vitamin B6, and vitamin B12 were compared with placebo; this intervention was not efficacious in reducing the overall risk of developing cancer.[27] An exploratory analysis of pooled data from two Norwegian randomized controlled trials showed an increase in both cancer incidence and cancer death in patients treated with folic acid and vitamin B12 versus those receiving placebo or vitamin B6 alone.[28] (Refer to the PDQ summaries on Breast Cancer Prevention; Colorectal Cancer Prevention; Lung Cancer Prevention; Prostate Cancer Prevention; and Prostate Cancer Screening for more information.)
Vitamin D has also generated interest as a potential anti-cancer agent. Sources of vitamin D include cutaneous synthesis upon exposure to sunlight, dietary intake, and supplements. Evidence on the efficacy of vitamin D supplements with or without calcium in preventing cancer incidence is available as a secondary endpoint from randomized controlled trials, with a summary of the results from three trials providing evidence of lack of efficacy.[29] A fourth randomized controlled trial further corroborates this lack of cancer chemopreventive effect.[30] Presently, the overall body of experimental evidence in humans indicates that at the doses studied (range: 400–1,100 IU daily), vitamin D supplements do not reduce the overall risk of cancer. This is a topic of ongoing interest, and a large-scale randomized trial of vitamin D (2,000 IU/day) and marine omega-3 fatty acid is under way that includes cancer as a primary endpoint.[31]
None of the randomized controlled trials mentioned above studied multivitamin supplements as commonly taken by the general U.S. population; however, a separate arm of the Physician Health Study (PHS) II directly studied this question. In the PHS II, 14,641 male physicians were randomly assigned to receive either a daily multivitamin supplement or a placebo for a median of 11 years.[32] Multivitamin supplements were associated with an 8% relative decrease in cancer incidence (HR, 0.92; 95% CI, 0.86–0.998; P = .04). The overall reduction in cancer risk was more pronounced in men who had been diagnosed with cancer before the study began (HR, 0.66; 95% CI, 0.50–0.88) than in those with no history of cancer (HR, 0.95; 95% CI, 0.87–1.03), suggesting that the small benefit of multivitamins in reducing overall cancer incidence largely stemmed from the prevention of second primary cancers.
Environmental Exposures and Pollutants
The relationship between environmental pollutants and cancer risk has been of long-standing interest to researchers and the public. When estimates of the potential burden of cancer have been calculated for different classes of exposure, the factors described earlier, such as cigarette smoking and infections have represented much greater proportions of the cancer burden than have environmental pollutants. Nevertheless, some associations between environmental pollutants and cancer have been clearly established. Perhaps because the lung is most heavily exposed to air pollutants, many of the most firmly established examples of pollutants and cancer relate specifically to lung cancer, including secondhand tobacco smoke, indoor radon, outdoor air pollution, and asbestos for mesothelioma. Another environmental pollutant linked with cancer is highly concentrated inorganic arsenic in drinking water, which is causally associated with cancers of the skin, bladder, and lung. Many other environmental pollutants, such as pesticides, have been assessed for risk with human cancer, but with indeterminate results. There are challenging methodological issues to address in these studies, such as accurately measuring exposures for long periods, which often make it difficult to clearly establish an association between an environmental pollutant and cancer.
The list of topics considered above is not exhaustive. Other lifestyle and environmental factors known to affect cancer risk (either beneficially or detrimentally) include certain sexual and reproductive practices, the use of exogenous estrogens, and certain occupational and chemical exposures.
In this summary, factors were selected that appear to impact the risk of several types of cancer and that have been identified as being potentially modifiable. These include cigarette smoking, which has been conclusively linked with a wide range of malignancies; avoidance of cigarette smoking has been shown to reduce cancer incidence. Other potential modifiable cancer risk factors include alcohol consumption and obesity; physical activity is inversely associated with the risk of certain cancers. More research is needed to determine whether these associations are causal and whether avoiding risk behaviors or increasing protective behaviors would actually reduce cancer incidence.
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Description of the Evidence
Added text about the Physician Health Study II in which 14,641 male physicians were randomly assigned to receive either a daily multivitamin supplement or a placebo for a median of 11 years, finding that multivitamin supplements were associated with an 8% relative decrease in cancer incidence; overall reduction in cancer risk was more pronounced in men who had been previously diagnosed with cancer than in those with no history of cancer, suggesting that the small benefit of multivitamins in reducing overall cancer incidence largely stemmed from the prevention of second primary cancers (cited Gaziano et al. as reference 32).
This summary is written and maintained by the PDQ Screening and Prevention Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ NCI's Comprehensive Cancer Database pages.
If you have questions or comments about this summary, please send them to Cancer.gov through the Web site's Contact Form. We can respond only to email messages written in English.
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about cancer prevention. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
Any comments or questions about the summary content should be submitted to Cancer.gov through the Web site's Contact Form. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Levels of Evidence
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Screening and Prevention Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
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The preferred citation for this PDQ summary is:
National Cancer Institute: PDQ® Cancer Prevention Overview. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://cancer.gov/cancertopics/pdq/prevention/overview/HealthProfessional. Accessed <MM/DD/YYYY>.
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AUGUSTA, Ga. — The echoes amid the pines at Augusta National provided evidence Wednesday that the excitement of the 78th Masters was kicking up. The annual par-three tournament produced its usual crowd-pleasing theatrics — from the aces delivered by Matt Jones, Buddy Alexander and Mark O'Meara to the dialed-in, six-birdie victory claimed by Ryan Moore.
But the serious business begins Thursday with 97 players teeing it up and many eager to see just how wide open the doors to contending will be.
Finding an obvious favorite seems as difficult as ever, particularly with the absence of the world No. 1 Tiger Woods. Two-time major champion Rory McIlroy, ranked No. 9, was asked how many players have a legitimate shot at winning.
"I would say 70," McIlroy said. "There's a few past champions who play that might not be able to compete. There might be a few first-timers or a few amateurs that won't compete. But then you've got the rest."
So, yeah, it would be wise to keep a close eye on Adam Scott, the defending champion and current Las Vegas favorite.
And watch out for Henrik Stenson, No. 3 in the world and confident with his game.
But don't overlook Jason Day or Dustin Johnson or Matt Kuchar or, well, about five dozen other players who could make serious noise over the next four days.
A Tiger-less Masters — the first since 1994 — may lack some of the usual juice for TV ratings and casual fans, but it shouldn't be void of Augusta's trademark roars and weekend drama.
Reigning U.S. Open champion Justin Rose squeezed McIlroy's contender estimate, surmising there's a group of 15 players he would call "pretty strong favorites," a list Rose said had to include McIlroy, Lee Westwood, Ian Poulter and Sergio Garcia.
You also have to believe Phil Mickelson registers on that radar. And as Mickelson pushes to join Jack Nicklaus, Arnold Palmer and Woods as the only players with at least four green jackets (Nicklaus has six), he's a credible source for how things might unfold.
So just how wide open is it this week?
Mickelson said it would depend on the firmness and speed of the course, noting Tuesday that the greens were "getting back to Masters speed" after rain and thunderstorms Monday.
And if that persists, he noted, the class of potential victors shrinks significantly, to less than a dozen.
"Because if that happens," Mickelson said, "the subtleties and the nuances and the penalty of Augusta National will come through."
Across the board, players assert that Masters first-timers — numbering two dozen this year — will face a greater challenge acclimating to the awe, pressure and intricacies of the course.
By the same token, Mickelson said, previous Masters winners — he's one of nine in the field under 45 — gain a greater serenity for handling the week's roller coaster.
At least that was the case for Mickelson after his breakthrough win in 2004. Each subsequent trip to the Masters found him far more at ease.
"Unequivocally, yes," Mickelson said. "Absolutely. Because you want it as a player and as a kid growing up so bad to win the Masters and to be part of the history here that sometimes you get in your own way.
"Sometimes you force things when you shouldn't. Sometimes your mind goes where it shouldn't and starts seeing what you don't want to have happen. And it's sometimes difficult to control your own thoughts."
Finding peace of mind, along with control off the tee and around the greens, seems a prerequisite to winning. But as the tournament begins, the doorstep for potential contenders seems plenty crowded.
Twitter: @danwiederer


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From some quick research over the top forwards in the league, we see that, generally, they haven't really shown an ability to consistently convert shots on target (SoT) into goals above the league average rate. The league average hovers around the 33% mark for forwards and 28% mark for midfielders, with very few players able to exceed those totals each year (and even then that would be expected purely based on statistical variance). In short then, whether it seems intuitive or not, if a player's SoT are turning into goals at a very high rate, we must expect some regression in the coming weeks.
Now then, a quick side bar as to what we mean by this, as this term is often misused and the difference can appear trivial but is actually key (long term readers will know that I too made this mistake once myself so this isn't the rant of a classically trained statistician, outraged that the masses are misusing his darling tools, more a warning message for those trying to use statistical analysis a bit more in their weekly decision making).
The first point is that regression accounts for what should happen in the future and has no interest in correcting for past anomalies. Take, for example, the basketball player with a career free throw percentage of 80% who hasn't suffered any significant ageing or reasons for decline/improvement. If, after half a season he's taken 100 free throws and made 70 of them (70%) what do we expect from his second half? To get his year end average back up to his career 80% rate he'd have to go 90/100 to give him 160/200 for the year, or 80%. But, on what basis will he suddenly perform above his career rate? Averages and regression care not for your 82 game sample size (or, in our case, 38 games) and thus it's simply not true to say we expect his season rate to regress all the way back to his 80% conversion rate. Instead, we expect the rest of the season to see him convert at his true talent level of 80%.
Let's look at a football example for clarity. Through eleven gameweeks, Wayne Rooney has hit the target 12 times and scored twice (17%). To get back to that 34% mark noted above, Rooney would have to convert six of his next 12 shots to give him the eight goals needed from 24 shots (33%), but that's not what we expect. We expect him to convert at that same 33% rate so four of his next 12 shots would be goals. This may sound pedantic but just in this crude example it's the difference between Rooney scoring four and six goals over a relatively short time frame and can obviously have a large impact on our forecasts.
We can however say that if player x is getting a lot of shooting opportunities and continues to do so, he should convert at a better rate than he has to date and thus appears undervalued by the market. It's a subtle distinction but an important one that needs making every now and again.
The second, and somewhat trivial point to make is that regression goes both ways so Rooney's conversion rate can regress up to the mean, rather than always having to cite the Steve Fletchers of the world whose conversion rate looks unsustainable and thus is pegged fro downwards regression.
Okay then, onto some data.
The below chart plots players' total shots per 90 minutes on the x axis against their goals per shot on target percentage on the y axis. The lines mark the league average for both measures for all forwards this year (the G/SoT% includes several years' data):
The bottom left if harder to be excited about as while they should convert at a higher rate in the future, their overall lack of chances may ultimately mean it doesn't make too much difference and thus they're tough to own. This is particularly true of someone like P Cisse, as while he appears to have been unfortunate in converting his chances, even at a league average rate he would have scored only one more goal, clearly not enough to justify his lofty price tag.
The top left quadrant is the real concern as this group appears to have overachieved versus league average in terms of G/SoT% so unless you believe they have a genuine skill to continue to do so, we're expecting some regression in the coming weeks and months. Fletcher is the stand out man here whose 63% conversion rate is clearly unsustainable, even for a player who has shown an ability to exceed the league average over the years. This data needs to be taken in context as someone like Crouch could still offer some value if he converted at a lower rate but care should be taken before we anoint anyone from this group as great fantasy options.
The top right quadrant is a mixed bag and one you'd label with 'caution' rather than a full on 'warning'. Take Berbatov for example. With five goals from just 11 SoT, his 45% rate looks a touch high and of his next 11 SoT we'd expect only 3.6 to hit the back of the net. However, for a cheaper player who comes with job security, genuine talent and who's getting more than the average total shots per game, that rate would still potentially make him good value and forecast him for a further 14 goals if he played every game from here on (1.57 SoT/90minutes x 27 games x 33% conversion rate). The caution more comes within players like Suarez or even the great van Persie who are getting a lot of hype and, while excellent prospects, might be getting a touch overvalued based on their production to date. Again, it's all relative as using the same calculation as for Berbatov, van Persie would still be on pace for another 13 goals even at a league average rate, but that is substantially less than some are foreseeing.
One final note here. You might wonder why I'm plotting SoT% against total shots per 90 minutes rather than only shots on target. It's a valid point but I've used total shots as my concern with only using SoT is that the sample sizes are so small that extrapolating them can get messy quickly. I'm more comfortable therefore to add the required note that not every shot is created equal, rather than relying on Benteke's six SoT and drawing too many inferences (with 24 total shots and 22 SiB one can expect a better on target rate in the future too).
As with pretty much every piece of analysis I post, other than the final model forecasts, the above should not be taken as 'sell player x' or 'buy player y' but more a way of identifying players to look closer at, one way or another. It doesn't, for instance, factor in strength of schedule played or upcoming, assist potential and a myriad of other factors, so it shouldn't be taken out of context. I like it's visual simplicity though and it's nice way to identify players and think "I didn't realise player x was benefiting from high shot conversion, maybe I should look closer at his stats".


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Purchasing Policy
Our goal at Jazz Events Limited t/a Jazz Events, is to make your purchasing experience easy, efficient and fair, so we can get your products or tickets to you as quickly as possible. The following purchase policies are designed to ensure your satisfaction and understanding of the purchase process on our websites – this purchase policy incorporates our Terms of Use by this reference.
If you do not agree with any part of our terms and conditions please do not place an order.
Jazz Events Ltd sells its own products as well as products on behalf of promoters and other companies, which means we do not necessarily set the product prices. Policies set forth by our clients, such as venues and promoters, prohibit us from issuing exchanges or refunds after a purchase has been made, or for lost, stolen, damaged or destroyed tickets. When you receive your tickets, please keep them in a safe place. Please note that direct sunlight or heat can sometimes damage tickets. Tickets purchased on our websites may be subject to a per ticket service charge and a non-refundable per order processing fee. When purchasing tickets on our websites, you may be limited to a specified number of tickets for each event. This amount is indicated on the order tickets page and its verified with every transaction. This policy is in effect to discourage unfair ticket buying practices.
We aim to dispatch tickets as soon as possible. We are not able to necessarily be specific with exact dates of dispatch - this is dependant on each type of event although are generally dispatched no sooner than 6 weeks before an event. Occasionally, for some events, the tickets may not be dispatched until very close to the event date. Tickets will be sent using the method selected at checkout, if an insured delivery option is selected you will be sent a tracking url when they have been dispatched. If your tickets have not arrived five days before the show or, if you are travelling, five days before you leave, please contact us. Please include your booking confirmation code, the full name and address submitted with the booking, and details of the event.
Event cancellations and amendments
Occasionally, events are cancelled or postponed by the promoter or venue for a variety of reasons. If the event is cancelled, please contact us for information on receiving a refund from the responsible party. If the event was moved or rescheduled, the venue or promoter may set refund limitations. Contact us for exact instructions.
For information about a purchase you've made please email email@example.com quoting your order id.
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As part of our ticket purchasing policy we regret that we can not cancel, exchange, refund or transfer tickets unless the event in question has been either cancelled or rescheduled.
If during your booking, you provided us with a valid email address or phone number, we will automatically attempt to contact you to inform you of the refund or exchange procedures if it is cancelled or rescheduled.
Cancelled Events - For the majority of cancelled events (please see individual events policies where appropriate), Jazz Events Ltd will issue a full refund automatically without you needing to return the tickets. Refunds are normally issued within 28 days of Jazz Events Ltd receiving notification of the cancellation and you should see the appropriate credit on your card statement.
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If you wish to receive a refund for rescheduled events, you will need to return all tickets in your original booking to us at the address below. Please ensure that all tickets in the booking are safely returned to us. Failure to do so will cause a delay or prevent a refund being issued. If some members of your party still wish to attend please enclose a note informing us of this and we'll be in touch to rebook these for you.
The address to return tickets to is:
Jazz Events
Ticket Refunds
The Old School
Higher Kinnerton
If you have not yet received your tickets, please contact us with the request including details of your booking.
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Other useful Information - If you did not purchase your ticket from Jazz Events but another seller, you will need to go back to them direct for instructions on obtaining your refund.
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For all intents and purposes the term 'Ticket' is used here to describe a method by which to gain entry to an event. It may be a paper based ticket, wristband, email, e-ticket etc.
Your ticket is issued subject to the Rules and Regulations of the venue, event organiser and promoter. Full details are available on each of our event websites.
Please check your ticket(s) as mistakes cannot always be rectified.
While we try and ensure that all prices on our website are accurate, errors may occur. If we discover an error in the price of tickets you have ordered, we will inform you as soon as possible and give you the option of reconfirming your order at the correct price (and credit or debit your account as applicable) or cancelling your order. If we are unable to contact you, you agree that we may treat the order as cancelled. If you choose to cancel after you already paid the incorrect ticket price for the tickets, you will receive a full refund from us.
It is the responsibility of the ticket holder to ascertain whether an event has been cancelled and the date and time of any re-arranged event. If an event is cancelled or scheduled, we will use reasonable endeavours to notify ticket holders of the cancellation once we have received the relevant authorisation from the event organiser. Please note that we cannot guarantee that ticket holders will be informed of such cancellation before the date of the event.
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We regret that unless paragraph 17 applies, tickets cannot be exchanged or refunded after purchase. Jazz Events Ltd cannot be held responsible for any tickets, which are lost or stolen reserves the right to cancel ticket bookings which it reasonably suspects to have been fraudulently.
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Tickets are generally dispatched no sooner than 6 weeks before an event. Occasionally, for some events, the tickets may not be dispatched until very close to the event date.
There can be a number of reasons for delays of this sort. Typically, this is due to the tickets for an event needing to be printed on special stock, where the promoter, event organiser or the venue have insisted that we use stock supplied by them, instead of our own. This can result in delays if we have to wait for this stock to arrive before we can commence fulfilling orders.
If your tickets have not arrived five days before the show or, if you are travelling, five days before you leave, please email firstname.lastname@example.com. You will need to include your booking confirmation code, the full name and address submitted with the booking and details of the event.
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Delivery Charge
The price you pay is the same price or less than what we pay to send your order.
Our delivery service is fully insured and trackable from the moment it is dispatched.
You will receive an email confirming delivery date and time with the option of rescheduling delivery to a time more convenient.
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Booking Fee is applied as a percentage of your order total excluding delivery, currently 4%.
These charges pay for our credit/debit card processing services, merchant fees, distribution network, installation and maintenance of computer hardware and software, telephone support, labour and all the other costs associated with a ticket transaction.
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It's rare for us to be able to offer group booking discounts. However, if you have a large group of people who want to attend specific event please firstname.lastname@example.com including the number you require to book and the event you wish to attend.
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Many people make a living as a video game beta tester. What this means is that they get paid to find bugs in beta versions of upcoming video games. The reason for this is quite simple. For the game company, it is financially beneficial to pay professional game testers to thoroughly test a game and all of it's features so that it meets consumer expectations, and so that it is the best quality that can possibly be achieved.Generally speaking, here's how you get started: you contact a few game developers & game companies and you persuade them to hire you as a beta tester. In a nutshell, that's basically what needs to be done. Sounds simple, right? Unfortunately though, it is much easier said than done.The best way to "persuade" these companies and developers is by showing them your overwhelming amount of expertise in the video game industry; things like your skill level as a gamer, your ability to accurately document glitches and bugs, your ability to follow instructions to the letter, and so on and so forth. Occasionally, it means making them an offer they can't refuse, such as testing a few video games for free (GULP). Why test them for free? Well, to get your foot in the door and show them that your a dedicated tester that just loves to play video games. Remember, they are looking for true blue game testers that can be remarkably efficient when testing video games.When you begin landing video game tester jobs, you are generally sent a free copy in the mail as well as a questionnaire and "report" to fill out. Typically, you'll be given an assignment to complete that either involves beating the entire game from start to finish or playing one level over & over & again. It really just depends on the information the developer needs.Once you get your assignment, it's time to go to work. Complete the assignment, fill out the form or questionnaire, and then mail it back to the game developer. It's important to be fast with your video game testing and, at the same time, you must be professional as well. With that being said, get the work done quickly but make sure it is done accurately and without mistakes. After they have received your report, you will be issued a check in the mail. Typically, the checks are paid every other week to the video game beta tester.To be a good game tester, you have to have an eye for detail, as well as the ability to play certain parts of a game repeatedly. At the same time, you have to be able to properly document errors and glitches that you find, which will be done via the bug reporting form.When it comes to getting started and finding your first video game tester job, there are two paths you can walk. Path 1: You go out on your own and do everything completely by yourself without any help from anyone or anything. Path 2: You research and read through the numerous resources & testing guides in order to find a "tried, tested, and proven" approach that others have achieved success with. Obviously, the path you choose is up to you, but personally, I'd go with option 2. Why? Because video game testing is an industry made up of teams, not solo gamers. Plus, why would you want to "reinvent the wheel" when you can just improve upon it?There you have it; a quick & simple guide on how to get paid as a video game beta tester.
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text: Share: December 20, 2009 Climate Change The recent hacking of e-mails at the Climatic Research Unit at the University of East Anglia Center — one of the world's foremost institutions for the study of climate change — offers a disconcerting view of how modern science is done. If the truth is manipulated by scientists, then who are we to believe? However, looking beneath the rough surface waters of scientific politics, the science of climate change — global warming — is as solid as ever. It is reassuring to note that despite the limited progress made in Copenhagen, the delegates found little reason to reopen the debate about the reality of the science behind global warming. Since the late 1800s, we've known carbon dioxide acts as a greenhouse gas to warm our planet. We know that without a natural level of carbon dioxide and water vapor (the other major greenhouse gas) in the atmosphere, our planet would be below the freezing point of water and higher life forms would not exist. We know carbon dioxide has been rising in Earth's atmosphere since the dawn of the Industrial Revolution and that the long-term average temperature of planet Earth has risen at least 1 degree Celsius during the past century. We don't see anything resembling these trends and conditions in the records of the past 10,000 years. Some delegates might have preferred to blame the recent temperature rise to external causes — something other than human activities — but the case for doing so is very weak. No studies show a significant increase in solar output during the same period, and satellite measurements suggest no large trends in the reflectivity of our planet to incoming radiation. The laws of physics show even small increases in the concentration of carbon dioxide and other greenhouse gases emitted by humans and added to the low, natural background concentrations in the atmosphere will translate to a warmer atmosphere. Climate, like daily weather, is variable from year to year, so it is sometimes difficult to see and assess the long-term trends amid the annual variability. An analogy is valuable: a few cold days in March don't suggest we should throw out our expectations of an overall warming trend each year between January and July in the northern hemisphere. Warmest years on record The warmest year on record was 1998; the last few years have been slightly cooler. Still, the eight years from 2000-08 are among the 10 warmest years on record. Barring a huge volcanic eruption, I would bet 2020 will be warmer than 1998, and the trend in global temperature will rise every decade in the 21st century. Bets are not science, but smart bets are informed by science. So it is reassuring the delegates in Copenhagen were able to ignore the foolishness in East Anglia. What was said in those e-mails was stupid and wrong, but it is clear a fair and open scientific process continued unabated. The antics of a few do not disprove the work of the overwhelming majority of the world's climate change scientists, who have shown that rapid global warming is real, because of humans. It is dangerous to our health, our food supply, our cities and our national security — in short, our future. It is unclear what all the posturing and political deals in Copenhagen accomplished, but our nation and the world need to get on with the job of reducing the emissions of carbon dioxide and other greenhouse gases to the atmosphere. Share: Feature Global warming is real - despite email hoax › December 20, 2009


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I am an early childhood consultant and writer and I offer lectures, workshops and mentoring around the world. Teachers and parents alike rave about their experiences and want me back for more!
Here is a song I recorded with a few friends. RISE UP
Watch an hour long talk on Creative Discipline from Santa Barbara in March 2017
Watch a 2 minute video to learn more about my approach.
I write Chamakanda Blogs which gives support for teachers and parents in connecting with and understanding young children. You might benefit by subscibing.
I was a kindergarten teacher at the Santa Cruz (California) Waldorf School for 24 years. My mixed-age kindergarten included children from 3-years-old until they were ready for first grade. Since the mid-1990's, I have given workshops, lectures and courses on many themes for various institutions and groups around the U.S. including Rudolf Steiner College and various schools in Indonesia and China. For the past 8 years I've been on the faculty of WISC(Waldorf Institute of Southern California). I'm a former Board member of WECAN (Waldorf Early Childhood Association of North America) as well as former editor of Gateways, the bi-annual newsletter of WECAN, and my many articles have been published in Gateways and various other publications. My first book, Connecting With Young Children: Educating the Will, was published in 2011. Conscious Parenting: A Guide to Living with Young Children and What's the Story: Storytelling as a Path Toward Living Happily Ever After were published in 2015.
I am available for teacher and parent mentoring and coaching, as well as workshops, lectures and courses on various themes including:Storytelling and Storymaking as Nourishment for the Young ChildThe Senses as the Windows to Connection with the WorldThe World of the Young ChildWalking, Speaking and ThinkingBeyond Sticks and CarrotsNurturing Imagination Through Creative PlayCircle Time with Young ChildrenInner Work/Self Development for teachers and parentsChild StudyCultural Diversity and Waldorf Education - Inclusiveness as a Practice
Check out this interview with me from The Wonder of Childhood
"Chamakanda was a very good friend to the children."
My blog is found at
Special thanks to Leslye Lawrence for everything!