Cassava Plant Is A Potential Cure For Cancer And Infertility

Until now, this exotic plant has been used in making bread and drinks, but now studies have shown that it is a potential cancer and infertility treatment! Cassava, or manioc, also known by its scientific name of Mahinot esculenta, is a plant that is indigenous to the South American areas that belongs to the spurge family of plants.
Recent studies have shown that the cassava can be invaluable to our health thanks to the many health benefits it offers. The leaves of the plant are rich in proteins, lysine and beta-carotene, while the root is full of calcium and vitamin C. Eating the plant regularly will surely improve the bone strength and resistance. Scientists have also discovered that the plant can be used as a cure for infertility, headaches and arthritis.
Lankacnews.com reports that several studies have shown that the plant can be powerful treatment against tumors. Furthermore, tapioca, an extract of the cassava has been found to be very versatile and useful in treatment of various health conditions. It can prevent diabetes, birth defects, improve the circulation and the red blood cell count, maintain the fluid balance in the body, lower cholesterol, protect the bone mineral density, improve the digestion, prevent Alzheimer’s disease, protect the cardiovascular health and aid weight gain. Some people believe that tapioca can help cure bladder, colon and prostate cancer.

Preparing cassava for consumption

The cassava plant needs to be cooked finely before consumption, as it contains a small amount of cyanide that needs to be eliminated. First, you need to peel the plant. Then, cut it into pieces, and alternate them between hot and cold water. When they’re soaked, put them in the fridge and leave them for a couple of hours. Pour the liquid in which the cassava pieces have soaked in into another liquid like a fruit juice or water, and drink the solution before breakfast every morning.
The vitamin B17 content of the cassava is the reason behind its powerful anti-cancer properties. Knowing this, Dr. Cynthia Jayasuriya, an ear, nose and throat surgeon, started investigating foods high in this vitamin when she was diagnosed with transitional cell cancer. She was struggling with the diseases for nearly a decade, when she decided to try a natural therapy when she read about the cassava on WorldWithoutCancer.org.
Dr. Jayasuriya learned that the cassava is rich in this vitamin, so she started consuming for a month. She ate a total of 100 gr. of the plant three times a day. In the morning, she ate boiled cassava, while in the afternoon and evening she ate it as a curry. After a month, she did a cystoscopy which revealed no sign of the cancer!
Once the cassava plant enters the body, the vitamin B17 mixes with Rhodanese, an enzyme which breaks down the vitamin into three sugars. The cancer cell is an immature cell which has a different enzyme, beta-glucosidase, which breaks vitamin B17 into glucose, benzaldehyde and hydrocyanic acid. The acid acts as a LTTE cyanide capsule, effectively killing the cancer cell.
If the vitamin combines with the cancer cell enzyme, it breaks down to 1 sugar, 1 benzaldehyde and 1 hydrocyanic acid, which kills the cancer cell locally.
Source: http://www.healthiestuniverse.com/

Blood sample new way of detecting cancer

A new RNA test of blood platelets can be used to detect, classify and pinpoint the location of cancer by analysing a sample equivalent to one drop of blood. Using this new method for blood-based RNA tests of blood platelets, researchers have been able to identify cancer with 96 per cent accuracy. This according to a study at Umeå University in Sweden recently published in the journal Cancer Cell.

"Being able to detect cancer at an early stage is vital. We have studied how a whole new blood-based method of biopsy can be used to detect cancer, which in the future renders an invasive cell tissue sample unnecessary in diagnosing lung cancer, for instance. In the study, nearly all forms of cancer were identified, which proves that blood-based biopsies have an immense potential to improve early detection of cancer," according to Jonas Nilsson, cancer researcher at Umeå University and co-author of the article.
In the study, researchers from Umeå University, in collaborations with researchers from the Netherlands and the US, have investigated how a new method of blood-based RNA tests of the part of the blood called platelets could be used in detecting and classifying cancer.
The results show that blood platelets could constitute a complete and easily accessible blood-based source for sampling and hence be used in diagnosing cancer as well as in the choice of treatment method.
Blood samples from 283 individuals were studied of which 228 people had some form of cancer and 55 showed no evidence of cancer. By comparing the blood samples RNA profiles, researchers could identify the presence of cancer with an accuracy of 96 per cent among patients. Among the 39 patients in the study in which an early detection of cancer had been made, 100 per cent of the cases could be identified and classified.
In follow-up tests using the same method, researchers could identify the origin of tumours with a so far unsurpassed accuracy of 71 per cent in patients with diagnosed cancer in the lung, breast, pancreas, brain, liver, colon and rectum. The samples could also be sorted in subdivisions depending on molecular differences in the cancer form, which can be of great use in the choice of treatment method.

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Story Source:
The above post is reprinted from materials provided by Umea University. Note: Materials may be edited for content and length.

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Journal Reference:

1. Myron G. Best, Nik Sol, Irsan Kooi, Jihane Tannous, Bart A. Westerman, François Rustenburg, Pepijn Schellen, Heleen Verschueren, Edward Post, Jan Koster, Bauke Ylstra, Najim Ameziane, Josephine Dorsman, Egbert F. Smit, Henk M. Verheul, David P. Noske, Jaap C. Reijneveld, R. Jonas A. Nilsson, Bakhos A. Tannous, Pieter Wesseling, Thomas Wurdinger. RNA-Seq of Tumor-Educated Platelets Enables Blood-Based Pan-Cancer, Multiclass, and Molecular Pathway Cancer Diagnostics. Cancer Cell, 2015; 28 (5): 666 DOI: 10.1016/j.ccell.2015.09.018

Source: Science Daily

WHO Confirms Eating Meat Causes Cancer

On Monday, the World Health Organization confirmed that our high-meat diets are in fact killing us. According to the WHO report, processed meats like sausage and bacon undoubtedly cause cancer, and red meats, such as beef and lamb, most probably do so as well. But why is a food that equipped our ancestors with the large brains needed to reach the top of the food chain now killing us?
This month, 22 scientists from 10 countries met at the International Agency for Research on Cancer (IARC) in Lyon, France, to assess more than 800 studies on the association between cancer and meat consumption in order to evaluate the carcinogenicity of high-meat diets. Their results are now published in the online journal The Lancet. For their report, the team looked specifically at the health effects of eating processed meat (meat that has been transformed from its original state, such as bacon and sausage), and the effects of eating red meat (unprocessed animal muscle, such as beef, pork, and lamb). In order to evaluate these risks, the researchers investigated the association of cancer and meat consumption in several countries and also looked into how rat populations are affected by these diets.
Based on their research, a majority of the group “concluded that there is sufficient evidence in human beings for the carcinogenicity of the consumption of processed meat,” with the report specifically naming ham, hot dogs, sausages, and jerky in this category. In addition, the team classified the consumption of red meat as “probably carcinogenic to humans,” but cited that there was “inadequate evidence in experimental animals” to definitively prove this link. This correlation between cancer and eating processed meats was strongest seen in the case of colon and stomach cancer, although eating red meat was also linked to pancreatic and prostate cancer.
The move from a plant-based to more meat-based diet is largely credited as the pivotal step in human evolution. The protein and calories available in meat allowed humans to dedicate more energy to building bigger brains, which in turn allowed us to become the planet’s most dominant creature, NPR reported. However, although meat-eaters commonly use this fact to back their carnivorous decision, there are many key differences between how our ancestors ate meat versus how we do so now that make the comparison ineffective.
First off, we no longer prepare our meat the same way our ancestors did 2.3 million years ago. According to the WHO report, one of the major culprits for meat's carcinogenic properties is its preparation. Common meat processing techniques, such as curing and smoking, can often result in the formation of carcinogenic chemicals. For red meat, although cooking makes meat both taste better and easier to digest, it can also produce known or suspected carcinogens. High temperature cooking, such as pan-frying, grilling, or barbecuing were identified in the report as producing the highest quality of these chemicals.
In addition, the cuts of meat that we consume today also look different from those of our ancestors. For example, today most cultures consume only the muscle meats, but hunter-gatherers were known to eat all parts of the animal, including the organs. Eating only muscle can cause an imbalance, giving meat-eaters an overload of protein and iron without the addition of nutrients found in other body parts. Above all, our ancestors, and even our grandparents for that matter, did not eat nearly as much meat as we are eating today. According to the Earth Policy Institute, U.S. meat consumption rose from about 80 pounds annually per person in 1940 to over 180 pounds person person in 2012.
Although the study’s results are surprising, the researchers are not suggesting a complete abstinence from meat, but rather explain that their findings "support current public health recommendations to limit meat intake," Dr. Christopher Wild, director of the IARC, said in a statement, NBC reported.
"For an individual, the risk of developing colorectal cancer because of their consumption of processed meat remains small, but this risk increases with the amount of meat consumed," said IARC's Dr. Kurt Straif, NBC reported.
Source: Bouvard V, Loomis D, Guyton K, et al. Carcinogenicity of consumption of red and processed meat. The Lancet Oncology. 2015.

Is The Malaria Parasite The Cancer Cure We’ve Been Looking For? Accidental Discovery Displays Remarkable Results

As far as accidents go, stumbling upon a potential cure for cancer is one we can all probably forgive. According to a recent study, a group of Danish scientists might have done just that by discovering that a potential malaria vaccine had the unexpected side effect of killing tumors.
Malaria is bloodborne disease caused by the Plasmodium parasite. It is spread through humans by mosquito bites and, according to UNICEF, kills up to a million people each year. Malaria is especially dangerous for pregnant women as the parasite may attack the placenta, which then puts the child’s life at risk. In their ongoing efforts to prevent these specific infections, scientists from the University of Denmark made a remarkable observation: Due to the similar characteristics between tumors and placentas, the same technique malaria uses to attack and destroy placentas could also be used to destroy cancer tumors.
“The placenta is an organ, which within a few months grows from only few cells into an organ weighing approximately 2 pounds, and it provides the embryo with oxygen and nourishment in a relatively foreign environment,” study author Ali Salanti said in a statement. “In a manner of speaking, tumors do much the same — they grow aggressively in a relatively foreign environment."
The researchers attempted to improve on this natural design by attaching a cancer-killing toxin to the malaria protein. They found that the combination was lethal; in lab tests, it was up to 90 percent effective in destroying various cancer samples. The lethal combination was also tested successfully in mice that were implanted with different types of human cancers. And while it may seem jarring to trade off cancer for malaria, Thomas Mandel Clausen, a PhD student involved with the research, explained that the the malaria protein only attaches to the tumor “without any significant attachment to other tissue.”
It will be at least four years before the treatment will be available for human testing, and researchers are hopeful it’ll be a significant step forward in cancer treatment research. However, since the protein they use attaches to carbohydrates found only in the placenta and cancer tumors, this life-saving characteristic will make the treatment too dangerous for cancer treatment in pregnant women. “Expressed in popular terms, the toxin will believe that the placenta is a tumor and kill it, in exactly the same way it will believe that a tumor is a placenta,” Salanti said.
Source: Salani A, Clausen, Agerbæk M Ø, et al. Targeting Human Cancer by a Glycosaminoglycan Binding Malaria Protein. Cancer Cell. 2015

Antioxidants Don't Kill Cancer? Study Suggests That Taking These Compounds Does More Harm Than Good

Antioxidants are often promoted for their “cancer-killing” properties, but in a recent study, researchers found strong evidence to suggest that these unique molecules may actually promote the spread of certain cancer cells — a finding that could change the way doctors advise cancer patients to eat.
Antioxidants are compounds that can help to neutralize free radicals, natural substances that attack our cells and DNA. By neutralizing free radicals, antioxidants can prevent or delay some types of cell damage. These compounds can be found naturally in many types of food, most notably fruits and vegetables, but can also be man-made and taken in supplement form.
In order to investigate what effect antioxidants had on cancer cells, a team of researchers from the Children’s Research Institute at UT Southwestern gave these compounds to mice that had been transplanted with melanoma cells from cancer patients. The team observed that cancer spread faster in mice that were administered antioxidants than it did in mice that were not. According to the press release, since the spread of cancer, also known as metastasis, is the leading cause of death in most cancer patients, the finding was significant. These results also directly contradict past research that has shown that increased levels of antioxidants prevented cell damage associated with cancer development. According to Morrison, these findings may lead doctors to revise their dietary recommendations for cancer patients.
This is not the first time researchers have linked antioxidants to increased progression of cancer. In 1994, a study in The New England Journal of Medicine found a higher incidence of lung cancer among men who took the antioxidants vitamin E and beta-carotene. And again last year, a study published in Science Translational Medicine found that taking high doses of antioxidants such as vitamin E could actually speed up the progression of lung cancer in smokers and other high-risk patients.
"The idea that antioxidants are good for you has been so strong that there have been clinical trials done in which cancer patients were administered antioxidants," said Dr. Sean Morrison in a statement, explaining that some trials had to be stopped because the patients getting the antioxidants were dying faster. "Our data suggest the reason for this: Cancer cells benefit more from antioxidants than normal cells do."
Based on these results, Morrison suggests that pro-oxidants, compounds that promote rather than inhibit oxidation, may instead be beneficial to cancer patients. However, despite the finding, not everyone needs to take antioxidants off their menu. The study suggests that healthy people who do not have cancer can continue to receive that many benefits, such as fighting obesity, and protecting their eyesight without worry of adverse effects.

How elephant crush cancer

Why elephants aren’t riddled with tumors poses a weighty problem for researchers. A new study shows that the animals harbor dozens of extra copies of one of the most powerful cancer-preventing genes. These bonus genes might enable elephants to weed out potentially cancerous cells before they can grow into tumors.
When it comes to cancer, elephants appear to have several strikes against them. At up to 4800 kg, an African elephant packs about 100 times as many cells as you do. The more cells an animal carries, the higher the odds that one of them will suffer the DNA damage that can lead to cancer. Producing all those cells also entails numerous rounds of cell division, each of which can result in a tumor-triggering DNA break. Moreover, elephants can survive for more than 60 years in the wild, providing plenty of time for tumors to arise. “Long-lived animals with lots of cells should all be dropping dead of cancer,” says pediatric oncologist Joshua Schiffman of the University of Utah’s Huntsman Cancer Institute in Salt Lake City, who is a co-author on the new study. “But they don’t or they’d go extinct.”
The surprisingly low cancer rates in elephants and other hefty, long-lived animals such as whales—known as Peto’s paradox after one of the scientists who first described it—have nettled scientists since the mid-1970s. So far, researchers have made little progress in solving the mystery or determining how other long-lived species beat cancer. One exception involves naked mole rats. Although these African rodents aren’t massive, they survive for up to 28 years, almost 10 times longer than lab rats, and they don’t develop cancer. Two years ago, cell and molecular biologists Vera Gorbunova and Andrei Seluanov of the University of Rochester in New York and colleagues reported that one of naked mole rats’ defenses against cancer was a complex sugar called hyaluronan, which prevents their cells from clumping together to form tumors.
In the new study, Schiffman teamed up with Carlo Maley, an evolutionary cancer biologist at Arizona State University, Tempe, and colleagues. To put elephants’ cancer-fighting abilities into perspective, the researchers wanted to pin down different species’ vulnerability to tumors. The team used data from the Elephant Encyclopedia, which tallies the births and deaths of all captive elephants worldwide, and from necropsies performed on animals of more than 30 species at the San Diego Zoo in California. Fewer than 5% of elephants die from cancer, the scientists estimated, a lower rate than for smaller animals such as African wild dogs (8%) and humans (up to 25%).
A possible reason for pachyderms’ reduced susceptibility to cancer turned up in the genome of the African elephant. The researchers found that it contains 40 copies of the gene that encodes the protein p53, one of the most important mechanisms for preventing cancer. If cells have DNA damage that could spawn tumors, p53 prevents them from dividing until they make repairs or spurs them to commit suicide. Asian elephants harbor 30 to 40 copies of the gene, the team reports online today in the Journal of the American Medical Association.
In contrast, humans sport only two copies of the gene for p53, and so does elephants’ closest living relative, the rock hyrax. The extra copies probably accumulated millions of years ago as the gene was accidentally duplicated many times in the ancestors of elephants, the researchers suggest.
To investigate how the extra copies of the p53 gene fend off tumors, the team dosed African elephant cells with radiation, damaging their DNA. “We expected to see that elephants were repairing DNA like nobody’s business,” Schiffman says. But the animals’ cells weren’t any better than human cells at fixing broken DNA. Instead, the elephant cells were twice as likely to die after radiation exposure than were human cells. “We think we’ve figured out—maybe—why elephants don’t get cancer,” Schiffman says. The extra copies of the p53 gene enable elephants to kill off potentially cancerous cells before they form tumors. The study is consistent with a paper published earlier this week on the preprint server bioRxiv, which also found 40 copies of the gene for p53 in the elephant genome.
“This is exciting evidence for how [Peto’s] paradox is resolved by one giant animal,” says Gorbunova, who wasn’t connected to the new study. However, biochemist Vadim Gladyshev of Harvard Medical School says he’s skeptical because the researchers haven’t demonstrated that the extra genes produce working versions of p53. “My question is whether any of these genes have a function.”
Schiffman says that he and his colleagues are trying to determine whether they can make human cells more elephantlike, for example by inserting additional copies of the p53 gene or by identifying compounds that duplicate the effects of the extra copies.
Naked mole rats and elephants protect against cancer in different ways, Seluanov notes. “We need to look at long-lived, usually big animals,” he says, and we might find yet more ways of preventing cancer that that could potentially be useful for our cells

Cancer Overall Risk Rises With Every 4-Inch Increase In Height

Cancer risk increases with height, suggest researchers from Karolinska Institutet and University of Stockholm in Sweden.
“In our preliminary report, we present that for every 10-centimeter [about 4 inches] increase in height, overall cancer is increased by 18 percent in women and 11 percent in men,” said the researchers in a statement accompanying their presentation at the European Society for Pediatric Endocrinology.
Past studies have shown that taller people have a higher risk of developing different types of cancer, including breast cancer and melanoma, say the researchers. To investigate, a team led by Emelie Benyi, a Ph.D. student at Karolinska, examined medical and other records and tracked a large group of people — a total of 5.5 million men and women, all born in Sweden between 1938 and 1991, ranging in height (as adults) from 100 cm (3-foot-3) to 225 cm (7-foot-3). The team derived information from various databases, including the Swedish Medical Birth, the Swedish Conscription, the Swedish Passport Registers, and the Swedish Cancer Register. Tracking the group until the end of 2011, the researchers came to some surprising results.
“We found that total cancer risk and risks of breast cancer and melanoma were higher with increasing height in the Swedish population,” wrote the authors.
With each 10 cm of height, cancer risk increased by 18 percent in women and 11 percent in men, the researchers say. For both men and women, the risk of developing melanoma increased by nearly 30 percent per 10 cm, while taller women had a 20 percent greater risk of developing breast cancer.

One Example & Three Possible Reasons

Confused by all these percentages? The researchers say their risk estimates are comparisons, not absolute risks, and give this example to explain how it works: Swedish women have a 10 percent risk of developing breast cancer in their lifetimes. This scientific esimate was calculated based on a woman's height of 170 cm.
“According to our data where breast cancer is increased by 20 percent for each 10 cm increase in height, women of a height of 160 cm would in this example instead have a life time risk of breast cancer of about 8  percent and women of 180 cm would have a life time risk of about 12 percent,” the researchers wrote.
Benyi and her colleagues emphasized their results are only preliminary and only apply to Sweden. Having controlled for education and income, they explained socioeconomic variables did not change the results in any significant way.
So how about answering the key question — why is height linked to cancer? Possibly, the team explained, taller people (while young) are exposed to higher levels of growth factors, which could possibly promote cancer development. This, though, has not been verified.
“Another hypothesis could be that taller people simply have a larger number of cells in their bodies that then could potentially transform into cancer,” they wrote. “A third possible explanation is that taller individuals have a higher caloric intake, which has also previously been linked to cancer.”

5 Genetic Mutations Linked To Brain Cancer Might Explain Why Tumors Grow In The Brain

Nearly 70,000 new cases of primary brain cancer will be diagnosed this year, and the cause may lie within a person’s DNA. The Institute for Cancer Research has linked glioma, the most common form of brain cancer, with five genes that can be inherited throughout a family line. Scientists came across the discovery in what’s considered the largest study to date on DNA from people with glioma.
"These are exciting results because identifying genetic mistakes that increase the risk of glioma could be a vital first step toward developing new treatments against the disease,” said Dr. Aine McCarthy, a science information officer at Cancer Research UK, in a press release. “Building on these findings and determining the exact role these genetic changes play in the development of glioma could help doctors personalize treatment for the disease in the future and save more lives."
The research team compared DNA from more than 5,637 people who were diagnosed with glioma to 9,158 people without the disease. There are three billion letters of DNA that create a person’s genetic makeup, and each variant is a one-letter difference in the DNA code that increases risk of glioma for those who have the disease. When researchers searched each patient’s DNA code, they found a total of 12 mistakes in the genes of people with glioma.
According to the American Brain Tumor Association, there are currently more than 120 different types of brain tumors identified. Researchers found only one genetic variant increased risk of glioblastoma (23 percent); however, despite representing 17 percent of all primary brain tumors, the number of people affected by this type of glioma is relatively small. The other four variants that were found in patients’ genes were increased risk of non-glioblastoma forms of glioma developing by approximately 5 percent.
Dr. Melissa Bondy, associate director of Cancer Prevention and Population Sciences at the National Cancer Institute, said it was widely believed throughout the medical community that there was no association between family history and the development of gliomas. But that was before Bondy’s team of researchers linked genes to gliomas. The influence genetics have on a person’s risk of developing a certain cancer is just beginning to be understood, as genetic testing becomes more widely used in diagnostics.
"It provides firm evidence that susceptibility to the disease is in part inherited,” said the study’s lead researcher Richard Houlston, a professor of Molecular and Population Genetics at the Institute of Cancer Research, in the press release. "One of the risk factors we identified is linked to quite a dramatically increased chance of developing glioblastoma, a particularly aggressive kind of brain cancer. Our study sheds fresh light on the biology of gliomas, and could provide clues to why the disease develops, and how it could be treated or prevented."

Experimental New Drug Enlists Your Immune System In The Fight Against Cancer

The Centers for Disease Control and Prevention states that there are around 650,000 cancer patients receiving chemotherapy in the U.S. annually. Chemotherapy drugs lower the body’s white blood cell count and block cell growth and replication, which halts cancer cells from growing. Chemotherapy patients, however, become more prone to infections and illnesses with a lowered immune system. So, the obvious next step in chemotherapy drugs would be to create some that make the immune system fight the cancer cells as well. A new study published in Cell describes a class of experimental drugs that are being put through clinical trials, which aim to do just that.

UK researchers found that a protein normally involved in healthy cell growth and its spread, called Focal Adhesion Kinase (FAK), tends to be overproduced in tumors, thus helping cancer cells to avoid detection by the immune system. An effect of this is that rather than the immune system working to seek out and destroy cancer cells, it actively protects them. In their research, the team found that the experimental drug acts as a FAK inhibitor, preventing the protein from camouflaging the cancer cells, and allowing the immune system to do its job and destroy them.

The research was tested on mice with squamous cell carcinoma, a type of skin cancer. But the researchers believe the drugs would work on other forms of cancer as well. "FAK is hijacked by cancer cells to protect them from the immune system," lead author Dr. Alan Serrels said in a press release. "This exciting research reveals that by blocking FAK, we've now found a promising new way to help the immune system recognize the cancer and fight it."

He went on to state that since the drug is already in the early stages of clinical trials, it has the potential to be an excellent sidekick to existing immunotherapy treatments. "Because it works within tumor cells rather than influencing the immune cells directly," he said, "it could offer a way to reduce the side effects of treatments that harness the power of the immune system against cancer."

Another recent study looking to improve immunotherapy found that adding aspirin to the treatment could lead to better outcomes. Using COX inhibitors, a group of chemicals that aspirin falls under, researchers were able to help stop the production of prostaglandin E2 , which is produced by skin, breast, and bowel cancer cells. These same inhibitors triggered the immune system into action and got it to fight the cancer cells

Lifestyle May Be The Reason Cancer Is The Leading Cause Of Death For Hispanics

A new study published in CA: A Cancer Journal for Clinicians found cancer is still the leading cause of death among Hispanics. But the data is much more nuanced than that.
First, the results of the study: After analyzing incidence and mortality data from national registries, the American Cancer Society (ACS) anticipates 125,900 new cancer cases and 37,800 cancer deaths among Hispanics and Latinos living in the United States in 2015. Lung cancer remains the leading cause of cancer death among Hispanic men, while breast cancer is the leading cause of death among women — after lung and breast cancer, colorectal and prostate cancer are the most prevalent types of cancer.
These rates, however, significantly vary between Hispanic subpopulations. The ACS found that death rates among Puerto Ricans and Cubans are similar to death rates among non-Hispanic whites (NHWs). For example, the total cancer death rate for Puerto Rican men is 12 percent lower than the rate for NHW men, but is an estimated 20 percent higher rate than the rate for Mexican men. Similarly, Mexicans have the lowest death rates for the four prevalent types of cancer, yet they have the highest rates for infection-related cancers.
In addition to subpopulations, age also factors into cancer incidence: For young Hispanics aged 25 and younger, cancer death rates are comparable to rates for NHWs, though rates among those aged 15 to 19 are slightly higher. The ACS said that the risk factors for these subpopulations were low education and socioeconomic levels, smoking, alcohol, obesity, and infectious agents, like hepatitis B and human papillomavirus.
While there’s no doubt this disease is a concern, the overall cancer death rates are actually 30 percent lower in Hispanics today — equal to the rate among NHWs — than they were in 1995. In fact, each year since 1995 (1996 for women), this rate has been dropping by 2.4 percent among Hispanic and Latino men and 0.5 percent among women. What’s more is that the ACS found cancer burdens second-generation Hispanics more than it does first-generation Hispanics.
“The growth in the population of U.S. residents of Hispanic origin is now driven primarily by births, not immigration, which will probably change the future cancer risk profile of this group,” lead study author Rebecca L. Siegel, director of surveillance information for the ACS, said in a press release. “The second generation, born and raised in the U.S. and more intertwined in our lifestyle, including our diet, has higher cancer rates than first-generation immigrants, so we may see a higher cancer burden in this group in the future.”
Regardless of how high or low that burden turns out to be, this study suggests that the still-high cancer rate is driven by Western lifestyle patterns. Yet, as the ACS mentioned, it's difficult to accurately assess the risk profile for Hispanics because the term itself aggregates data. Using a single term to define several subpopluations just masks the distinct differences between them.
Hispanics face greater cultural and language differences in the U.S., too, decreasing the likelihood they'll get screened for prevalent cancers. The ACS reported the majority of Hispanics struggle with barriers, like a lack of health insurance.
"Efforts to further progress in cancer control must consider the dramatic differences in cancer risk within this heterogeneous population," the researchers concluded. "Effective strategies for decreasing cancer rates among Hispanics include the use of culturally appropriate lay health advisors and patient navigators; targeted, community-based intervention programs to increase screening and vaccination rates, and encourage healthy life-style behaviors; and further funding for subgroup- and site-specific research

3-D model of solid tumors explains cancer evolution

They're among the most powerful tools for shedding new light on cancer growth and evolution, but mathematical models of the disease for years have faced an either/or stand off.

Though models have been developed that capture the spatial aspects of tumors, those models typically don't study genetic changes. Non-spatial models, meanwhile, more accurately portray tumors' evolution, but not their three-dimensional structure.
A collaboration between Harvard, Edinburgh, and Johns Hopkins Universities including Martin Nowak, Director of the Program for Evolutionary Dynamics and Professor of Mathematics and of Biology at Harvard, has now developed the first model of solid tumors that reflects both their three-dimensional shape and genetic evolution. The new model explains why cancer cells have a surprising number of genetic mutations in common, how driver mutations spread through the whole tumor and how drug resistance evolves. The study is described in an August 26 paper in Nature.
"Previously, we and others have mostly used non-spatial models to study cancer evolution," Nowak said. "But those models do not describe the spatial characteristics of solid tumors. Now, for the first time, we have a computational model that can do that."
A key insight of the new model, Nowak said, is the ability for cells to migrate locally.
"Cellular mobility makes cancers grow fast, and it makes cancers homogenous in the sense that cancer cells share a common set of mutations. It is responsible for the rapid evolution of drug resistance," Nowak said. "I further believe that the ability to form metastases, which is what actually kills patients, is a consequence of selection for local migration."
Nowak and colleagues, including Bartek Waclaw of the University of Edinburgh, who is the first author of the study, Ivana Bozic of Harvard University and Bert Vogelstein of Johns Hopkins University, set out to improve on past models, because they were unable to answer critical questions about the spatial architecture of genetic evolution.
"The majority of the mathematical models in the past counted the number of cells that have particular mutations, but not their spatial arrangement," Nowak said. Understanding that spatial structure is important, he said, because it plays a key role in how tumors grow and evolve.
In a spatial model cells divide only if they have the space to do so. This results in slow growth unless cells can migrate locally.
"By giving cells the ability to migrate locally," Nowak said, "individual cells can always find new space where they can divide.
The result isn't just faster tumor growth, but a model that helps to explain why cancer cells share an unusually high number of genetic mutations, and how drug resistance can rapidly evolve in tumors.
As they divide, all cells -- both healthy and cancerous -- accumulate mutations, Nowak said, and most are so called "passenger" mutations that have little effect on the cell.
In cancer cells, however, approximately 5 percent are what scientists call "driver" mutations -- changes that allow cells to divide faster or live longer. In addition to rapid tumor growth, those mutations carry some previous passenger mutations forward, and as a result cancer cells often have a surprising number of mutations in common.
Similarly, drug resistance emerges when cells mutate to become resistant to a particular treatment. While targeted therapies wipe out nearly all other cells, the few resistant cells begin to quickly replicate, causing a relapse of the cancer.
"This migration ability helps to explain how driver mutations are able to dominate a tumor, and also why targeted therapies fail within a few months as resistance evolves," Nowak said. "So what we have is a computer model for solid tumors, and it's this local migration that is of crucial importance."
"Our approach does not provide a miraculous cure for cancer." said Bartek Waclaw, "However, it suggests possible ways of improving cancer therapy. One of them could be targeting cellular motility (that is local migration) and not just growth as standard therapies do