Researchers Find the Existence of another Immune System in Humans

The good news is that doctors can determine which antigens a patient’s cancer cells release. By targeting sequestered antigens – the ones unknown to the immune system – doctors could greatly increase vaccines’ chances of success. NeuroscienceNews.com image is credited to United States Department of Health and Human Services and is for illustrative purposes only.

A groundbreaking new study reveals an unexpected interaction between men’s testes and the immune system. Additionally, the findings could help explain the development of certain autoimmune disorders and why some cancer vaccines are ineffective.

Unexpected connection likely sabotaging vaccines designed to treat cancer.
The University of Virginia, School of Medicine, has again shown that a part of the body thought to be disconnected from the immune system actually interacts with it, and that discovery helps explain cases of male infertility, certain autoimmune diseases and even the failure of cancer vaccines.

Scientists developing such vaccines may need to reconsider their work in light of the new findings or risk unintentionally sabotaging their own efforts. UVA’s Kenneth Tung, MD, said that many vaccines likely are failing simply because researchers are picking the wrong targets – targets that aren’t actually foreign to the immune system and thus won’t provoke the desired immune responses.

Overturning Orthodoxy
Tung, of UVA’s Beirne B. Carter Center for Immunology Research, and a team of collaborators have discovered an unexpected interaction between men’s testes and the immune system. While science textbooks insist the testes are barricaded from the immune system by an impenetrable wall of cells, the researchers have determined there’s actually a very small door in that wall, a door that appears to open in only one direction.



The team discovered that the testes release some, but not all, of the antigens – substances that can spur an immune response – that are created during the production of sperm. Because the testes release these antigens naturally, the immune system ignores them. That’s a normal, healthy response, but it also may explain why cancer vaccines are failing. Cancer vaccines target antigens, so if vaccine developers rely on antigens that are ignored by the immune system, the vaccine won’t work.

“In essence, we believe the testes antigens can be divided into those which are sequestered [behind the barrier] and those that are not,” Tung said. “Antigens which are not sequestered would not be very good cancer vaccine candidates.”

The good news is that doctors can determine which antigens a patient’s cancer cells release. By targeting sequestered antigens – the ones unknown to the immune system – doctors could greatly increase vaccines’ chances of success.



Treating Infertility
The finding also may prove important for couples seeking to have children. Up to 12 percent of men who suffer from infertility have an autoimmune response to their own reproductive cells. That means their immune systems are attacking their sperm, essentially. Tung and his collaborators shed light on what may be happening, showing that a particular step during the creation of sperm is responsible for determining whether the sperm antigens will spark an immune response. Cells called “regulatory T cells” then help control the immune system’s response to the non-sequestered antigens. In men who are infertile because of an autoimmune disorder, something is going wrong with the process, leading the immune system to attack when it shouldn’t. With that knowledge, doctors may be able to develop new treatments for the autoimmune disorders and the resulting infertility.

Rethinking the Immune System
The discovery of the unknown immune interaction comes less than two years after UVA’s Jonathan Kipnis and Antoine Louveau rewrote textbooks when they discovered that the brain has a direct connection to the immune system, a connection long thought not to exist. That discovery could have profound effects in the quest to defeat diseases ranging from Alzheimer’s to multiple sclerosis.
Source: University of Virginia Health System.

YOUR INPUT IS MUCH APPRECIATED! LEAVE YOUR COMMENT BELOW.

Breakthrough in the fight against Decease including Cancer

A treatment billed as a potential breakthrough in the fight against disease, including cancer, could back-fire and make the disease fitter and more damaging, new research has found.

Ground-breaking research has found that introducing 'friendlier' less-potent strain into a population of disease-causing microbes can lead to increased disease severity.

The surprise findings by a team of scientists at the University of Exeter has led to call for urgent research into the implications of using 'fire to fight fire' to combat disease. The research shows that far from being a 'silver bullet' to weaken disease, the practice of introducing pacifist microbes into a host could make the aggressive pathogen stronger, which could hamper disease management.

Until now, introducing friendlier cousins which do not cause severe disease, into a population of pathogens has been shown to reduce disease severity and damage to the infected host. It has been suggested that this approach could be an effective way of treating cancer, and research so far has proved effective and promising. For example, scientists have already produced encouraging results in the fight against Clostridium difficile infections that are so common in our hospitals.


This photograph depicts Clostridium difficile colonies after 48hrs growth on a blood agar plate; Magnified 4.8X. C. difficile, an anaerobic gram-positive rod, is the most frequently identified cause of antibiotic-associated diarrhea (AAD).

But the University of Exeter scientists tested this strategy using a plant pathogen, and found the therapy could go dramatically wrong, with devastating consequences for the host plant.

A team lead by Professors Ivana Gudelj, a mathematical biologist and Nick Talbot, a plant disease specialist, investigated the devastating rice blast disease. They introduced a mixed population of the fungus that causes this disease into rice, where the mixture included an aggressive strain and a pacifist mutant. They expected that the overall disease severity would decrease because of the presence of the pacifist strain. However, they found the opposite. The rice plants succumbed to much more severe disease.

The Exeter University research, published in eLife, shows that the therapy can in some circumstances have the opposite effect and that the way the pathogen will behave can be unpredictable, leading to more severe disease. The research highlights the need for these new strategies to be carefully tested before they are used therapeutically.

The scientists used cooperation theory and mathematical modelling, to identify the reason for their surprising result. They found that in some circumstances pacifists "helped" aggressive microbes to be more efficient in utilizing resources obtained from the host.



Professor Ivana Gudelj, who led the research, said: "Our study shows that a promising disease management strategy may not always be effective and indeed may has damaging unforeseen consequences. Importantly, our work also provides a foundation for the analysis of when, and why, this can happen. We find that the mechanisms driving our unexpected findings when treating rice blast infection are pertinent for many diseases involving bacterial and fungal pathogens"

Developing new ways of treating infectious disease has become more pressing with the development of resistance to antibiotics.

One strategy being explored to treat infections that resist current drugs involves neutralizing the disease-causing agent. This strategy involves extracting the agent from the patient so that scientists can remove components of the microbe's DNA in order to neutralize the disease.

This new harmless agent is then grown in the lab and re-introduced to the disease site with the expectation that it will out-compete its more harmful cousin by stealing resources, the disease needs to proliferate. Such research has proved effective in several lab tests.



The University of Exeter scientists tested this method in rice blast infections, but they found more severe disease symptoms.

Professor Nick Talbot, Professor of Molecular Genetics and expert in plant diseases, said: "The strategy of introducing less aggressive microbes to fight more aggressive ones may prove effective to control some crop disease, but our study shows that they are not a silver bullet and caution needs to be exercised. We need to understand how microbes interact with each other in natural settings, before we can try to alter their ability to cause disease in this way. Our study also shows why mathematicians and biologists need to work together more often, because we would not have understood this phenomenon at all without the mathematical analysis carried out."

Richard Lindsay, a PhD student who worked on the research team, added: "Our findings are of central importance in understanding how microbial infections evolve, but also have wider significance for the treatment of cancer and the therapeutic control of disease in humans, animals and plants."
Source: Discovery Magazine

YOUR INPUT IS MUCH APPRECIATED! LEAVE YOUR COMMENT BELOW.

New Glowing technique is been used in Brain surgery

The fluorescent dye technique, originally developed to treat lung cancer, illuminated brain tumors in real-time during surgery, helping physicians distinguish between healthy and cancerous tissue an experimental cancer imaging tool that makes tumors glow brightly during surgery has shown promise again in a new Penn Medicine clinical study, this time in patients with brain cancer. The fluorescent dye technique, originally developed by surgeons at the Penn Center for Precision Surgery to treat lung cancer, illuminated brain tumors in real-time during surgery, helping physicians distinguish between healthy and cancerous tissue. Each year, over 15,000 people in the United States undergo surgeries to remove brain tumors.

Findings from the pilot study, led by first author John Y.K. Lee, MD, MSCE, an associate professor of Neurosurgery in the Perelman School of Medicine at the University of Pennsylvania, and co-director of the Center for Precision Surgery, were reported in this week in Neurosurgery.

A big challenge with brain surgery is ensuring the entire tumor is removed. It is difficult to identify the margins of the tumor with current approaches. Cancer tissue not visible to the naked eye or felt by fingers is often missed during tumor removal, leading to recurrence in some patients -- about 20 to 50 percent.



Penn's approach, which relies on an injectable dye that accumulates in cancerous tissues more so than normal tissues, may help change that. "Fluorescent contrast agents take visualization to a whole new level," Lee said. "It has the potential for real-time imaging, identification of disease, and most importantly, precise detection of the tumor's margins. With this, we know better where to cut."

The study also includes co-author, Sunil Singhal, MD, an associate professor of Surgery, and co-director the Center for Precision Surgery at Penn's Abramson Cancer Center, who first started work on this approach in his lab nearly 10 years ago.
The technique uses near-infrared, or NIR, imaging and the contrasting agent indocyanine green (ICG), which fluoresce a bright green under NIR light. ICG was developed during World War II as a dye in photography and, in 1958 it was approved by the U.S. Food and Drug Administration (FDA) for use in medicine, primarily in liver diagnostics and later in cardiology.

However, for this study, researchers used a modified version of ICG at a higher concentration delivered intravenously about 24 hours before surgery to ensure margins were included. This is the first time, to the author knowledge, that this delayed imaging of ICG has been used to visualize brain tumors. Patients enrolled in the clinical study were between the ages of 20 and 81 with a diagnosis of a solitary brain tumor and a presumed glioma based on imaging or prior surgery or biopsy.

Twelve of the 15 tumors demonstrated strong intraoperative fluorescence. The lack of glow in the three remaining tumors could potentially be due to their disease grade and timing of the injection, the authors suggested. Eight of the 15 patients demonstrated a visible glow through the dura, a thick membrane on the meninges of the brain, was opened, demonstrating the technology's ability to see deeply within the brain before the tumor is exposed. Once opened, all tumors were picked up by NIR imaging. The researchers also studied the surgical margins using neuropathology and magnetic resonance imaging, (MRI) to assess the accuracy and precision of NIR fluorescence in identifying tumor tissue.



Of the 71 specimens collected from MRI-enhanced tumors and their surgical margins, 61 (85.9 percent) fluoresced and 51 of these (71.8 percent) were classified as glioma tissue of the 12 MRI-enhancing gliomas, four patients had biopsy specimens that were both non-fluorescent and negative for tumor, which matched the gross total resection seen on their MRI. In contrast, 8 patients had residual fluorescent signal in the resection cavity. Only 3 of these patients showed gross total resection on MRI. This suggests a benefit of true-negative NIR signal after resection, the authors said
Over the past three plus years, Singhal, Lee, and their colleagues have performed more than 300 surgeries with the imaging tool in patients with various types of cancer, including lung, brain, bladder and breast. "This technique, if approved by the FDA, may offer great promise to physicians and patients," Singhal said. "It's a strategy that could allow greater precision across many different cancer types, help with early detection, and hopefully better treatment success."

Source: Materials provide by Perelman School of Medicine at the University of Pennsylvania.

YOUR INPUT IS MUCH APPRECIATED! LEAVE YOUR COMMENT BELOW.

Bitter Almonds: Banned Because They Cure Cancer?

By: Alexandria Addesso

Carcinogens, substances that are capable of causing cancer in living tissue, seem to be everywhere. Processed foods, microwaves, and plastic goods are just a few of the many, many everyday items that can cause cancer. With known carcinogens becoming more apparent in the collective societal consciousness, alternative treatments and natural preventative measures have become more popular.

Bitter almonds are known to contain vitamin B17. B17 is a glycoside nutrient used by alternative medical practitioners in cancer prevention, and some have even claimed that it is a cure for cancer yet no medical studies have backed up that claim. The commercial sales of bitter almonds have been illegal since 1995. The commercial sale of the supplement form of B17 has been banned by the FDA since the 1980s.



Recently there has been a swarm of controversy around the ban of the commercial sale of bitter almonds, with some coming to the inaccurate conclusion that the use of bitter almonds in any fashion is illegal in the United States. This has caused many conspiracy theories to form as to why the government would make such a ban on a natural substance that could combat cancer.

Is the government simply making laws to keep its citizens ill and fully reliant on drugs made by big pharmaceutical corporations? Although that statement may not be totally incorrect, there is another reason why the commercial sale bitter almonds and most forms of B17 in general iare banned. The extract of B17, laetrile, contains prussic acid which is a chemical precursor for cyanide. Yet other natural foods also contain benign forms of prussic acid such as apple seeds.



Human beings have been eating bitter almonds for thousands of years with little to no documented reports of poisoning. Yet lawmakers cite that the commercial sales of bitter almonds are banned due to a possible link to the commercial sale and production of cyanide. Currently possession and the consumption of bitter almonds is not illegal. Bitter almond trees grow wildly in the US and cooks are allowed to farm small quantities of bitter almonds for specific dishes and pastes.

YOUR INPUT IS MUCH APPRECIATED! LEAVE YOUR COMMENT BELOW.

Cannabis: A Cure For Cancer?

By: Alexandria Addesso

Cannabis has been utilized for medical purposes for thousands of years. Yet in many counties throughout the world it is still viewed as an illegal drug. In the United States cannabis on the federal level is listed as a Schedule 1 drug, classifying it as having “high potential for abuse and no known medical use,” even though it is legal for medicinal use in 25 states and recreational use in four states plus Washington DC.

While marijuana has been known to cure many illnesses from insomnia to depression to pms, one of its most significant uses in a treatment being studied for quite some time is with cancer. According to cancer.gov, tests have shown that the use of cannabinoid oils helped lessen or eliminate nausea, loss of appetite, and pain management better than more conventional pharmaceutical drugs. Oncologists are more likely to recommend or prescribe cannabis to their patients than any other types of physicians, but usually always in conjunction with more “conventional” treatments.



But the real question that needs to be answered is whether or not cannabis can be used to treat and cure cancer itself and not just it’s side effects? Cannabinoids are known to possess antitumor properties and be successful in limiting inflammation, cell proliferation, and cell survival. Yet not all cannabinoids come from the marijuana plant, there are also types that come from the human endorphin system as well synthetically made cannabinoids. Cannabidiol (CBD) makes up 40 percent of the cannabinoids extracted from the cannabis plant and is known for its anti-inflammatory and anti-anxiety properties. Tetrahydrocannabinol (THC) is the chemical in cannabis that, according to cancer.gov, is effective in shrinking tumors. Yet most if not all studies suggest that treatment for cancer using marijuana should be paired with other treatments such as chemotherapy to be most effective.



Even though studies have yet to deem cannabis as the cure-all for cancer, it has definitely been shown to be very effective. So why isn’t it legal for cancer treatment across the board? Pharmaceutical companies have too much to lose on patents on cancer drugs that have long been on the market. Being that there is still such a surging black market for cannabis, even in the extremely pure and medically useful distilled oil form, capitalism has too much to lose. Even those vendors in the cannabis industry legally pose a threat to big pharm being that most are locally owned business.

The bottom-line is, greed kills.

YOUR INPUT IS MUCH APPRECIATED! LEAVE YOUR COMMENT BELOW.

French Fries are the real killers

What is acrylamide?
Acrylamide is a chemical used primarily as a building block in making polyacrylamide and acrylamide copolymers. Polyacrylamide and acrylamide copolymers are used in many industrial processes, such as the production of paper, dyes, and plastics, and in the treatment of drinking water and wastewater, including sewage. They are also found in consumer products, such as caulking, food packaging, and some adhesives. Trace amounts of acrylamide generally remain in these products.

Is there acrylamide in food?
Researchers in Europe and the United States have found acrylamide in certain foods that were heated to a temperature above 120 degrees Celsius (248 degrees Fahrenheit), but not in foods prepared below this temperature (1). Potato chips and French fries were found to contain higher levels of acrylamide compared with other foods (2). The World Health Organization and the Food and Agriculture Organization of the United Nations stated that the levels of acrylamide in foods pose a “major concern” and that more research is needed to determine the risk of dietary acrylamide exposure (2).

How does cooking produce acrylamide?
Asparagine is an amino acid (a building block of proteins) that is found in many vegetables, with higher concentrations in some varieties of potatoes. When heated to high temperatures in the presence of certain sugars, asparagine can form acrylamide. High-temperature cooking methods, such as frying, baking, or broiling, have been found to produce acrylamide (3), while boiling and microwaving appear less likely to do so. Longer cooking times can also increase acrylamide production when the cooking temperature is above 120 degrees Celsius (4, 5).

Is there anything in the cooking process that can be changed to lower dietary acrylamide exposure?
Decreasing cooking time, blanching potatoes before frying, and postdrying (drying in a hot air oven after frying) have been shown to decrease the acrylamide content of some foods (6, 7).

Should I change my diet?
Acrylamide levels in food vary widely depending on the manufacturer, the cooking time, and the method and temperature of the cooking process (8, 9). The best advice at this time is to follow established dietary guidelines and eat a healthy, balanced diet that is low in fat and rich in high-fiber grains, fruits, and vegetables.

Are there other ways humans are exposed to acrylamide?
Food and cigarette smoke are the major sources of acrylamide exposure (10). Exposure to acrylamide from other sources is likely to be significantly less than that from food or smoking, but scientists do not yet have a complete understanding of all sources of exposure. Acrylamide and polyacrylamide are used in some industrial and agricultural procedures, and regulations are in place to limit exposure in those settings.

Does acrylamide increase the risk of cancer?
Studies in rodent models have found that acrylamide exposure poses a risk for several types of cancer (11, 12,13). However, the evidence from human studies is still incomplete. The National Toxicology Program and the International Agency for Research on Cancer consider acrylamide to be a “probable human carcinogen,” based on studies in laboratory animals given acrylamide in drinking water. However, toxicology studies have shown differences in acrylamide absorption rates between humans and rodents (14).

A series of case-control studies have investigated the relationship between dietary intake of acrylamide and the risk of developing cancers of the oral cavity, pharynx, esophagus, larynx, large bowel, kidney, breast, and ovary. These studies generally found no excess of tumors associated with acrylamide intake (15, 16, 17, 18, 19). In the studies, however, not all acrylamide-containing foods were included in estimating exposures. In addition, information in case-control studies about exposures is often based on interviews (personal or through questionnaires) with the case and control subjects, and these groups may differ in the accuracy of their recall about exposures. One factor that might influence recall accuracy in cancer-related dietary studies is that diets are often altered after receiving a diagnosis of cancer.

To avoid such limitations in accurately determining acrylamide exposure, biomarkers of exposure were recently used in a Danish cohort study designed to evaluate the subsequent risk of breast cancer in postmenopausal women (20). Among women with higher levels of acrylamide bound to the hemoglobin in their blood, there was a statistically significant increase in risk of estrogen receptor-positive breast cancer. This finding suggests an endocrine hormone-related effect, which would be consistent with the results of a questionnaire-based cohort study in the Netherlands that found an excess of endometrial and ovarian cancer—but not of postmenopausal breast cancer—associated with higher levels of acrylamide exposure (21). Another cohort study from the Netherlands suggested a positive association between dietary acrylamide and the risk of renal cell cancer, but not of prostate or bladder cancer (22).

What are other health effects of acrylamide?
High levels of acrylamide in the workplace have been shown to cause neurological damage, e.g., among workers using acrylamide polymers to clarify water in coal preparation plants (23).

Are acrylamide levels regulated?
The U.S. Environmental Protection Agency (EPA) regulates acrylamide in drinking water. The EPA established an acceptable level of acrylamide exposure, set low enough to account for any uncertainty in the data relating acrylamide to cancer and neurotoxic effects. The U.S. Food and Drug Administration regulates the amount of residual acrylamide in a variety of materials that come in contact with food, but there are currently no guidelines governing the presence of acrylamide in food itself.

What research is needed?
Although studies in rodent models suggest that acrylamide is a potential carcinogen, additional epidemiological cohort studies are needed to help determine any effects of dietary acrylamide intake on human cancer risk. It is also important to determine how acrylamide is formed during the cooking process and whether acrylamide is present in foods other than those already tested. This information will enable more accurate and comprehensive estimates of dietary exposure. Biospecimen collections in cohort studies will provide an opportunity to avoid the limitations of interview-based dietary assessments by examining biomarkers of exposure to acrylamide and its metabolites in relation to the subsequent risk of cancer.

For information about acrylamide from the World Health Organization (WHO) and the Food and Agriculture Organization of the United Nations, please visit WHO's Food Safety: AcrylamideExit Disclaimer page.

For information about acrylamide from the National Toxicology Program (NTP), please visit NTP's Report on Carcinogens.

Selected References

1. Stadler RH, Blank I, Varga N, et al. Acrylamide from Maillard reaction products. Nature 2002; 419(6906):449–450.

2. Food and Agriculture Organization of the United Nations. World Health Organization. Summary report of the sixty-fourth meeting of the Joint FAO/WHO Expert Committee on Food Additives (JECFA). Retrieved July 24, 2008, from: http://www.who.int/entity/ipcs/food/jecfa/summaries/summary_report_64_final.pdf

3. Mottram DS, Wedzicha BL, Dodson AT. Acrylamide is formed in the Maillard reaction. Nature 2002; 419(6906):448–449.

4. Gertz C, Klostermann S. Analysis of acrylamide and mechanisms of its formation in deep-fried products.European Journal of Lipid Science and Technology 2002; 104(11):762–771.

5. Rydberg P, Eriksson S, Tareke E, et al. Investigations of factors that influence the acrylamide content of heated foodstuffs. Journal of Agricultural and Food Chemistry 2003; 51(24):7012–7018.

6. Kita A, Brathen E, Knutsen SH, Wicklund T. Effective ways of decreasing acrylamide content in potato crisps during processing. Journal of Agricultural and Food Chemistry 2004; 52(23):7011–7016.

7. Skog K, Viklund G, Olsson K, Sjoholm I. Acrylamide in home-prepared roasted potatoes. Molecular Nutrition and Food Research 2008; 52(3):307–312.

8. Tareke E, Rydberg P, Karlsson P, Eriksson S, Tornqvist M. Analysis of acrylamide, a carcinogen formed in heated foodstuffs. Journal of Agricultural and Food Chemistry 2002; 50(17):4998–5006.

9. Mojska H, Gielecinska I, Szponar L. Acrylamide content in heat-treated carbohydrate-rich foods in Poland.Roczniki Panstwowego Zakladu Higieny 2007; 58(1):345–349.

10. Urban M, Kavvadias D, Riedel K, Scherer G, Tricker AR. Urinary mercapturic acids and a hemoglobin adduct for the dosimetry of acrylamide exposure in smokers and nonsmokers. Inhalation Toxicology 2006; 18(10):831–839.

11. Dearfield KL, Abernathy CO, Ottley MS, Brantner JH, Hayes PF. Acrylamide: Its metabolism, developmental and reproductive effects, genotoxicity, and carcinogenicity. Mutation Research 1988; 195(1):45–77.

12. Dearfield KL, Douglas GR, Ehling UH, et al. Acrylamide: A review of its genotoxicity and an assessment of heritable genetic risk. Mutation Research 1995; 330(1–2):71–99.

13. Friedman M. Chemistry, biochemistry, and safety of acrylamide. A review. Journal of Agricultural and Food Chemistry 2003; 51(16):4504–4526.

14. Fuhr U, Boettcher MI, Kinzig-Schippers M, et al. Toxicokinetics of acrylamide in humans after ingestion of a defined dose in a test meal to improve risk assessment for acrylamide carcinogenicity. Cancer Epidemiology Biomarkers and Prevention 2006; 15(2):266–271.

15. Pelucchi C, Galeone C, Levi F, et al. Dietary acrylamide and human cancer. International Journal of Cancer2006; 118(2):467–471.

16. Mucci LA, Dickman PW, Steineck G, Adami HO, Augustsson K. Dietary acrylamide and cancer of the large bowel, kidney, and bladder: Absence of an association in a population-based study in Sweden. British Journal of Cancer 2003; 88(1):84–89.

17. Mucci LA, Lindblad P, Steineck G, Adami HO. Dietary acrylamide and risk of renal cell cancer. International Journal of Cancer 2004; 109(5):774–776.

18. Mucci LA, Adami HO, Wolk A. Prospective study of dietary acrylamide and risk of colorectal cancer among women. International Journal of Cancer 2006; 118(1):169–173.

19. Mucci LA, Sandin S, Balter K, et al. Acrylamide intake and breast cancer risk in Swedish women. Journal of the American Medical Association 2005; 293(11):1326–1327.

20. Olesen PT, Olsen A, Frandsen H, et al. Acrylamide exposure and incidence of breast cancer among postmenopausal women in the Danish Diet, Cancer and Health Study. International Journal of Cancer 2008; 122(9):2094–2100.

21. Hogervorst JG, Schouten LJ, Konings EJ, Goldbohm RA, van den Brandt PA. A prospective study of dietary acrylamide intake and the risk of endometrial, ovarian, and breast cancer. Cancer Epidemiology Biomarkers and Prevention 2007; 16(11):2304–2313.

22. Hogervorst JG, Schouten LJ, Konings EJ, Goldbohm RA, van den Brandt PA. Dietary acrylamide intake and the risk of renal cell, bladder, and prostate cancer. American Journal of Clinical Nutrition 2008; 87(5):1428–1438.

23. Mulloy KB. Two case reports of neurological disease in coal mine preparation plant workers. American Journal of Industrial Medicine 1996; 30(1):56–61.

http://www.oncologynurseadvisor.com/fact-sheets/acrylamide-in-food-and-cancer-risk-fact-sheet/article/426628/#