Older men with early-stage prostate cancer are not taking a big risk if they keep an eye on the disease instead of treating it right away, suggests the largest study to look at this issue since PSA tests became popular.
Only 10 percent of the 9,000 men in the study who chose to delay or skip treatment had died of prostate cancer a decade later. The vast majority were alive without significantly worsening symptoms or had died of other causes.
Even the 30 percent who eventually sought treatment were able to delay it for an average of 11 years.
“It is important news,” said Dr. Otis Brawley, chief medical officer of the American Cancer Society. “It may persuade some middle-of-the-roaders that we are overtreating this disease,” and that PSA testing may be amplifying the problem, he said. The PSA blood test to help detect tumors has been widely used since the 1990s.
Grace Lu-Yao of Robert Wood Johnson Medical School in New Jersey led the study and will report results at a cancer conference later this week in San Francisco.
Whether to treat prostate cancer is one of the biggest medical dilemmas today. The disease is the most common cancer in American men – about 220,000 cases will be diagnosed this year – but most tumors grow so slowly they never threaten lives. There is no sure way to tell which tumors will.
PSA tests can help find tumors many years before they cause symptoms, but routine screening of men at average risk of the disease is not recommended, because there is no proof it saves lives.
Prostate cancer treatments are tough, especially on older men. Many men are left with sexual or bladder control problems. Some doctors instead recommend “watchful waiting” to monitor signs of the disease and treat only if they worsen, but smaller studies have given conflicting views of the safety of that approach.
The new study looked at the natural course of the disease in men who chose that option. It is the first involving so many older men – half were over 75 – and so many whose tumors were found through PSA tests.
Using the federal government’s cancer database, researchers studied 9,018 men diagnosed from 1992-2002 with early-stage prostate cancer who did not get surgery, radiation or hormone therapy for at least six months. Most never got any treatment at all.
A decade later, 3 percent to 7 percent of those with low- or moderate-grade tumors (rated by how aggressive the cells appear) had died of prostate cancer, versus 23 percent of those with high-grade tumors. Overall, prostate cancer killed 10 percent of them.
“The great majority of patients … are going to die of something else,” so most older men with early-stage tumors could delay treatment, Lu-Yao said.
“If people are younger or have more advanced disease, I wouldn’t say this is a safe option,” but most cases are diagnosed in men 68 or older, and most are early stage, she noted.
The National Cancer Institute paid for the study. It is not the final word – that usually comes from studies where similar groups of patients are randomly assigned to get one treatment or another, and the results compared. But absent that kind of evidence, this large study “does show that a large number of men do well with no initial treatment and indeed with no treatment long term,” Brawley said.
Dr. Howard Sandler, a radiation and prostate specialist at the University of Michigan, agreed, but cautioned, “there are exceptions to every rule,” and some very active, healthy older men may do better having treatment right away, along with older men who have higher-grade tumors.
Earlier this month, a scientific review published in the Annals of Internal Medicine concluded that evidence was too thin to recommend treatment over watchful waiting, or one treatment over another. Studies do show that prostate cancer surgery mostly helps men under 65, said Dr. Timothy Wilt of the Minneapolis VA Center for Chronic Disease Outcomes Research, who led the review.
The new study shows that for men older than that, “observation is a very reasonable approach,” he said. “Many men do quite well for a long period of time with no treatment.”
The cancer conference is sponsored by the American Society of Clinical Oncology and several other groups.
Although routine PSA testing is not recommended for all men, the cancer society does advise giving men information and the option to have it starting at age 50. Screening is recommended starting at age 45 for men with a family history of prostate cancer and for black men, because of their higher risk of the disease.
February 17th, 2008
ALMOST 3000 men die of prostate cancer each year in Australia and an estimated 18,700 are diagnosed with the disease. With baby boomers now reaching their 50s and 60s, those figures are set to increase.
So, is enough being done to reduce the emotional toll that surgery can take on men?
Not surprisingly, sexual dysfunction tops the list of the most common post-operative side effects that men complain about in a study published in a recent issue of Urologic Nursing.
Significantly, it is urinary dysfunction issues that are troubling men most and many are not emotionally prepared for these complications, says lead author Bryan Weber, assistant professor in the University of Florida College of Nursing.
Professor Weber said, given the various treatment options for prostate cancer, men who undergo radical prostatectomy might initially decide the risk of physical dysfunction was worth the benefit of improved survival. However, many did not know what to expect in the months after surgery.
“The effects of this treatment are quite immediate and can lead to depression and frustration,” she said.
The authors evaluated 72 men six weeks after they underwent prostatectomy, measuring their physical function and assessing whether they had urinary, bowel and sexual dysfunction. Measurement of self-confidence, social support and uncertainty about their disease and treatment were also recorded.
“Almost immediately after treatment, men may experience depression, awkwardness and emasculation, which will have a great effect on their quality of life.”
Over half the men reported low to moderate social support, indicating that many of the topics proved embarrassing for them to discuss with others. The level of social support was significantly related to urinary problems, revealing those with incontinence may need additional support compared to those with greater bladder control.
Asked by Consult if greater access to formal counselling services was needed for this group of patients, Professor Weber agreed.
“Yes – men have indicated that little information is provided pre and post surgery that highlights available options in dealing with treatment side effects.
“After an initial diagnosis of prostate cancer, men may be so focused on eradicating the disease that they don’t realise the effects the treatment will have on their quality of life, both for them and their families.”
Physical side effects of prostate cancer treatment limit daily activities and may interfere with a man’s sense of masculinity and self-confidence. Urinary incontinence requires the use of pads which can create concern about leakage and odour, Professor Weber said.
“Sexual dysfunction interferes with a man’s sense of self and may limit the relationship he has with his significant other.”
Professor Weber suggests clinicians assess men and their support systems, identify changes in physical function that may occur as a result of treatment and direct them to products and services designed to help them cope with the immediate effects of sexual dysfunction and urinary and bowel incontinence.
Men also need to be made aware of the numerous medications to ease sexual dysfunction, their cost and potential side effects.
“Education and counselling should be provided to these men to better inform and prepare patients for the physical side effects they are likely to experience postoperatively.
“Since we know that men are less likely to rely on support groups or be more embarrassed to discuss these items with family and friends, it’s even more vital for health-care professionals to stress these issues and include options for patients.
“Men need to be introduced to different options, make choices and regain control over their lives.”
Source
Urologic Nursing
February 7th, 2008
An important paper on the interaction of antioxidants and radiation therapy was recently published in the International Journal of Cancer. Interestingly, despite the significance of its findings, this study has received virtually zero attention from the scientific community or the media.
As background, in April 2005, Isabelle Bairati, MD, PhD, and her colleagues at the Hôtel-Dieu de Québec Research Centre and the Université Laval completed a ten-year study on the interaction of antioxidants and radiation therapy. This was hailed as the first placebo-controlled, double-blind, randomized trial assessing the effect of supplementation with antioxidant vitamins during radiation therapy. The study concluded that supplements of synthetic beta-carotene (30 mg per day) or alpha tocopherol (400 IU per day) had a harmful effect on cancer patients. In particular, the authors claimed that the cancer recurrence rate was 40 percent higher among patients who had been randomly assigned to the supplementation arm of the trial. They therefore called on patients and physicians to exert caution in using antioxidants until new evidence could be provided by future trials.
Kedar Prasad, PhD, and other proponents of the concurrent use of antioxidants during cancer treatment criticized the Bairati paper. They were disappointed that Bairati and colleagues had used ordinary alpha tocopherol as their choice of vitamin E when Prasad’s previous work had shown that it was not just alpha tocopherol but alpha tocopherol succinate that had the anticancer efficacy. They also felt that natural forms of the vitamin were more effective than synthetic, drug store-type vitamins. But, by and large, the medical world accepted the Bairati trial as definitive proof that antioxidants interfered with radiation therapy. Word spread like wildfire in oncology circles, confirming a long-held belief that antioxidants interfered with standard cancer treatments such as radiation and chemotherapy. The take away message, as stated in a Université Laval press release, was that “Supplements May Speed Up Development of Cancer.” Advocates of complem! entary and alternative medicine (CAM) were confounded by this large and impressive study.
But now the other shoe has dropped.
In December 2007, Dr. Bairati and her Québec colleagues published a major modification of their previous conclusions. Further analysis revealed, they said, that the danger of synthetic antioxidants was limited to one particular sub-population: cigarette smokers – specifically, those who continued to smoke during radiation treatment. The authors analyzed the outcome in 540 patients who had been given radiation for head and neck cancers. During the follow-up period, 119 patients had a recurrence of their disease and 179 died. Smokers were the group with the worst prognosis. However, astonishingly, smoking in the period leading up to or following radiation therapy did not modify the effects of the two supplements. It was only smoking during the course of radiation therapy that led to a statistically significant increase in the risk of a recurrence. It was a large enough increase to skew the statistics for the group as a whole, leading to the erroneous conclus! ion that antioxidants interfered with radiotherapy in the general patient population.
Statistically, increased risk is generally expressed as a “hazard ratio” (abbreviated HR). In this study, current smokers had an HR of 2.41 for recurrence, in other words more than double the chance of a recurrence compared to the rest of the patient population. The HR for death from any cause was a similar 2.26. But the hazard ratio for dying of their initial head and neck cancer was a whopping 3.38 in patients who got radiation, smoked and also received a single synthetic antioxidant.
“These results could best be explained by the hypothesis that the combined exposures reduced the efficacy of radiation therapy,” Bairati and her colleagues now say. “Particular attention should be devoted to prevent patients from both smoking and taking antioxidant supplements during radiation therapy” (Meyer 2007).
According to the National Cancer Institute, 85 percent of head and neck cancers are linked to tobacco use. (Alcohol use further exacerbates this trend.) This has been widely known for years, and so it is shocking that there are still people so hopelessly addicted to tobacco that they not only continue to smoke after they’ve been diagnosed with head and neck cancer but continue to smoke right through their radiation therapy. It was in this subset of particularly unhealthy individuals that antioxidants were associated with an increased risk of disease progression. As Bairati and colleagues suggest, such individuals should definitely not compound their problems by then taking a synthetic antioxidant.
But the more important lesson for patients and practitioners is that antioxidants do NOT generally interfere with the effects of radiation therapy, as was previously suggested. They do NOT increase the risk of a recurrence, of death from head and neck cancer, or of overall mortality in the average patient. In this updated study, the harmful effect of synthetic antioxidants was entirely limited to those relatively few tobacco-addicted patients who continued to smoke during their radiation therapy. Thus, the major premise underpinning oncologists’ condemnation of antioxidants during radiation therapy has crumbled, although few seem to have noticed so far.
References:
Bairati I, Meyer F, Jobin E, et al. Antioxidant vitamins supplementation and mortality: a randomized trial in head and neck cancer patients. Int J Cancer. 2006;119:2221-4.
Bairati I, Meyer F, Gélinas M, et al. Randomized trial of antioxidant vitamins to prevent acute adverse effects of radiation therapy in head and neck cancer patients. J Clin Oncol. 2005;23:5805-5813.
Bairati I, Meyer F, Gélinas M, et al. A randomized trial of antioxidant vitamins to prevent second primary cancers in head and neck cancer patients. J Natl Cancer Inst. 2005;97:481-488.
Meyer F, Bairati I, Fortin A, et al. Interaction between antioxidant vitamin supplementation and cigarette smoking during radiation therapy in relation to long-term effects on recurrence and mortality: A randomized trial among head and neck cancer patients. Int J Cancer. 2007 Dec 4;122(7):1679-168.
February 4th, 2008
New evidence from the Million Women Study finds increased risk for six cancers not previously associated with high BMI.
Increased body-mass index (BMI) raises the risk for adenocarcinoma of the esophagus, endometrial cancer, kidney cancer, and postmenopausal breast cancer in women. But researchers have not conclusively associated high BMI with the risk for other cancers in women. In this large cohort study, investigators in the U.K. recruited 1.2 million women aged 50 to 64 without cancer (except for nonmelanoma skin cancer) between 1996 and 2001. The team assessed the effect of BMI (adjusted for 10 clinical factors) on the incidence of and mortality risk for 17 of the most common types of cancer.
Mean follow-up was 5.4 years. The researchers confirmed the association between increasing BMI and the cancers previously associated with obesity. They also found significant associations between increasing BMI and the risks for leukemia, multiple myeloma, non-Hodgkin lymphoma, pancreatic cancer, ovarian cancer, and — in premenopausal women only — colon cancer. In the 10 cancers that were positively associated with increasing BMI, the risks for cancer mortality were similar to those for cancer incidence. Increasing BMI did not affect risks for malignant melanoma, colorectal cancer, and cancers of the stomach, cervix, bladder, or brain. Increasing BMI decreased risks for lung cancer and squamous-cell carcinoma of the esophagus.
Comment: These sound findings suggest that more cancers are linked to obesity than previously thought. Since the worldwide obesity epidemic shows no signs of abating, we need new approaches to help patients to avoid weight gain, which could prevent many cancers as well as cardiovascular events.
Published in Journal Watch Cardiology January 9, 2008
February 4th, 2008
Overweight and obesity were associated with increased risk for many types of cancer.
The prevalence of obesity is increasing in developed countries. Almost one quarter of women in England are reported to be obese (BMI >30), and about one third are overweight (BMI, 25.0–29.9), whereas in the U.S., one third are obese and almost two thirds are overweight or obese. In the Million Women Study, English and Scottish women (age range, 50–64) self-reported demographic characteristics (BMI, age, geographic region, socioeconomic status, age at first delivery, parity, smoking, alcohol intake, physical activity, menopausal status, and use of hormone therapy) from 1996 through 2001. Investigators analyzed these data in relation to cancer incidence and mortality as reported in the National Health Service central registers.
Increasing BMI was associated with a significant positive trend in relative risk for adenocarcinoma of the esophagus (RR, 2.38); however, risk for squamous carcinoma of the esophagus decreased (RR, 0.26). Melanoma and stomach, colorectal, cervical, bladder, and brain cancers showed no variation in overall risk in relation to BMI. Premenopausal women (but not postmenopausal women who never used HT) had increased risk for colorectal cancer (RR, 1.61) or melanoma (RR, 1.62) with increasing BMI. However, increasing BMI was associated with a decreased risk for breast cancer in premenopausal women (RR, 0.86) and an increased risk in postmenopausal women (RR, 1.36). Endometrial cancer risk increased with BMI in both premenopausal (RR, 1.77) and postmenopausal (RR, 3.98) women. Other cancers for which risk increased with BMI were kidney cancer, leukemia, multiple myeloma, pancreatic cancer, non-Hodgkin lymphoma, and ovarian cancer. Lung cancer incidence decreased with increasing BMI (RR, 0.74); excluding smokers did not substantially alter the results. Overall, for 10 out of 17 specific cancer types examined, increasing BMI was associated with increased incidence and mortality.
Comment: The results of this large prospective study substantiate another potential health risk associated with being overweight or obese: cancer. According to these data, almost half of endometrial cancer and esophageal adenocarcinoma cases can be attributed to being overweight or obese. Menopausal status affects the relation between BMI and cancer risk, not only for hormonally related breast and endometrial cancers but also for colorectal cancer and melanoma. Women at risk for particular cancers because of personal or family history might be especially motivated by these findings to attain or maintain a BMI below 24.9.
Reeves GK et al. Cancer incidence and mortality in relation to body mass index in the Million Women Study: Cohort study. BMJ 2007 Dec 1; 335:1134.
January 30th, 2008
Some oncologists contend that patients undergoing chemotherapy and/or radiation therapy should not use food supplement antioxidants and other nutrients. Oncologists at an influential oncology institution contended that antioxidants interfere with radiation and some chemotherapies because those modalities kill by generating free radicals that are neutralized by antioxidants, and that folic acid interferes with methotrexate. This is despite the common use of amifostine and dexrazoxane, 2 prescription antioxidants, during chemotherapy and/or radiation therapy.
To assess all evidence concerning antioxidant and other nutrients used concomitantly with chemotherapy and/or radiation therapy, the MEDLINE® and CANCERLIT® databases were searched from 1965 to November 2003 using the words vitamins, antioxidants, chemotherapy, and radiation therapy. Bibliographies of articles were searched. All studies reporting concomitant nutrient use with chemotherapy and/or radiation therapy (280 peer-reviewed articles including 62 in vitro and 218 in vivo) were indiscriminately included.
Results: Fifty human clinical randomized or observational trials have been conducted, involving 8,521 patients using
beta-carotene; vitamins A, C, and E; selenium; cysteine; B vitamins; vitamin D3; vitamin K3; and glutathione as single agents or in combination.
Conclusions: Since the 1970s, 280 peer-reviewed in vitro and in vivo studies, including 50 human studies involving 8,521 patients, 5,081 of whom were given nutrients, have consistently shown that non-prescription antioxidants and other nutrients do not interfere with therapeutic modalities for cancer. Furthermore, they enhance the killing of therapeutic modalities for cancer, decrease their side effects, and protect normal tissue. In 15 human studies, 3,738 patients who took non-prescription antioxidants and other nutrients actually had increased survival.
(Altern Ther Health Med. 2007;13(1):22-28.)
January 29th, 2008
Extracts of black raspberries might protect Barrett’s esophagus patients against oesophageal cancer and also might shift premalignant oral lesions from progression to squamous cell carcinoma (SCC) back toward normal differentiation, Ohio State researchers reported at the AACR’s 6th Annual International Conference on Frontiers in Cancer Prevention Research.
Laura Kresty, PhD, assistant professor in the Ohio State University Cancer Chemoprevention Program, Columbus, reported that 58% of 20 Barrett’s oesophagus patients who ate a freeze-dried preparation of black raspberries daily for 26 weeks had a significant decline in mean urinary levels of 8-isoprostane, an indicator of global oxidative stress and DNA damage (abstract B34).
“Many of these patients had suffered from gastroesophageal reflux for a decade,” Dr. Kresty said at a press briefing. “Injury from acids results in generation of reactive oxygen species, which then cause damage. We tested this preparation in an attempt to decrease the ongoing oxidative stress in these patients.”
The take-home message, she said: “We need to increase fruit and vegetable consumption, and patients can do something to modify some pathways that lead to cancer.”
She recommended that the lyophilized black raspberry formulation be further studied in a randomized, placebo-controlled phase II trial.
An oral gel
Susan Mallery PhD, DDS, and her colleagues took a different approach. Her group tested a highly concentrated, bioadhesive black raspberry gel as a topical treatment for precancerous oral lesions (abstract B35). Dr. Mallery is a professor in the Department of Oral Maxillofacial Surgery and Pathology at Ohio State University’s College of Dentistry.
“The major problem with patients who have these premalignant lesions is recurrent disease that appears postop despite clear surgical margins,” Dr. Mallery said. “Black raspberries are full of anthocyanins, potent antioxidants that give the berries their rich, dark color, and our findings show that these compounds may have a role in silencing precancerous cells.”
This phase I/II trial included 20 patients with oral intraepithelial neoplasia (IEP) lesions and 10 normal controls. “There are lots of sugars and carbohydrates in black raspberries, and we wanted to control for risk of iatrogenic fungal infection,” Dr. Mallery said.
The “very motivated” participants applied the 10% (by weight) dried black raspberry gel four times a day to the target sites. Each patient served as his or her own internal control. None were smokers. The study continued for 42 days, the approximate amount of time necessary for 1½ cycles of surface epithelial turnover.
At the end of the study, Dr. Mallery said that comparison of pre- and post-treatment biopsies showed improvement (a decrease in lesion grade) in 35% of the patients, stable disease in 45%, and an apparent increase in lesion grade in 20%, but she suspects the latter is due to sampling bias.
More detailed examination showed decreased loss of heterozygosity (suggesting that cells were returning to a normal genetic state) and upregulation of cell differentiation markers.
Dr. Mallery said that the next step should be a longer (3-month), placebo-controlled, multicenter study. She also recommended further evaluation of berry gels for chemoprevention of oral IEP.
A more colorful diet
Navindra Seeram, PhD, MRSC, said that Dr. Mallery’s method is “a great approach” to many of the problems of taking a food into drug use because it overcomes the problem of degeneration of active components during the digestive process.
“The active compounds need to be in surface contact with the oral epithelium. If you are eating this berry, it spends a miserably short time in contact with the oral mucosa. This bioadhesive topical appears to be much better,” said Dr. Seeram, assistant professor in the Department of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island, Kingston.
Dr. Seeram recently reviewed the cancer preventive potential of blackberry, black raspberry, blueberry, cranberry, red raspberry, and strawberry extracts (J Agric Food Chem 54:9329-9339, 2006).
A problem solved
Dr. Seeram also said that the lyophilized black raspberry preparation used in the study reported by Dr. Kresty solves another problem by permitting preparation of a large amount of standardized powdered extract that can be used in clinical trials.
He said that the studies reinforce the fact that “we should be eating more colors in our diet, particularly more berries.”
Cranberries are effective against urinary tract infections, Dr. Seeram said, and blueberries have anti-neurodegenerative effects.
“And now we see that black raspberries seem to have some anticancer activity. We need a rainbow of colors in our diets,” Dr. Seeram said.
Oncology News
January 2008 • Volume 17 Number 1
January 25th, 2008
Tumorigenesis or carcinogenesis is a multi-step process that is induced primarily by carcinogens leading to the development of cancer. Extensive research in the last few years has revealed that regular consumption of certain fruits and vegetables can reduce the risk of acquiring specific cancers. Phytochemicals derived from such fruits and vegetables, referred to as chemopreventive agents include genistein, resveratrol, diallyl sulfide, S-allyl cysteine, allicin, lycopene, capsaicin, curcumin, 6-gingerol, ellagic acid, ursolic acid, silymarin, anethol, catechins and eugenol. Because these agents have been shown to suppress cancer cell proliferation, inhibit growth factor signaling pathways, induce apoptosis, inhibit NF-κB, AP-1 and JAK-STAT activation pathways, inhibit angiogenesis, suppress the expression of anti-apoptotic proteins, inhibit cyclooxygenase-2, they may have untapped therapeutic value. These chemopreventive agents also have very recently been found to reverse chemoresistance and radioresistance in patients undergoing cancer treatment. Thus, these chemopreventive agents have potential to be used as adjuncts to current cancer therapies.
written by: Thambi Doraia and Bharat B. Aggarwalb
Cancer Letters
Volume 215, Issue 2, 25 November 2004, Pages 129-140 doi:10.1016/j.canlet.2004.07.013
January 24th, 2008
From the perspective of curative and preventive therapy, we have lost the war against cancer. Deaths from cancer are stable or increasing at 570,000 deaths in 2005.1 One in 3 people will get cancer in his or her lifetime.1 Given the average latent period of 30 years for solid tumours,2 17 million Americans are walking around with cancer that is somewhere along the continuum from initiation of a cancer cell to clinical manifestation of the disease.3 Clinical cancer care focuses almost entirely on eradicating the tumour through chemotherapy, radiation, or surgery, none of which addresses cancer early in the continuum of its natural history.
Emerging novel treatments, including vaccines and immunotherapy, hold promise. But are they enough? Are we focusing on late stage curative care and missing assessments and interventions that could change the landscape of cancer treatment and help those 17
million Americans prevent or reverse latent cancers?
In my oncology rotation in medical school, I asked my professor what percentage of cancers was related to diet and was shocked
by his answer—70%. Is there a different approach to cancer that allows for late stage interventions but asks a different set of questions based on a different set of assumptions? Rather than asking what is the right treatment for cancer, we might ask what genetic, lifestyle, and environmental factors trigger the development of cancer and what clinical strategies we can use to alter its trajectory.
Consider this fact: 16% of all cancers are new primary cancers in patients who have had cancer, not recurrences.4 This means that people who have cancer are more likely to get a second and independent cancer. Why is this so? Is it because of the toxic effects of the treatment of the first primary cancer, or is it something else? This is a compelling area for research and inquiry.
Another fertile area for inquiry and therapy might be based on an analysis of the etiology and mechanisms of cancer and how they influence the core physiological systems that determine our health. This might be called milieu therapy, or regulation therapy.
Rather than treating cancer per se, might we enhance immune function and surveillance through dietary and lifestyle changes, nutrient or phytonutrient therapies? Are there mechanisms that are common to most cancers, such as inflammation, altered hormone metabolism, oxidative stress, and impaired detoxification? With our current understanding of the mechanisms of cancer development and progression, we can reframe our treatment approach to include interventions that support the biological systems
that, when dysfunctional, allow the initiation, progression, and acceleration of cancer. The solution will come only through a systems approach. We have seen the flaws in reductionistic models of intervention, such as the CARET trials.5 Hundreds of millions of dollars were spent following the reductionist model of inquiry rather than a systems approach, with predictable and, unfortunately, negative
outcomes.6 Epidemiological evidence that vegetable consumption reduced cancer risk led to the assumption that betacarotene
was the “active agent.” This led to trials on thousands of smokers at risk for lung cancer using doses 100 times greater than what is normally consumed. The outcome of increased cancer risk among the treatment group should not have been a surprise— giving high doses of an antioxidant in an oxygen-rich environment (the lung), heated by smoke, led to increased oxidative
stress and the promotion of large amounts of reactive oxygen species, which facilitate cancer initiation and progression. A high dose of any one antioxidant can upset the equilibrium, leading to an uncontrolled free-radical chain reaction. This is what
happened in the CARET study. The lesson to be learned is not that vitamins don’t prevent cancer, but that single interventions in a complex physiology are likely to fail. The future of cancer care lies not in finding the best cocktail of chemotherapeutic agents, but in customizing treatments to correct patients’ individual imbalances. We must use our understanding of mechanisms of disease and physiologic and metabolic balance to design a treatment approach that uses diet, lifestyle, nutrient, phytonutrient, mind-body, and pharmacological
interventions to restore normal function and optimize gene expression patterns in the key systems that modulate cancer risk.
REFERENCES
1. American Cancer Society. Cancer facts & figures 2005. Available at: http://www.cancer.org/docroot/STT/content/STT_1x_Cancer_Facts__Figures_2005.asp. Accessed December 9, 2006.
2. O’Shaughnessy JA, Kelloff GJ, Gordon GB, et al. Treatment and prevention of intraepithelial neoplasia: an important target or accelerated new agent development. Clin Cancer Res. 2002;8(2):314-346.
3. Wattenberg LW. Prevention—therapy—basic science and the resolution of the cancer problem. Cancer Res. 1993;53(24):5890-5896.
4. National Cancer Institute. Tumors included in prevalence estimates. Available at: http://srab.cancer.gov/prevalence/methods.html. Accessed December 10, 2006.
5. Omenn GS, Goodman GE, Thornquist MD, et al. Risk factors for lung cancer and for intervention effects in CARET, the Beta-Carotene and Retinol Efficacy Trial. J Natl Cancer Inst. 1996;88(21):1550-1559.
6. Burton GW, Ingold KU. Beta-Carotene: an unusual type of lipid antioxidant. Science. 1984;224(4649):569-573.
Mark A. Hyman, MD, is the editor-in-chief of Alternative Therapies in Health and Medicine. ALTERNATIVE THERAPIES, jan/feb 2007, VOL. 13, NO. 1 (Altern Ther Health Med. 2007;13(1):10.)
January 22nd, 2008
Each year, the American Cancer Society (ACS) estimates the number of new cancer cases and deaths expected in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival based on incidence data from the National Cancer Institute, Centers for Disease Control and Prevention, and the North American Association of Central Cancer Registries and mortality data from the National Center for Health Statistics. This report considers incidence data through 2003 and mortality data through 2004. Incidence and death rates are age-standardized to the 2000 US standard million population. A total of 1,444,920 new cancer cases and 559,650 deaths for cancers are projected to occur in the United States in 2007. Notable trends in cancer incidence and mortality rates include stabilization of the age-standardized, delay-adjusted incidence rates for all cancers combined in men from 1995 through 2003; a continuing increase in the incidence rate by 0.3% per year in women; and a 13.6% total decrease in age-standardized cancer death rates among men and women combined between 1991 and 2004. This report also examines cancer incidence, mortality, and survival by site, sex, race/ethnicity, geographic area, and calendar year, as well as the proportionate contribution of selected sites to the overall trends. While the absolute number of cancer deaths decreased for the second consecutive year in the United States (by more than 3,000 from 2003 to 2004) and much progress has been made in reducing mortality rates and improving survival, cancer still accounts for more deaths than heart disease in persons under age 85 years. Further progress can be accelerated by supporting new discoveries and by applying existing cancer control knowledge across all segments of the population.
Jemal A, Siegel R, Ward E, Murray T, Xu J, Thun MJ.
Cancer Occurrence, Department of Epidemiology and Surveillance Research, American Cancer Society, Atlanta, GA, USA.
CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66.
January 20th, 2008
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