Research - Cancer General
Diterpenoid Tanshinones, the extract from Danshen (Radix Salviae Miltiorrhizae) induced apoptosis in nine human cancer cell lines
ObjectiveTo identify the active anti-tumor constituents in the extract from Danshen (Radix Salviae Miltiorrhizae) and investigate the mechanisms underlying the actions.
MethodsFirst, we introduced a two-step counter-current chromatography to extract the therapeutically active diterpenoid, tanshinone from Danshen (Radix Salviae Miltiorrhizae). The cholecystokinin (CCK-8) method was used to evaluate the inhibitory effect of diterpenoid tanshinone in liver cancer QGY-7703, lung cancer PC9, lung cancer A549, gastric cancer MKN-45, gastric cancer HGC-27, colon cancer HCT116, myeloma cellU266/RPMI8226, and human breast cancer MCF-7 in vitro. Fluorescence staining was used to observe the cytotoxicity ofditerpenoid tanshinone on PC9 cells. The Western blot was used to detect apoptosis-related protein poly ADP-ribose polymerase (PARP), cysteinyl aspartate specific proteinase3/9 (caspase3/9), and cleaved-cysteinyl aspartate specific proteinase3/9 (cleaved-caspase3/9). The endoplasmic reticulum stress-related activating transcription factor 4 (ATF4), phosphorylated eukaryotic initiation factor 2α (p-eIF2α), and phosphorylated jun amino-terminal kinase (p-JNK), and caspase-12 were also analyzed using the Western blot.
ResultsDiterpenoid tanshinone inhibited the nine human tumor cell lines, with an IC50 of 4.37–29 μg/mL, with the PC9 and MCF-7 displaying the lowest values. Fluorescence staining showed a lethal effect of diterpenoid tanshinone on PC9 cells. The Western blot showed that the expression of caspase3/9 protein and ATF-4 protein decreased gradually. However, the PARP, cleaved-caspase 3/9 and the expression of p-eIF2 α, P-JNK, and caspase-12 increased gradually, in a dose-dependent fashion.
ConclusionWe successfully introduced a two-step counter-current chromatography method to extract diterpenoid tanshinone, and demonstrated its antitumor activity. Diterpenoid tanshinone can induce apoptosis in nine human cancer cell lines.
Source : Journal of Traditional Chinese Medicine
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Investigation of 2 Types of Self-administered Acupressure for Persistent Cancer-Related Fatigue in Breast Cancer Survivors A Randomized Clinical Trial
Suzanna M. Zick, ND, MPH; Ananda Sen, PhD; Gwen K. Wyatt, PhD, RN; Susan L. Murphy, PhD; J. Todd Arnedt, PhD; Richard E. Harris, PhD
IMPORTANCE Fatigue is a common and debilitating late-term effect of breast cancer that is associated with poor sleep and decreased quality of life, yet therapies remain limited. Acupressure has reduced fatigue in previous small studies, but rigorous clinical trials are needed.
OBJECTIVES To investigate if 6 weeks of 2 types of self-administered acupressure improved fatigue, sleep, and quality of life vs usual care in breast cancer survivors and to determine if changes were sustained during a 4-week washout period. DESIGN,
SETTING, AND PARTICIPANTS Phase 3 randomized, single-blind, clinical trial conducted from March 1, 2011, through October 31, 2014. Women were recruited from the Michigan Tumor Registry.
INTERVENTIONS Randomization (1:1:1) to 6 weeks of daily self-administered relaxing acupressure, stimulating acupressure, or usual care.
MAIN OUTCOMES AND MEASURES The primary outcome was change in the Brief Fatigue Inventory score from baseline to weeks 6 and 10. Secondary analyses were sleep (Pittsburgh Sleep Quality Index) and quality of life (Long-Term Quality of Life Instrument).
RESULTS A total of 424 survivors of stages 0 to III breast cancer who had completed cancer treatments at least 12 months previously were screened, and 288 were randomized, with 270 receiving relaxing acupressure (n = 94), stimulating acupressure (n = 90), or usual care (n = 86). One woman withdrew owing to bruising at the acupoints. At week 6, the percentages of participants who achieved normal fatigue levels (Brief Fatigue Inventory score <4) were 66.2% (49 of 74) in relaxing acupressure, 60.9% (42 of 70) in stimulating acupressure, and 31.3% (26 of 84) in usual care. At week 10, a total of 56.3% (40 of 71) in relaxing acupressure, 60.9% (42 of 69) in stimulating acupressure, and 30.1% (25 of 83) in usual care continued to have normal fatigue. At neither time point were the 2 acupressure groups significantly different. Relaxing acupressure, but not stimulating acupressure, showed significant improvements in sleep quality compared with usual care at week 6, but not at week 10. Only relaxing acupressure significantly improved quality of life vs usual care at weeks 6 and 10.
CONCLUSIONS AND RELEVANCE Both acupressure arms significantly reduced persistent fatigue compared with usual care, but only relaxing acupressure had significant effects on sleep quality and quality of life. Relaxing acupressure offers a possible low-cost option for managing symptoms.
Source : JAMA Oncology
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Alcohol consumption as a cause of cancer
Background and aims There is increasing research evidence about the causal role of alcohol in cancer, accompanied by unclear and conflicting messages in the media. This paper aimed to clarify the strength of the evidence for alcohol as a cause of cancer, and the meaning of cause in this context.
Methods Recent epidemiological and biological research on alcohol and cancer was reviewed and summarized, drawing upon published meta-analyses identified from the Medline database and the archives of the International Agency for Research on Cancer. More recent epidemiological studies not included in these publications were also reviewed. A brief description of the nature of causal inference in epidemiology was used to frame discussion of the strength of the evidence that alcohol causes cancer, and contrast this with the case for a protective association of alcohol with cardiovascular disease.
Results The usual epidemiological understanding of a cause is a factor that increases the incidence of a condition in the population. In the context of a body of epidemiological evidence of an association of alcohol consumption with a disease, the inference that it is a causal association requires alternative explanations of the observed finding to be judged unlikely. Even without complete knowledge of biological mechanisms, the epidemiological evidence can support the judgement that alcohol causes cancer of the oropharynx, larynx, oesophagus, liver, colon, rectum and breast. The measured associations exhibit gradients of effect that are biologically plausible, and there is some evidence of reversibility of risk in laryngeal, pharyngeal and liver cancers when consumption ceases. The limitations of cohort studies mean that the true effects may be somewhat weaker or stronger than estimated currently, but are unlikely to be qualitatively different. The same, or similar, epidemiological studies also commonly report protection from cardiovascular disease associated with drinking but a high level of scepticism regarding these findings is now warranted.
Conclusions There is strong evidence that alcohol causes cancer at seven sites in the body and probably others. Current estimates suggest that alcohol-attributable cancers at these sites make up 5.8% of all cancer deaths world-wide. Confirmation of specific biological mechanisms by which alcohol increases the incidence of each type of cancer is not required to infer that alcohol is a cause.
Source : Journal Addiction
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Sugar and Cancer: Mitigating the Affects of Diet on Cancer
Food speaks to our genes; its message or signal can turn the immune system on or off. Consumption of a high carbohydrate or sugar diet can increase risk of cancer. The affect of diet on cancer risk and prevention were explained in an oral presentation at the 2nd AnnualOncology Nurse Advisor Navigation Summit.1
Epigenetics is the variations caused by external modifications to DNA such as environment, exercise, stress, meditation, spirituality, and diet, explained Sharon Meyer, DiplON, CNC, of Integrative Nutrition. Sugar or glucose feeds cancer, although not directly. Insulin chaperones sugar or glucose into the cells. Insulin docks onto an insulin receptor on the cell surface enabling sugar/glucose to enter the cell, where the mitochondria convert it into energy. Too much sugar increases blood sugar and insulin levels. Over time, healthy cells are no longer able to receive sugar. Insulin receptors become sensitive to insulin and no longer respond; this is insulin resistance.
Cancer cells are poor energy metabolizers. Their surfaces are covered with insulin receptors that continually chaperone glucose into the cancer cells. Therefore, even when healthy cells become insulin resistant, cancer cells continue to accept and metabolize sugar. Insulin releases glucose into the cancer cells, it goes through the nucleus causing an epigenetic effect of turning on genes that prompt cell division. Meyer described this effect as “Like a foot on a gas pedal, stimulating cancer growth.”
“If the foods you ate could turn off the expression of your cancer genes, and turn on tumor suppressor genes, what would you have for dinner?” asked Meyer. Her answer: Vegetables. A lot of them and a variety of them. “Eat from the rainbow,” advised Meyer.
Vegetables are high in phytochemicals, which protect plants from the environment, stressors, sun, toxins, and more; humans need phytochemicals to be healthy. They are major communicators to our genes. They support detoxification, boost immunity, improve heart health, promote healthy estrogen metabolism, stimulate apoptosis, reduce inflammation, and feed the gut bugs (microbiome).
Other components of a healthy diet include fats and oils and protein. Healthy choices for fats and oils include foods such as avocadoes, fish (eg, sardines, herring, salmon), nuts and seeds, nut butters, butter, and ghee. Extra virgin olive oil, flaxseed oil, coconut oil/butter/milk, nut oils (eg, walnut, hazelnut, macadamia), and avocado oils are better choices.
Protein sources include eggs, fish, poultry, beef, lamb, and lean pork. Whole-milk dairy and whey protein are other recommendations. Animal protein should be free-range, pasture raised, or organic, and wild fish.
In closing, Meyer's advice for patients with cancer is to eat appealing foods when they can, and not to stress over their diet. “Plenty of time to clean up later!”
1. Meyer S. Nutrition & Cancer. Oral presentation at: Oncology Nurse Advisor Navigation Summit; April 7-9, 2016; Orlando, FL.
Source : Oncology Nurse Advisor
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Bioactive Components of Chinese Propolis Water Extract on Antitumor Activity and Quality Control
Hongzhuan Xuan,1,2 Yuehua Wang,2 Aifeng Li,3 Chongluo Fu,2 Yuanjun Wang,2 and Wenjun Peng1
To understand the material basis of antitumor activity of Chinese propolis water extract (CPWE), we developed a simple and efficient method using macroporous absorptive resin coupled with preparative high performance liquid chromatography and separated and purified eleven chemical components (caffeic acid, ferulic acid, isoferulic acid, 3,4-dimethoxycinnamic acid, pinobanksin, caffeic acid benzyl ester, caffeic acid phenethyl ester, apigenin, pinocembrin, chrysin, and galangin) from CPWE; then we tested the antitumor activities of these eleven components using different human tumor cell lines (MCF-7, MDA-MB-231, HeLa, and A549). Furthermore, cell migration, procaspase 3 level, and reactive oxygen species (ROS) of effective components from CPWE were investigated. Our data showed that antitumor activities of the eleven components from CPWE were different from each other. CPWE and its effective components induced apoptosis by inhibiting tumor cell migration, activating caspase 3, and promoting ROS production. It can be deduced that the antitumor effects of propolis did not depend on a single component, and there must exist “bioactive components,” which also provides a new idea for Chinese propolis quality control.
Previous studies from our group reported the biological activities of Chinese propolis [15–17] and the present study was the first one to investigate the effective components on antitumor activity in CPWE. Four phenolic acids (caffeic acid, ferulic acid, isoferulic acid, and 3,4-dimethoxycinnamic acid) had little cytotoxicity on four tumor cell lines; the other seven constituents (pinobanksin, caffeic acid benzyl ester, caffeic acid phenethyl ester, apigenin, pinocembrin, chrysin, and galangin) obviously decreased four tumor cells’ proliferation, although the inhibitory effects of the seven components were different from each other, which indicated that the antitumor effects of CPWE did not depend on a single component, and at least the seven effective components might be “bioactive components” of antitumor activity. Admittedly, there must be other effective components needed to be studied further.....
Source : Evidence Based Complementary and Alternative Medicine
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Forest adjuvant anti-cancer therapy to enhance natural cytotoxicity in urban women with breast cancer: A preliminary prospective interventional study
Studies have shown both significantly diminished natural cytotoxicity and immunosuppression in breast cancer patients after standard anti-cancer treatments. Therefore, an integrative approach employing adjuvant therapy in addition to current treatments is required to enhance immunoactivation. This preliminary prospective interventional study aimed to assess the feasibility of forest therapy as an adjuvant to enhance natural cytotoxicity.
Methods This was a feasibility study of 11 volunteer women aged 25–60 years with stage III breast cancer. All subjects were exposed to daily forest therapy for 14 days whilst living in accommodation in a forest. Interventions included a relaxing daily 2-h morning walk (3 miles), free time tailored to subjects interest, group interaction and prepared meals based on nutritional standards. Outcome measures included natural killer (NK) cell populations and levels of perforin and granzyme B.
Results Data from all participants were analysed. The mean volume of NK cells increased from 319.4 μL in the city to 444.6 μL in the forest after forest therapy (p < 0.01). The mean level of perforin increased from 216.9 pg/mL in the city to 344.9 pg/mL in the forest and then further increased to 463.2 pg/mL after subjects returned to the city (p < 0.02). The mean level of granzyme B increased from 4.4 pg/mL in the city to 11.2 pg/mL in the forest and then further increased to 20.2 pg/mL after subjects returned to the city (p < 0.02).
Conclusions This study demonstrates the potential of forest therapy as an adjuvant anti-cancer therapy after standard treatments. A definitive trial with a control group should now be performed with larger sample sizes and long-term follow-up periods to confirm the feasibility and potential therapeutic effectiveness of this approach.
Source : European Journal of Integrative Medicine
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Gas Chromatography-Mass Spectrometry Analysis of Ulva fasciata (Green Seaweed) Extract and Evaluation of Its Cytoprotective and Antigenotoxic Effects
Idania Rodeiro,1 Sitlali Olguín,2 Rebeca Santes,2 José A. Herrera,3 Carlos L. Pérez,4 Raisa Mangas,3 Yasnay Hernández,1 Gisselle Fernández,4 Ivones Hernández,1 Sandra Hernández-Ojeda,2 Rafael Camacho-Carranza,2 Ana Valencia-Olvera,2 and Jesús Javier Espinosa-Aguirre2
The chemical composition and biological properties of Ulva fasciata aqueous-ethanolic extract were examined. Five components were identified in one fraction prepared from the extract by gas chromatography-mass spectrometry, and palmitic acid and its ethyl ester accounted for 76% of the total identified components. Furthermore, we assessed the extract’s antioxidant properties by using the DPPH, ABTS, and lipid peroxidation assays and found that the extract had a moderate scavenging effect. In an experiment involving preexposition and coexposition of the extract (1–500 µg/mL) and benzo[a]pyrene (BP), the extract was found to be nontoxic to C9 cells in culture and to inhibit the cytotoxicity induced by BP. As BP is biotransformed by CYP1A and CYP2B subfamilies, we explored the possible interaction of the extract with these enzymes. The extract (25–50 µg/mL) inhibited CYP1A1 activity in rat liver microsomes. Analysis of the inhibition kinetics revealed a mixed-type inhibitory effect on CYP1A1 supersome. The effects of the extract on BP-induced DNA damage and hepatic CYP activity in mice were also investigated. Micronuclei induction by BP and liver CYP1A1/2 activities significantly decreased in animals treated with the extract. The results suggest that Ulva fasciata aqueous-ethanolic extract inhibits BP bioactivation and it may be a potential chemopreventive agent.
Source : Evidence Based Complementary and Alternative Medicine
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Combinations of 'safe' chemicals may increase cancer risk, study suggests
Lots of chemicals are considered safe in low doses. But what happens when you ingest a little bit of a lot of different chemicals over time?
In some cases, these combinations may conspire to increase your risk of cancer, according to a new report.
“Many [chemicals] have the possibility, when they are combined, to cause the initiation of cancer,” said Hemad Yasaei, a cancer biologist at Brunel University in England, one of the authors of the report. “They could have a synergistic or enhanced effect.”
This is not the way regulators typically think about cancer risk when they evaluate a compound’s safety.
Normally, they test an individual chemical on laboratory animals, exposing them to progressively smaller amounts until it no longer causes malignant tumors to grow. Then they take that dose, determine the equivalent for humans, and apply what is called a “margin of safety” by declaring that some small fraction of that low dose is safe for people.
The big assumption driving the margin of safety is that a smaller amount of a chemical is less dangerous than a larger amount. (Think of the familiar axiom, “The dose makes the poison.”)
But that’s not true for all chemicals, experts say. Some chemicals, such as those that mimic hormones, may actually be more dangerous at lower doses because the human body is exquisitely attuned to respond to minute amounts of natural hormones such as estrogen and testosterone.
And regulators haven’t required testing of mixtures of chemicals at all.
“Everybody had been working under the assumption that when we tested these chemicals individually and they didn’t cause cancer below a certain dose, then we’re fine to spray that particular pesticide on your breakfast cereal before it goes into the box,” said Leroy Lowe, president of Canadian nonprofit Getting to Know Cancer and leader of the report published this week by the journal Carcinogenesis.
The new report raises questions about whether this approach is adequate.
Lowe has been making this point for years. One of his organization’s primary aims is to change the way regulators assess the health effects of chemical mixtures.
Humans are exposed to about 80,000 man-made chemicals over their lifetimes, experts say. These chemicals are in the foods we eat, the water we drink and the air we breathe.
“We live in a chemical soup,” said toxicologist Linda Birnbaum, director of the National Institute of Environmental Health Sciences, who was not involved in the new study.
The research team — a coalition of 174 researchers from 28 countries — set out to determine whether mixtures of these chemicals, at the very tiny concentrations found in the environment, could plausibly trigger the formation of cancerous tumors. They focused on 85 particular chemicals that were impossible to avoid in modern life, that were likely to disturb biological function and were not thought to pose cancer risks at the very low doses that people tend to ingest them.
“We were only looking at the tip of the iceberg,” Yasaei said.
The researchers scoured the scientific literature to understand how each of these chemicals could affect 10 important processes that are essential to cancer development. Among them: tumor-promoting inflammation, resistance to cell death and the formation of new blood vessels to feed malignant cells.
In addition, they categorized whether each of the chemicals exerted biological effects at very low doses to which humans are ubiquitously exposed. (These doses are so small that they tend to be measured in parts per million or parts per billion.)
Of the 85 chemicals researchers examined, 50 were found to affect cancer-causing processes in the body, even at very low doses.
These 50 everyday chemicals included bisphenol A (used in manufacturing plastics), triclosan (often found in hand sanitizer and anti-bacterial soap) and atrazine (a commonly used herbicide). Since each of these chemicals affects different processes that could lead to cancer — bisphenol A makes cells less sensitive to signals to stop reproducing, for example, while atrazine encourages inflammation — it’s plausible that consuming mixtures of these chemicals is riskier than consuming any one individually.
“To me, it’s not a surprise,” said Birnbaum of the NIEHS. Scientists know that small effects from many chemicals can add up to cause other diseases, she said. For instance, chemicals known as endocrine disruptors can lead to neurological, immune system and reproductive problems, among others.
Considering the safety of individual chemicals is a lot like looking at the trees, but missing the forest, Birnbaum said. When doing research to determine chemical safety, “we’ve got to start thinking more about what reality is,” she said.
This could mean sweeping changes in rules about the levels of chemicals considered safe in drinking water, food, and air.
“I’d like to see regulators and policy makers start looking at the totality of the exposure instead of one chemical at a time,” she said.
Source : LA Times
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Caramel Color in Soft Drinks and Exposure to 4-Methylimidazole: A Quantitative Risk Assessment
- Tyler J. S. Smith,
- Julia A. Wolfson,
- Ding Jiao,
- Michael J. Crupain,
- Urvashi Rangan,
- Amir Sapkota,
- Sara N. Bleich,
- Keeve E. Nachman
Caramel color is added to many widely-consumed beverages as a colorant. Consumers of these beverages can be exposed to 4-methylimidazole (4-MEI), a potential carcinogen formed during its manufacture. California’s Proposition 65 law requires that beverages containing 4-MEI concentrations corresponding to exposures that pose excess cancer risks > 1 case per 100,000 exposed persons (29 μg 4-MEI/day) carry warning labels. Using ultrahigh-performance liquid chromatography-tandem mass spectrometry, we assessed 4-MEI concentrations in 12 beverages purchased in California and a geographically distant metropolitan area (New York) in which warning labels are not required. In addition, we characterized beverage consumption by age and race/ethnicity (using weighted means calculated from logistic regressions) and assessed 4-MEI exposure and resulting cancer risks and US population cancer burdens attributable to beverage consumption. Data on beverage consumption were obtained from the National Health and Nutrition Examination Survey, dose-response data for 4-MEI were obtained from the California Environmental Protection Agency Office of Environmental Health Hazards Assessment, and data on population characteristics were obtained from the U.S. Census Bureau. Of the 12 beverages, Malta Goya had the highest 4-MEI concentration (915.8 to 963.3μg/L), lifetime average daily dose (LADD - 8.04x10-3 mg/kgBW-day), lifetime excess cancer risk (1.93x10-4) and burden (5,011 cancer cases in the U.S. population over 70 years); Coca-Cola had the lowest value of each (4-MEI: 9.5 to 11.7μg/L; LADD: 1.01x10-4 mg/kgBW-day; risk: 1.92x10-6; and burden: 76 cases). 4-MEI concentrations varied considerably by soda and state/area of purchase, but were generally consistent across lots of the same beverage purchased in the same state/area. Routine consumption of certain beverages can result in 4-MEI exposures > 29 μg/day. State regulatory standards appear to have been effective in reducing exposure to carcinogens in some beverages. Federal regulation of 4-MEI in caramel color may be appropriate.
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Fiber consumption and all-cause, cardiovascular, and cancer mortalities: A systematic review and meta-analysis of cohort studies
Lihua Liu1, Shan Wang2 and Jianchao Liu3
1 Institute of Hospital Management, Chinese PLA General Hospital, Beijing, P. R. China
2 Department of Epidemiology and Biostatistics, School of Basic Medical Sciences, Peking Union Medical College/Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences Beijing, P. R. China
3 Office of Hospital Informatization, Institute of Hospital Management, Chinese PLA General Hospital, Beijing, P. R. China
The present meta-analysis aimed to investigate fiber consumption and all-cause mortality, and cause-specific mortality. MEDLINE and web of science database were searched for cohort studies published from inception to August 2014. Studies were included if they provided a hazard ratio (HR) and corresponding 95% CI for mortality in relation to fiber consumption.We found that, compared with those who consumed lowest fiber, for individuals who ate highest fiber, mortality rate was lower by 23% (HR, 0.77; 95% CI, 0.72–0.81) for CVD, by 17% (HR, 0.83; 95% CI, 0.74–0.91) for cancer, by 23% (HR, 0.77; 95% CI, 0.73–0.81) for all-cause mortality. For each 10 g/day increase in fiber intake, the pooled HR was estimated to be 0.89 (95% CI, 0.86–0.93) for all-cause mortality, 0.80 (95% CI, 0.72–0.88) for CHD mortality, and 0.66 (95% CI, 0.40–0.92) for IHD mortality, 0.91 (95% CI, 0.88–0.94) for cancer. Dietary fiber and CVD mortality showed a strong dose–response relation. Apparently, fiber consumption is inversely associated with all-cause mortality and CVD, IHD, cancer mortality.
Source : Molecular Nutrition and Food Research
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Exercise boosts tumor-fighting ability of chemotherapy
Combining exercise with chemotherapy shrunk tumors more than chemotherapy alone, according to research performed in a mouse model of melanoma.
Exercise has long been recommended to cancer patients for its physical and psychological benefits. This research team was particularly interested in testing whether exercise could protect against the negative cardiac-related side effects of the common cancer drug doxorubicin. Though effective at treating a variety of types of cancer, doxorubicin is known to damage heart cells, which could lead to heart failure in the long term.
The study was led by Joseph Libonati, PhD, FAHA, an associate professor in the School of Nursing and director of the Laboratory of Innovative and Translational Nursing Research at the University of Pennsylvania in Philadelphia. This research study was published in the American Journal of Physiology (2014; doi:10.1152/ajpregu.00082.2014).
“The immediate concern for these patients is, of course, the cancer, and they'll do whatever it takes to get rid of it,” Libonati said. “But then when you get over that hump you have to deal with the long-term elevated risk of cardiovascular disease.”
Previous studies had shown that an exercise regime prior to receiving chemotherapy could protect heart cells from the toxic effects of doxorubicin, but few had looked to see whether an exercise regimen during chemotherapy could be beneficial.
To do so, Libonati's team set up an experiment with four groups of mice. All were given an injection of melanoma cells in the scruffs of their neck. During the next 2 weeks, two of the groups received doxorubicin in two doses while the other two groups received placebo. The mice in one treated group and one placebo group were put on exercise regimens, walking 45 minutes 5 days a week on mouse-sized treadmills, while the rest of the mice remained sedentary.
After the 2-week trial, the researchers examined the animals' hearts using echocardiogram and tissue analysis. As expected, doxorubicin was found to reduce the heart's function and size and increased fibrosis, which is a damaging thickening of tissue. Mice that exercised were not protected from this damage.
“We looked, and the exercise didn't do anything to the heart. It didn't worsen it, it didn't help it,” Libonati said. “But the tumor data—I find them actually amazing.”
The amazing result was that the mice that both received chemotherapy and exercised had significantly smaller tumors after 2 weeks than mice that only received doxorubicin. This could be partly because exercise increases blood flow to the tumor, bringing with it more of the drug in the bloodstream.
“If exercise helps in this way, you could potentially use a smaller dose of the drug and get fewer side effects,” Libonati said.
“People don't take a drug and then sit down all day,” Libonati said. “Something as simple as moving affects how drugs are metabolized. We're only just beginning to understand the complexities.”
Source : Oncology Nurse Advisor
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Intravenous Vitamin C May Boost Chemo's Cancer-Fighting Power
Large doses of intravenous vitamin C have the potential to boost chemotherapy's ability to kill cancer cells, according to new laboratory research involving human cells and mice. Vitamin C delivered directly to human and mouse ovarian cancer cells helped kill off those cells while leaving normal cells unharmed, University of Kansas researchers report.
"In cell tissue and animal models of cancer, we saw when you add IV vitamin C it seems to augment the killing effect of chemotherapy drugs on cancer cells," said study co-author Dr. Jeanne Drisko, director of integrative medicine at the University of Kansas Medical Center.
In follow-up human trials, a handful of cervical cancer patients given intravenous vitamin C along with their chemotherapy reported fewer toxic side effects from their cancer treatment, according to the study published in the Feb. 5 issue of Science Translational Medicine.
"In those patients, we didn't see any ill effects and we noticed they had fewer effects from the chemotherapy," Drisko said. "It seemed to be protecting the healthy cells while killing the cancer cells."
Intravenous vitamin C has been considered an integrative medical therapy for cancer since the 1970s, Drisko noted.
But vitamin C's cancer-killing potential hasn't been taken seriously by mainstream medicine ever since clinical trials performed by the Mayo Clinic with oral vitamin C in the late 1970s and early 1980s found no anti-cancer effects, she explained.
Researchers have since argued that those trials were flawed because vitamin C taken orally is absorbed by the gut and excreted by the kidneys before its levels can build up in the bloodstream.
But it's been hard to attract funding for further research. There's no reason for pharmaceutical companies to fund vitamin C research, and federal officials have been uninterested in plowing research dollars into the effort since the Mayo research was published, Drisko said.
This latest investigation began with researchers exposing human ovarian cancer cells to vitamin C in the lab. They found that the cells suffered DNA damage and died off, while normal cells were left unharmed.
The researchers then tested vitamin C on mice with induced ovarian cancer. The vitamin appeared to help chemotherapy drugs either inhibit the growth of tumors or help shrink them.
Finally, the team conducted a pilot phase clinical trial involving 27 patients with stage III or stage IV ovarian cancer.
The patients who received intravenous vitamin C along with their chemotherapy reported less toxicity of the brain, bone marrow and major organs, the investigators found.
These patients also appeared to add nearly 8.75 months to the time before their disease relapsed and progressed, compared with people who only received chemotherapy. The researchers did note that the study was not designed to test the statistical significance of that finding.
Vitamin C in the bloodstream helps kill cancer cells because it chemically converts into hydrogen peroxide when it interacts with tumors, Drisko said.
"If you can get your blood levels of vitamin C very high, it gets driven into the space around the cancer cells," she explained. "In that space, it's converted into hydrogen peroxide. It's very similar to what our white blood cells do. They create hydrogen peroxide to fight infection."
Dr. Stephanie Bernik, chief of surgical oncology at Lenox Hill Hospital in New York City, said intravenous vitamin C therapy is not unheard of among cancer doctors.
"I've had patients come in and say they were doing vitamin C intravenous therapy," Bernik said. "I always tell them we don't know enough to know whether it is good or bad."
This new research raises interesting possibilities, but until larger clinical trials are conducted Bernik says her advice to patients will not change.
"You have to do a bigger study with patients and look at outcomes. You also have to make sure these treatments don't interfere with the treatments we're giving currently," she said. "There may be some efficacy in what they're doing. It just needs to be proven. This is just the start of more studies looking at this in-depth."
Dr. Michael Seiden, chief medical officer for The US Oncology Network, agreed.
"It is important to emphasize that many vitamin therapies have shown interesting results when applied to cancer cells in test tubes yet, to date, these approaches typically are not effective and occasionally prove harmful in human studies," he said. "At this time, there is still no evidence that high-dose vitamin C should be part of the treatment for women with ovarian cancer."
While she agreed that larger trials need to be conducted, Drisko was not as hesitant.
"It's safe. It's inexpensive. There's a plausible mechanism we're investigating for why it works," she said. "We should be using this in patients, rather than dragging our feet and worrying about using it at all."
SOURCES: Jeanne Drisko, M.D., endowed professor and director, integrative medicine, University of Kansas Medical Center, Kansas City; Stephanie Bernik, M.D., chief, surgical oncology, Lenox Hill Hospital, New York City; Michael Seiden, M.D., chief medical officer, The US Oncology Network; Feb. 5, 2014, Science Translational Medicine
Source : Medline
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Antitumor and Wound Healing Properties of Rubus ellipticus Smith.
Blassan Plackal George, Thangaraj Parimelazhaga, Yamini T. Kumar, Thankarajan Sajeesh
The present investigation has been undertaken to study the antioxidant, antitumor, and wound healing properties of Rubus ellipticus. The R. ellipticus leaves were extracted using organic solvents in Soxhlet and were subjected to in vitro antioxidant assays. R. ellipticus leaf methanol (RELM) extract, which showed higher in vitro antioxidant activity, was taken for the evaluation of in vivo antioxidant, antitumor, and wound healing properties. Acute oral and dermal toxicity studies showed the safety of RELM up to a dose of 2 g/kg. A significant wound healing property was observed in incision, excision, and Staphylococcus aureus-induced infected wound models in the treatment groups compared to the control group. A complete epithelialization period was noticed during the 13th day and the 19th day. A 250-mg/kg treatment was found to prolong the life span of mice with Ehrlich ascite carcinoma (EAC; 46.76%) and to reduce the volume of Dalton's lymphoma ascite (DLA) solid tumors (2.56 cm3). The present study suggests that R. ellipticus is a valuable natural antioxidant and that it is immensely effective for treating skin diseases, wounds, and tumors.
Source : Journal of Acupuncture and Meridian Studies
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American Ginseng Root Clinically Safe and Effective for Reducing Cancer-Related Fatigue
by Amy C. Keller
Reviewed: Barton DL, Liu H, Dakhil S, et al. Wisconsin ginseng (Panax quinquefolius) to improve cancer-related fatigue: a randomized, double-blind trial, N07C2. J Natl Cancer Inst. August 2013;105(16):1230-1238.
Cancer-related fatigue (CRF) can severely disrupt the lives of both those recovering from cancer and patients currently receiving cancer treatment. Although standard medications such as psychostimulants have been studied for the treatment of CRF, clinical studies have not confirmed their efficacy. Both American ginseng (Panax quinquefolius, Araliaceae) and Asian ginseng (P. ginseng) have been used in Traditional Chinese Medicine as adaptogens, among other uses. Compounds known as ginsenosides, found in ginseng, are broadly bioactive.1 This randomized, double-blind, placebo-controlled study was based on a prior clinical pilot study of American ginseng for patients with CRF. In the pilot study, American ginseng with 5% ginsenoside content was given to participants in 750, 1000, or 2000 mg doses for eight weeks versus a placebo. The results from that trial showed that 1000 and 2000 mgs of P. quinquefolius were most efficacious at four and eight weeks compared to placebo.2 Based on these results, this larger study investigated the efficacy and tolerability of 2000 mg daily of American ginseng with a reported level of 3% ginsenosides in patients with CRF. (The ginseng root material was further assessed for “quality” and “potency” by an unnamed company.)
Enrolled patients were randomly assigned to either active treatment (2000 mg daily of ground American ginseng root commercially cultivated in Wisconsin) or a rice powder placebo for eight weeks, taken in the morning and noon. American ginseng and placebo were procured from the Ginseng Board of Wisconsin (Wausau, WI) and produced with good manufacturing practices (GMPs) by Beehive Botanicals in Hayward, WI.
Patients with CRF (having a score ≥ [greater than or equal to] four using a scale ranging from 0=no fatigue to 10=severe fatigue) present one month or more prior to the study were included as long as their cancer diagnosis was made within the preceding two years. Patients with brain tumors or central nervous system lymphoma and those with a score of four or higher for pain or insomnia using the scale above were excluded. Also excluded were those taking steroids, opioids, ginseng, or other treatments for fatigue. The randomization process controlled for baseline fatigue, recurrent fatigue, cancer treatment type and length, and tumor characteristics.
An impact score on the Multidimensional Fatigue Symptom Inventory-Short Form (MFSI-SF) at four weeks was the primary outcome. This scale rates fatigue from 0 (no fatigue) to four (extreme fatigue). Change in scores on the Profile of Mood States (POMS) fatigue-inertia and vigor-activity subscales and the Brief Fatigue Inventory (BFI) scale were secondary outcomes. These assessments were administered at baseline, four, and eight weeks into the study. Patients described the type and severity of adverse side effects at the study’s start and weekly thereafter. Study administrators also gauged adverse side effects during clinic visits. Scales from 0-10 were used to assess fatigue, pain, and sleep quality.
Initially, 364 patients were enrolled, with 133 patients in the treatment group and 128 patients in the placebo group completing the study (n=261). At the four-week primary endpoint analysis, 147 patients were in the treatment group, and 153 patients were in the placebo group (n=300). At baseline, no differences were observed between groups’ fatigue assessments or demographic measurements. At four weeks into the study, the change in the MFSI-SF in those in the treatment group was a non-significant difference of 14.4±27.1 as compared with 8.2±24.8 for those in the placebo group (P=0.07). The difference in score change at eight weeks, however, was significant (20±27 vs. 10.3±26.2, treatment group vs. control group, respectively; P=0.003).
After eight weeks of treatment, the MFSI-SF physical subscore change from baseline was significantly greater in those in the treatment group as compared to the placebo group (3.0±17.9 vs. -1.7±18.2, P=0.004). This also was observed with MFSI-SF total score change from baseline at the end of the study (6.7± 4.0 vs. 3.7±14.6, P=0.02). The change from baseline in POMS fatigue inertia scores after eight weeks of treatment also was significantly greater in the treatment group as compared to the placebo group (18.6±24.8 vs. 10.2±26.1, P=0.008).
While the BFI total score was not significantly different between groups, the subscores for “worst fatigue” and “fatigue now” after eight weeks of treatment in the ginseng group were significantly improved as compared to the placebo group (P value and data not reported). Additionally, when only those patients undergoing cancer treatment were compared in both groups, the percentage change in MFSI-SF score from baseline of those in the treatment group was significantly more than that of the placebo group after both four and eight weeks (P=0.02 and 0.01, respectively).
Adverse side effects that occurred more frequently than 1% included agitation, anxiety, insomnia, nausea, and vomiting, while nervousness, sleep disturbances, and loose stools were also noted. The adverse effects of greater frequency were not significantly different between groups, suggesting that American ginseng supplementation seems well tolerated but does not alleviate adverse side effects inherent to this population. Both loose stools and pain were worse after baseline but occurred only in the placebo group over the course of the study.
In conclusion, this study reports the safety and efficacy of eight weeks of American ginseng supplementation for the alleviation of CRF. The authors state that these results were “clinically meaningful” (more than 10 points difference using a scale from 0 to 100). Due to the significant improvement in fatigue in those undergoing current cancer treatment versus those who had completed chemotherapy, American ginseng may be a possible treatment for CRF. Stated strengths of the study include its randomized and double-blind design, and that fatigue was distinguished from sleep deficit or pain. The authors cited the study’s limited duration and general difficulty of measuring fatigue as weaknesses.
Variations among studies of efficacy measures — such as improvement of BFI — may be due to variable concentrations of ginsenosides, which can result from agricultural inconsistencies and lack of content standardization during processing. Ideally, future studies also should investigate potential herb-drug interactions with chemotherapy. In summary, this study suggests that American ginseng may be a well-tolerated treatment of CRF, particularly during cancer treatment, for which no other pharmacotherapy has shown significant clinical benefit.
Source : HerbalGram (ABC)
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Active Component of Grape Seed Extract Effective Against Cancer Cells
A University of Colorado Cancer Center study published online ahead of print in the journal Nutrition and Cancer describes the laboratory synthesis of the most active component of grape seed extract, B2G2, and shows this synthesized compound induces the cell death known as apoptosis in prostate cancer cells while leaving healthy cells unharmed.
"We've shown similar anti-cancer activity in the past with grape seed extract (GSE), but now we know B2G2 is its most biologically active ingredient which can be synthesized in quantities that will allow us to study the detailed death mechanism in cancer cells," says Alpna Tyagi, PhD, of the University of Colorado Skaggs School of Pharmacy and Pharmaceutical Sciences. Tyagi works in the lab of CU Cancer Center investigator and Skaggs School of Pharmacy faculty member, Chapla Agarwal, PhD.
The group has spent more than a decade demonstrating the anti-cancer activity of GSE in controlled, laboratory conditions. For example, previous studies have shown the GSE effectiveness against cancer cells and have also shown its mechanism of action. "But until recently, we didn't know which constituent of GSE created this effect. This naturally occurring compound, GSE, is a complex mixture of polyphenols and also so far it has been unclear about the biologically active constituents of GSE against cancer cells," Tyagi says.
Eventually the group pinpointed B2G2 as the most active compound, but, "it's expensive and it takes a long time to isolate B2G2 from grape seed extract," Tyagi says.
This expense related to the isolation of B2G2 has limited the group's further exploration. So instead of purifying B2G2 from GSE, the group decided to synthesize it in the lab. The current study reports the success of this effort, including the ability to synthesize gram-quantity of B2G2 reasonably quickly and inexpensively.
In the paper's second half, the group shows anti-cancer activity of synthesized B2G2 similar in mechanism and degree to overall GSE effectiveness.
"Our goal all along has been a clinical trial of the biologically active compounds from GSE against human cancer. But it's difficult to earn FDA approval for a trial in which we don't know the mechanisms and possible effects of all active components. Therefore, isolating and synthesizing B2G2 is an important step because now we have the ability to conduct more experiments with the pure compound. Ongoing work in the lab further increases our understanding of B2G2's mechanism of action that will help for the preclinical and clinical studies in the future," Tyagi says.
Source : PRWeb
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Honey as a Potential Natural Anticancer Agent: A Review of Its Mechanisms
Sarfraz Ahmed and Nor Hayati Othman
Department of Pathology, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia
The main treatment for cancer is by using chemotherapy and radiotherapy which themselves are toxic to other viable cells of the body. Recently, there are many studies focusing on the use of natural products for cancer prevention and treatment. Of these natural products, honey has been extensively researched. The mechanism of the anti-cancer activity of honey as chemopreventive and therapeutic agent has not been completely understood. The possible mechanisms are due to its apoptotic, antiproliferative, antitumor necrosis factor (anti-TNF), antioxidant, anti-inflammatory, estrogenic and immunomodulatory activities. We collate the findings of several studies published in the literature in order to understand the mechanism of its action.
Evidence is growing that honey may have the potential to be anticancer agent through several mechanisms (Figure 3). Though the full mechanism is yet to be fully understood, studies have shown that honey has anticancer effect through its interference with multiple cell-signaling pathways, such as inducing apoptosis, antiproliferative, anti-inflammatory, and antimutagenic pathways. Honey modulates the body immune system. There are still many unanswered questions; why sugar is carcinogenic, while honey which is basically sugar has anticarcinogenic properties. Honey of different floral sources may give different effects. More research is needed to improve our understanding of the positive effect of honey and cancer. What is seen in cell cultures or animal experimentations may not apply to humans. Prospective randomized controlled clinical trials are needed to validate the authenticity of honey either alone or as adjuvant therapy.
Source : Evidence Based Complementary and Alternative Medicine
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Nut Consumption with Total and Cause-Specific Mortality
Ying Bao, M.D., Sc.D., Jiali Han, Ph.D., Frank B. Hu, M.D., Ph.D., Edward L. Giovannucci, M.D., Sc.D., Meir J. Stampfer, M.D., Dr.P.H., Walter C. Willett, M.D., Dr.P.H., and Charles S. Fuchs, M.D., M.P.H.
Increased nut consumption has been associated with a reduced risk of major chronic diseases, including cardiovascular disease and type 2 diabetes mellitus. However, the association between nut consumption and mortality remains unclear.
We examined the association between nut consumption and subsequent total and cause-specific mortality among 76,464 women in the Nurses' Health Study (1980–2010) and 42,498 men in the Health Professionals Follow-up Study (1986–2010). Participants with a history of cancer, heart disease, or stroke were excluded. Nut consumption was assessed at baseline and updated every 2 to 4 years.
During 3,038,853 person-years of follow-up, 16,200 women and 11,229 men died. Nut consumption was inversely associated with total mortality among both women and men, after adjustment for other known or suspected risk factors. The pooled multivariate hazard ratios for death among participants who ate nuts, as compared with those who did not, were 0.93 (95% confidence interval [CI], 0.90 to 0.96) for the consumption of nuts less than once per week, 0.89 (95% CI, 0.86 to 0.93) for once per week, 0.87 (95% CI, 0.83 to 0.90) for two to four times per week, 0.85 (95% CI, 0.79 to 0.91) for five or six times per week, and 0.80 (95% CI, 0.73 to 0.86) for seven or more times per week (P<0.001 for trend). Significant inverse associations were also observed between nut consumption and deaths due to cancer, heart disease, and respiratory disease.
In two large, independent cohorts of nurses and other health professionals, the frequency of nut consumption was inversely associated with total and cause-specific mortality, independently of other predictors of death. (Funded by the National Institutes of Health and the International Tree Nut Council Nutrition Research and Education Foundation.)
Source : The New England Journal of Medicine
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Orange Juice and Cancer Chemoprevention
Silvia Isabel Rech Frankeab, Temenouga Nikolova Guechevab, João Antonio Pêgas Henriquescb & Daniel Práab
Orange juice (OJ) is among the most consumed fruit juices worldwide, and its chemopreventive action is fairly addressed in the literature. This review critically presents the available evidence linking OJ with cancer chemoprevention and on discussing the putative mechanisms and negative health effects. The chemopreventive action of OJ is related to its effect on metabolic enzymes and its antiinflammatory, cytoprotective/apoptotic, hormonal, cell signaling-modulating, antioxidant, and antigenotoxic effects. Most studies on OJ are in vitro, and few are conducted in vivo. Results from in vitro studies must be interpreted carefully because these findings do not consider in vivo bioavailability. However, such results are useful for studying the impact of different processing and storage methods on OJ's chemopreventive effect. Evidence of OJ's chemoprevention in humans is limited. OJ is antimutagenic in bacteria and antigenotoxic in humans and rodents. Studies using rodent cancer models showed that OJ is cancer chemopreventive, influencing either the induction stage or the promotion stage. The composition and, therefore, the chemopreventive action of OJ might be influenced by different cultivars, climates, extraction methods, packaging, storage temperatures, and shelf lives, among other factors. Epidemiological studies and randomized controlled intervention studies in humans evaluating the chemopreventive effect of OJ, taking into consideration variability in OJ composition, are needed
Source : Nutrition and cancer
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Potential of olive oil phenols as chemopreventive and therapeutic agents against cancer: A review of in vitro studies
Ivan Casaburi, Francesco Puoci, Adele Chimento, Rosa Sirianni, Carmen Ruggiero, Paola Avena and Vincenzo Pezzi
Olive oil is a common component of Mediterranean dietary habits. Epidemiological studies have shown how the incidence of various diseases, including certain cancers, is relatively low in the Mediterranean basin compared to that of other European or North America countries. Current knowledge indicates that the phenolic fraction of olive oil has antitumor effects. In addition to the ability to be chemopreventive, with its high antioxidant activity, the antitumor effects of olive oil phenols (OO-phenols) has been studied because of their capacity to inhibit proliferation and promote apoptosis in several tumor cell lines, by diverse mechanisms. This review will summarize and discuss the most recent relevant results on the antitumor effect of OO-phenols on leukemia tumor cells, colorectal carcinoma cells, and breast cancer (BC) cells. In particular, very recent data will be reported and discussed showing the molecular signaling pathways activated by OO-phenols in different histopathological BC cell types, suggesting the potential use of OO-phenols as adjuvant treatment against several subsets of BC. Data summarized here represent a good starting point for more extensive studies for better insight into the molecular mechanisms induced by OO-phenols and to increase the availability of chemopreventive or therapeutic drugs to fight cancer.
Source : Journal Molecular Nutrition and Food Research
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Green Tea and cancer Prevention
Chung S. Yanga & Xin Wanga
Extracts of green tea and green tea polyphenols have exhibited inhibitory effects against the formation and development of tumors at different organ sites in animals. These include animal models for skin, lung, oral cavity, esophagus, stomach, intestine, colon, liver, pancreas, bladder, mammary gland, and prostate cancers. In addition to suppressing cell proliferation, promoting apoptosis, and modulating signaling transduction, green tea polyphenols, especially (-)-epigallocatechin-3-gallate, also inhibit cell invasion, angiogenesis, and metastasis. This article reviews data on the cancer preventive activities of green tea polyphenols, possible mechanisms involved, and the relationship between green tea consumption and human cancer risk.
The inhibitory activities of tea and tea catechins against carcinogenesis have been demonstrated in different animal models. Studies in cell lines have also showed that tea catechins can affect a variety of signaling and metabolic pathways. These molecular events could result in cancer cell growth inhibition, apoptosis, and inhibition of invasion, angiogenesis, and metastasis. These activities and the prevention of carcinogenesis have been demonstrated in animal model, but the cancer preventive activity of tea has not been consistently observed in human studies. This may be due to the relatively lower levels of tea consumption by some human populations (than animal studies) and the various confounding factors in epidemiological studies in different populations. The low bioavailability of tea polyphenols, such as EGCG, is also an issue. For agents with low systematic bioavailability, their direct contact with the digestive tract could be important for their cancer preventive activity. This point should be applicable to the activities of EGCG and polyphenols in many other foods or beverages. This information, as well as the biological properties and activities of tea polyphenols reviewed here, may be useful in design of prospective studies and in the selection of the agent, dosage, and biomarkers for intervention trials. The results of such well-designed studies will provide more definitive information on the possible use of tea for the reduction of cancer risk in different populations.
Source : Nutrition and cancer
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Study Shows How Vitamin E Can Help Prevent Cancer
COLUMBUS, Ohio – Researchers have identified an elusive anti-cancer property of vitamin E that has long been presumed to exist, but difficult to find.
Many animal studies have suggested that vitamin E could prevent cancer, but human clinical trials following up on those findings have not shown the same benefits.
In this new work, researchers showed in prostate cancer cells that one form of vitamin E inhibits the activation of an enzyme that is essential for cancer cell survival. The loss of the enzyme, called Akt, led to tumor cell death. The vitamin had no negative effect on normal cells.
“This is the first demonstration of a unique mechanism of how vitamin E can have some benefit in terms of cancer prevention and treatment,” said lead author Ching-Shih Chen, professor of medicinal chemistry and pharmacognosy at The Ohio State University and an investigator in Ohio State’s Comprehensive Cancer Center.
The study appears in the March 19, 2013, issue of the journal Science Signaling.
Chen cautioned that taking a typical vitamin E supplement won’t offer this benefit for at least two reasons: The most affordable supplements are synthetic and based predominantly on a form of the vitamin that did not fight cancer as effectively in this study, and the human body can’t absorb the high doses that appear to be required to achieve the anti-cancer effect.
“Our goal is to develop a safe pill at the right dose that people could take every day for cancer prevention. It takes time to optimize the formulation and the dose,” he said.
Chen has filed an invention disclosure with the university, and Ohio State has filed a patent application for the agent.
Vitamin E occurs in numerous forms based on their chemical structure, and the most commonly known form belongs to a variety called tocopherols. In this study, researchers showed that, of the tocopherols tested, the gamma form of tocopherol was the most potent anti-cancer form of the vitamin.
The scientists manipulated the structure of that vitamin E molecule and found that the effectiveness of this new agent they created was 20-fold higher than the vitamin itself in cells. In experiments in mice, this agent reduced the size of prostate cancer tumors.
These findings suggest that an agent based on the chemical structure of one form of vitamin E could help prevent and treat numerous types of cancer – particularly those associated with a mutation in the PTEN gene, a fairly common cancer-related genetic defect that keeps Akt active.
The researchers began the work with both alpha and gamma forms of the vitamin E molecule. Both inhibited the enzyme called Akt in very targeted ways, but the gamma structure emerged as the more powerful form of the vitamin.
In effect, the vitamin halted Akt activation by attracting Akt and another protein, called PHLPP1, to the same region of a cell where the vitamin was absorbed: the fat-rich cell membrane. PHLPP1, a tumor suppressor, then launched a chemical reaction that inactivated Akt, rendering it unable to keep cancer cells alive.
“This is a new finding. We have been taking vitamin E for years but nobody really knew about this particular anti-cancer mechanism,” Chen said.
The gamma form was most effective because its chemical shape allowed it to attach to Akt in the most precise way to shut off the enzyme.
Because of how the various molecules interacted on the cell membrane, the scientists predicted that shortening a string of chemical groups dangling from the main body, or head group, of the gamma-tocopherol molecule would make those relationships even stronger. They lopped off about 60 percent of this side chain and tested the effects of the new agent in the prostate cancer cells.
“By reducing two-thirds of the chain, the molecule had a 20 times more potent anti-tumor effect, while retaining the integrity of vitamin E’s head group,” Chen said. This manipulation enhanced the anti-tumor potency of the molecule by changing its interaction with the cell membrane, so that the head group was more accessible to Akt and PHLPP1.
When mice with tumors created by these two prostate cancer cell lines were inSource : jected with the agent, the treatment suppressed tumor growth when compared to a placebo, which had no effect on tumor size. Chemical analysis of the treated tumors showed that the Akt enzyme signal was suppressed, confirming the effects were the same in animals as they had been in cell cultures.
The animal study also suggested the experimental agent was not toxic. Chen’s lab is continuing to work on improvements to the molecule.
Source : Ohio State University
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Spirituality May Boost Outcomes in Ovarian Cancer
Ovarian cancer patients who reported high levels of spirituality presurgery had better outcomes for stress and depression, as well as factors known to regulate tumor angiogenesis and inflammation, researchers reported here.Self-report of high spirituality was associated with significantly lower perceived stress and depression (P<0.001), according to Premal Thaker, MD of the Washington University School of Medicine in St. Louis, and colleagues.
These same patients also had significantly lower levels of IL-6, both in peripheral blood (P=0.001) and in ascites (P=0.013) after adjusting for stress and depression, Thaker reported at the meeting of the Society of Gynecologic Oncology.
"Spirituality is an important psychosocial resource that positively influences quality of life," Thaker noted, adding that "less is known about the role of positive stress buffers, such as spirituality and cytokines, in tumor angiogenesis and inflammation in ovarian cancer patients."
She also noted that patient's spirituality was defined as "an individual's sense of peace, purpose, and connection to others, and beliefs about the meaning of life." These beliefs and feelings are important for patients at the time of diagnosis and at the end of life by offering comfort, hope, improved quality of life, and meaning, she explained.
To analyze the effects of spirituality on preoperative patients with ovarian cancer, the researchers performed a prospective cohort study of 165 women with histologically confirmed epithelial ovarian cancer.
Patients were surveyed for stress, depression, and self-reported spirituality through the Perceived Stress Scale, Beck Depression Inventory, and FACT-Spirituality survey, respectively.
Participants also had blood drawn on the morning of surgery, which was used to obtain data on concentrations of patients' IL-6, IL-8, and vascular endothelial growth factor (VEGF).
Thaker noted that earlier studies had linked depression with worse IL-6 outcomes and high social support with better IL-6 outcomes.
Participants were mostly white (96.1%), married or living with a partner (64%), normal or overweight (61%), and had an average age of 59.9. Disease in patients was mostly at stage III or 1V (72%), grade III (86.6%), had serous histology (75%), and had optimal debulking (76.8%).
A regression analysis showed a significantly negative association between spirituality and depression, stress, and IL-6, which maintained significance after adjustment for disease stage, histology, disease grade, age, and body mass index. Additional adjustment for stress and depression showed that the relationship between spirituality and IL-6 outcomes were unaffected (P=0.002).
There was no significant associations between spirituality and VEGF or IL-8 concentrations.
"These results indicate relationships between patient self-reports of spirituality presurgery and an important proinflammatory and proangiogenic cytokine, as well as important psychosocial correlates of spirituality," the authors concluded, noting potential implications for future patient treatment.
Thaker noted the study was limited by self-reported measures and a single measure of spirituality.
Source : MedPage Today via Society of Gynecologic Oncology
Thaker PH, et al. "Spirituality, depression, and interleukin-6 in ovarian cancer patients" SGO 2013; Abstract 14.
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Meditation Combined With Art Therapy Can Change Your Brain and Lower Anxiety
Cancer and stress go hand-in-hand, and high stress levels can lead to poorer health outcomes in cancer patients. The Jefferson-Myrna Brind Center of Integrative Medicine combined creative art therapy with a Mindfulness-based Stress Reduction (MBSR) program for women with breast cancer and showed changes in brain activity associated with lower stress and anxiety after the eight-week program. Their new study appears in the December issue of the journal Stress and Health.
Daniel Monti, MD, director of the Jefferson-Myrna Brind Center of Integrative Medicine and lead author on the study, and colleagues have previously published on the success of Mindfulness-based Art Therapy (MBAT) at helping cancer patients lower stress levels and improve quality of life.
"Our goal was to observe possible mechanisms for the observed psychosocial effects of MBAT by evaluating the cerebral blood flow (CBF) changes associated with an MBAT intervention in comparison with a control of equal time and attention," says Monti. "This type of expressive art and meditation program has never before been studied for physiological impact and the correlation of that impact to improvements in stress and anxiety."
Eighteen patients were randomly assigned to the MBAT program or an education program control group. All had received the diagnosis of breast cancer between six months and three years prior to enrollment and were not in active treatment. The MBAT group consisted of the MBSR curriculum (awareness of breathing, awareness of emotion, mindful yoga, walking, eating and listening), paired with expressive art tasks to provide opportunities for self-expression, facilitate coping strategies, improve self-regulation, and provide a way for participants to express emotional information in a personally meaningful manner.
Patient response to the MBAT program was measured using a 90-item symptom checklist, completed by each patient before and after the eight-week program. In addition, functional magnetic resonance imaging (fMRI) was used pre and post-program to evaluate cerebral blood flow, corresponding to changes in the brain's activity. Scans were performed at rest, during a "neutral task" (control), meditation task, stressor task and at rest again -- designed to evaluate the general as well as specific effects and provide a thorough analysis of the CBF changes between the pre and post-program scans.
Participants in the MBAT group demonstrated significant effects on cerebral blood flow compared with the control group. The MBAT group showed increases in the emotional centers of the brain including the left insula which helps us to perceive our emotions, the amygdala which helps us experience stress, the hippocampus that regulates stress responses, and the caudate nucleus that is part of our brain's reward system. These increases correlated significantly with a lowering of stress and anxiety, as also reflected in the results of the pre and post-program anxiety scores among the MBAT intervention group.
The observed psychological and neuropsychological changes are consistent with current literature that states that MBSR interventions have shown to reduce anxiety, depression and psychological distress in a variety of populations. These have been associated with improved immune function, quality of life and coping effectiveness in women with breast cancer.
Given the improvements in anxiety levels and observed changes in CBF in the MBAT participants, these findings suggest that the MBAT program helps mediate emotional responses in women with breast cancer. "With the sample size enlarged, perhaps we can extrapolate these results to other disease populations and gain a fuller understanding of the physiological mechanisms by which mindfulness practices confer psychological benefits," says Monti.
Source : Science Daily
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A New Study on Breast Cancer Highlights the Need for Chemical Reform
How many of us have been rocked to the core by that malicious word, “cancer”? If you haven’t been slapped in the face with this fearsome news, then consider yourself a member of the fortunate few. One of every four deaths in the United States is due to cancer. Down with cancer. Seriously.
Its mysteries are maddening. Why do the people we love get cancer? Why do people who lead intentionally careful and healthful lives get cancer? Can we prevent our likelihood of being diagnosed? Is it genetic and inevitable, or environmentally triggered? Can we stop it?! How many family members and friends have asked themselves these questions? Consequently, cancer researchers are asking themselves the same things. A new study of breast cancer done in Ontario, Canada was released this week. It explores increased breast cancer risks in relation to occupational exposures to known carcinogenic chemicals.
Next to skin cancer, breast cancer is the most commonly diagnosed cancer in women in the United States. Fewer than half of the cases can be explained by recognized risk factors like family or reproductive history. Breast cancer is likely caused by a combination of environmental, genetic, hormonal, and lifestyle influences. No one fully understands how these factors interplay to increase your risk of a diagnosis.
Yet, scientists do have a hunch or two regarding the identification of specific risk factors. In industrialized countries, breast cancer incidence increased dramatically in the second half of the twentieth century as thousands of new chemicals with unknown health effects were introduced. This lead scientists to wonder, is this toxic soup of chemicals that we’re exposed to everyday increasing our risk of getting cancer? What about women exposed to exceptionally high levels of suspected carcinogens by virtue of their occupation? Are these women diagnosed with breast cancer at a higher rate than the general population? This is the set of questions that the scientists in Ontario set out to explore.
This study involved the participation of 1005 women with breast cancer and 1147 women without the disease to act as the control group. All women were asked to provide occupational histories in order to determine potential exposures to carcinogens and endocrine disruptors.
An endocrine disruptor is a chemical that creates hormone imbalance that results in some cancers, reproductive disorders, immune system dysfunction, birth defects, and neurological effects. Certain occupations require exposures to endocrine-disrupting chemicals on a daily basis.
So, what are these high-risk jobs?
Women in farming showed a 36% increased breast cancer risk.
- Several pesticides commonly used in agriculture act as mammary carcinogens and endocrine disrupting chemicals. Women often begin working on the farm at early ages, when they are even more vulnerable to the effects of these toxic pesticides.
- They work with a variety of potentially hazardous metals and chemicals that metal working processes entail.
- Women in food canning are exposed to residual toxic pesticides, as well as emissions for the polymer linings of cans.
- Women working in the automotive plastics industry are exposed to many plastics that have been found to release carcinogenic chemicals. Cumulative exposures to mixtures of these chemicals are a significant concern.
- For women who are pre-menopausal in either industry, their breast cancer risk becomes 5-fold.
- This may largely be attributable to the greater exposure to second-hand smoke as well as the night work, which has been found to disrupt the endocrine system.
To date, no women in Canada from any these high-risk industries have received worker compensation. It’s not like these industries don’t know that the chemicals they’re using have been identified as probable carcinogens. How is this acceptable? These workers are shouldering all of the risks and all of the costs (in the form of medical bills) so that these industries can save a dime by using carcinogenic chemicals as opposed to safer chemical alternatives. It’s not fair; it’s not right.
These findings have important implications not only for women workers, but for the general population as well. There are over 80,000 chemicals registered for production today, but fewer than 200 of these chemicals have been tested for human health and safety. These chemicals aren’t being tested because federal regulations, dictated by the Toxic Substances Control Act of 1976, puts the burden of safety determination on the Environmental Protection Agency rather than the chemical manufacturers. The EPA must prove that a chemical presents an “unreasonable risk” for consumers before it can be banned or restricted for use. This has made it really difficult for the EPA to protect us from harmful exposures. In fact, they can’t do much to protect us until after people begin to sicken or die, and undeniable evidence begins piling up linking these illnesses to a specific chemical exposure. That is too little protection too late for some.
As a result, we are exposed every day to the same chemicals that are making women workers in this study sick, albeit at much lower levels. However, some studies are finding that lower exposure to certain endocrine disruptors can actually be more harmful to our bodies than higher exposures. And it’s not like we’re being exposed to one or two carcinogenic chemicals every day, we’re being exposed to hundreds, maybe even thousands every day in the products all around us! That is not what I want for my loved ones or for myself. If safer chemical alternatives exist, we need to begin using them NOW.
Source : Michigan Network for Children's Environmental
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Link to Study : Breast cancer risk in relation to occupations with exposure to carcinogens and
endocrine disruptors: a Canadian case--control study
Green Tea Could Modify the Effect of Cigarette Smoking On Lung Cancer Risk
Drinking green tea could modulate the effect of smoking on lung cancer.
Results of this hospital-based, randomized study conducted in Taiwan were presented at the AACR-IASLC Joint Conference on Molecular Origins of Lung Cancer, Jan. 11-14, 2010.
"Lung cancer is the leading cause of all cancer deaths in Taiwan," said I-Hsin Lin, M.S., a student at Chung Shan Medical University in Taiwan. "Tea, particularly green tea, has received a great deal of attention because tea polyphenols are strong antioxidants, and tea preparations have shown inhibitory activity against tumorigenesis."
However, previous studies of green tea have been inhibited by the flaws of the epidemiologic model with its inherent biases.
Lin and colleagues enrolled 170 patients with lung cancer and 340 healthy patients as controls. The researchers administered questionnaires to obtain demographic characteristics, cigarette smoking habits, green tea consumption, dietary intake of fruits and vegetables, cooking practices and family history of lung cancer. They also performed genotyping on insulin-like growth factors as polymorphisms on the following insulin-like growth factors: IGF1, IGF2 and IGFBP3, which have all been reported to be associated with cancer risk.
Among smokers and non-smokers, those who did not drink green tea had a 5.16-fold increased risk of lung cancer compared with those who drank at least one cup of green tea per day. Among smokers, those who did not drink green tea at all had a 12.71-fold increased risk of lung cancer compared with those who drank at least one cup of green tea per day.
Lin and colleagues suspect genetics may play a role in this risk differential. Green tea drinkers with non-susceptible IGF1 (CA)19/(CA)19 and (CA)19/X genotypes reported a 66 percent reduction in lung cancer risk as compared with green tea drinkers carrying the IGF1 X/X genotype.
Heavy smokers carrying susceptible IGF1, IGF2 and IGFBP3 genotypes also had a higher risk of lung cancer compared with nonsmokers carrying non-susceptible IGF1, IGF2 and IGFBP3 genotypes.
"Our study may represent a clue that in the case of lung cancer, smoking-induced carcinogenesis could be modulated by green tea consumption and the growth factor environment," said Lin.
Source : Science Daily
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Acupuncture Relieves Symptoms of a Dry Mouth Caused by Radiotherapy for Head and Neck Cancers, Study Suggests
Patients who have received radiotherapy for head and neck cancer often suffer from the unpleasant and distressing side-effect of a dry mouth, caused by damage to their salivary glands from the radiation.
Now, a new study has shown that acupuncture can relieve the symptoms of dry mouth (known as xerostomia). The findings from the largest trial yet to investigate this are published in the cancer journal Annals of Oncology on October 24.
Around half a million people worldwide develop head and neck cancer each year and, at present, there are few effective treatments for dry mouth, which is a common side effect of radiotherapy; as many as 41% of patients can still be suffering from it five years later. Xerostomia affects the patients' quality of life, interfering with taste, chewing, speaking and sleeping. Short-term solutions such as mouthwashes, gels and toothpastes provide some respite, while treatment with a drug called pilocarpine has its own unwanted side-effects.
Doctors at seven cancer centres in the UK* recruited 145 patients suffering from radiation-induced xerostomia to a trial comparing acupuncture with education about oral care. The patients were randomised to receive group acupuncture sessions for 20 minutes every week for eight weeks, or two oral care educational sessions for one hour, one month apart. Four weeks after the end of these two different types of care, the patients swapped over to receive the other treatment.
Symptoms of xerostomia were measured objectively by means of paper strips, called Schirmer strips, which measure the amount of saliva in the mouth. A tried and tested quality of life questionnaire measured patients' subjective reporting of how their mouths felt, with questions about changes in individual symptoms such as sticky saliva, dry lips, needing to sip water to relieve a dry mouth, needing to sip water to help swallow food, and waking at night to sip water.
Although the researchers found there were no significant changes in saliva production, patients who had received nine weeks of acupuncture were twice as likely to report improved dry mouth than patients receiving oral care. Individual symptoms were also significantly improved among the group receiving acupuncture.
Dr Richard Simcock, consultant clinical oncologist at the Sussex Cancer Centre and one of the authors of the study, said: "Time had an important effect on key symptoms, with patients receiving acupuncture showing a quick response, which was sustained over several weeks."
The researchers said that the subjective reporting of improvements in xerostomia was of more significance than the lack of changes in the objective test with the Schirmer strips. "There was no clear relationship between a patient indicating they had a very dry mouth and the measurement of saliva on the Schirmer strips," explained Dr Simcock. "By definition these patients with chronic xerostomia produced little or no saliva, making objective measurements really difficult. Many studies have focused on the objective measurement of how much saliva is produced, but the amount of saliva produced does not necessarily influence the experience of a dry mouth. Xerostomia is therefore an entirely subjective symptom -- it is what the patient says it is, regardless of salivary measurement."
They also believed that the improvements in the experience of xerostomia were unlikely to be due to a placebo effect. Dr Valerie Jenkins, Deputy Director of Sussex Health Outcomes Research & Education in Cancer (SHORE-C) at Brighton & Sussex Medical School, University of Sussex, who supervised the research, said: "The profound impact that xerostomia exerts on functions such as eating, talking and sleeping, which were relieved by the acupuncture means that if it is entirely a placebo effect than this is a pretty powerful placebo. In addition, the results showed that patients were less likely to wake at night to sip water after treatment -- this effect seems difficult to ascribe solely to placebo."
She concluded: "The scepticism that exists about complementary therapies such as these is often due to inadequately designed and reported studies. This was a well-controlled, randomised trial conducted in major cancer centres throughout UK with good governance and reporting of adverse events."
The researchers say that further studies are needed to refine the acupuncture technique and discover how long its effect lasts and whether booster sessions might be required. But they believe it could be easily incorporated into the care of patients with xerostomia.
Dr Simcock said: "This is a very neglected group of patients suffering from a most unpleasant side-effect of treatment for which all other ameliorative interventions have failed to address adequately. The acupuncture intervention has been designed in a way that allows it to be delivered simply and cheaply in normal hospital surroundings and yet still produces a significant benefit for patients with a chronic symptom."
* The seven UK centres were: Royal Sussex County Hospital, Brighton; Guy's & St Thomas's Hospital Trust, London; Mount Vernon Hospital, London; Maidstone Hospital, Kent; Queen Elizabeth Hospital, Birmingham; Royal Surrey County Hospital, Guildford; The Royal Marsden, Sutton.
Source : Science Daily
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Researcher documents links between nutrients, genes and cancer spread
More than 40 plant-based compounds can turn on genes that slow the spread of cancer, according to a first-of-its-kind study by a Washington State University researcher.
Gary Meadows, WSU professor and associate dean for graduate education and scholarship in the College of Pharmacy, says he is encouraged by his findings because the spread of cancer is most often what makes the disease fatal. Moreover, says Meadows, diet, nutrients and plant-based chemicals appear to be opening many avenues of attack. "We're always looking for a magic bullet," he says. "Well, there are lots of magic bullets out there in what we eat and associated with our lifestyle. We just need to take advantage of those. And they can work together." Meadows started the study, recently published online in the journal Cancer and Metastasis Reviews, with some simple logic: Most research focuses on the prevention of cancer or the treatment of the original cancer tumor, but it's usually the cancer's spread to nearby organs that kills you. So rather than attack the tumor, said Meadows, let's control its spread, or metastasis. He focused in particular on genes that suppress metastasis. As search engine terms go, it took him down many a wormhole in the PubMed research database, as the concept of nutrients and metastasis suppressor genes is rarely identified by journals. It's even an afterthought of some of the researchers who find the genes. "People for the most part did not set out in their research goals to study metastasis suppressor genes," says Meadows. "It was just a gene that was among many other genes that they had looked at in their study." But Meadows took the studies and looked to see when metastasis suppressor genes were on or off, even if original authors didn't make the connection. In the end, he documented dozens of substances affecting the metastasis suppressor genes of numerous cancers.
He saw substances like amino acids, vitamin D, ethanol, ginseng extract, the tomato carotenoid lycopene, the turmeric component curcumin, pomegranate juice, fish oil and others affecting gene expression in breast, colorectal, prostate, skin, lung and other cancers. Typically, the substances acted epigenetically, which is to say they turned metastasis suppressor genes on or off. "So these epigenetic mechanisms are influenced by what you eat," he says. "That may also be related to how the metastasis suppressor genes are being regulated. That's a very new area of research that has largely not been very well explored in terms of diet and nutrition." Meadows says his study reinforces two concepts. For one, he has a greater appreciation of the role of natural compounds in helping our bodies slow or stop the spread of cancer. The number of studies connecting nutrients and metastasis suppressor genes by accident suggests a need for more deliberate research into the genes. "And many of these effects have not been followed up on," he says. "There's likely to be more compounds out there, more constituents, that people haven't even evaluated yet." Meadows also sees these studies playing an important role in the shift from preventing cancer to living with it and keeping it from spreading. "We've kind of focused on the cancer for a long time," he says. "More recently we've started to focus on the cancer in its environment. And the environment, your whole body as an environment, is really important in whether or not that cancer will spread."
Source : Medicalxpress
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High dietary antioxidant intake might cut pancreatic cancer risk
Increasing dietary intake of the antioxidant vitamins C, E, and selenium could help cut the risk of developing pancreatic cancer by up to two thirds, suggests research published online in the journal Gut.
If the association turns out to be causal, one in 12 of these cancers might be prevented, suggest the researchers, who are leading the Norfolk arm of the European Prospective Investigation of Cancer (EPIC) study. Cancer of the pancreas kills more than a quarter of a million people every year around the world. And 7500 people are diagnosed with the disease every year in the UK, where it is the six commonest cause of cancer death. The disease has the worst prognosis of any cancer, with just 3% of people surviving beyond five years. Genes, smoking, and type 2 diabetes are all risk factors, but diet is also thought to have a role, and may explain why rates vary so much from country to country, say the authors. The researchers tracked the health of more than 23,500 40 to 74 year olds, who had entered the Norfolk arm of the EPIC study between 1993 and 1997. Each participant filled in a comprehensive food diary, detailing the types and amount of every food they ate for 7 days, as well as the methods they used to prepare it. Each entry in the food diary was matched to one of 11,000 food items, and the nutrient values calculated using a specially designed computer programme (DINER). Forty nine people (55% men) developed pancreatic cancer within 10 years of entering the study. This increased to 86 (44% men) by 2010. On average, they survived 6 months after diagnosis. The nutrient intakes of those diagnosed with the disease within 10 years of entering EPIC were compared with those of almost 4000 healthy people to see if there were any differences. The analysis showed that a weekly intake of selenium in the top 25% of consumption roughly halved their risk of developing pancreatic cancer compared with those whose intake was in the bottom 25%. And those whose vitamins C, E, and selenium intake was in the top 25% of consumption were 67% less likely to develop pancreatic cancer than those who were in the bottom 25%. If the link turns out to be causal, that would add up to the prevention of more than one in 12 (8%) of pancreatic cancers, calculate the authors. Antioxidants may neutralise the harmful by-products of metabolism and normal cell activity—free radicals—and curb genetically programmed influences, as well as stimulating the immune system response, explain the authors. Other trials using antioxidant supplements have not produced such encouraging results, but this may be because food sources of these nutrients may behave differently from those found in supplements, they say. "If a causal association is confirmed by reporting consistent findings from other epidemiological studies, then population based dietary recommendations may help to prevent pancreatic cancer," they conclude. More information: Dietary antioxidants and the aetiology of pancreatic cancer: a cohort study using data from food diaries and biomarkers, Banim PJR, Luben R, McTaggart A, et al. Gut (2012). doi:10.1136/gutjnl-2011-301908
Source : Medical Xpress
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Green Tea Compound Shows Promise for Tackling Cancer
A compound found in green tea could be a weapon in treatments for tackling cancer, according to newly published research at the University of Strathclyde.
The extract, known as epigallocatechin gallate, has been known to have preventative anti-cancer properties but fails to reach tumours when delivered by conventional intravenous administration.
However, in initial laboratory tests at the Universities of Strathclyde and Glasgow, researchers used an approach which allowed the treatment to be delivered specifically to the tumours after intravenous administration. Nearly two-thirds of the tumours it was delivered to either shrank or disappeared within one month and the treatment displayed no side effects to normal tissues.
The tests are thought to be the first time that this type of treatment has made cancerous tumours shrink or vanish.
In the tests, on two different types of skin cancer, 40% of both types of tumour vanished, while 30% of one and 20% of another shrank. A further 10% of one of the types were stabilised.
The researchers encapsulated the green tea extract in vesicles that also carried transferrin, a plasma protein which transports iron through the blood. Receptors for transferrin are found in large amounts in many cancers.
Dr Christine Dufès, a senior lecturer at the Strathclyde Institute of Pharmacy and Biomedical Sciences, led the research. She said: "These are very encouraging results which we hope could pave the way for new and effective cancer treatments.
"When we used our method, the green tea extract reduced the size of many of the tumours every day, in some cases removing them altogether. By contrast, the extract had no effect at all when it was delivered by other means, as every one of these tumours continued to grow.
"This research could open doors to new treatments for what is still one of the biggest killer diseases in many countries."
Source : Science Daily via Antitumor activity of the tea polyphenol epigallocatechin-3-gallate encapsulated in targeted vesicles after intravenous administration. Nanomedicine, 2012; DOI: 10.2217/nnm.12.83
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