The results of a study released by the CDC on April 6 show that more than 1 in 5 U.S. adults are infected with cancer-causing HPV.

“We tend to overlook the fact that 20 percent of us are carrying the virus that can cause cancer,” said Geraldine McQuillan, lead author of the report and a senior infectious-disease epidemiologist in the Division of Health and Nutrition Examination Surveys at the CDC's National Center for Health Statistics. “People really need to realize that this is a serious concern.”

During 2011-14, prevalence of any oral HPV among adults aged 18-69 was 7.3 percent and high-risk oral HPV was 4.0 percent. Prevalence of any and high-risk oral HPV was lowest among non-Hispanic Asian adults and any oral HPV was highest among non-Hispanic black adults.

During 2013–2014, any genital HPV prevalence among adults aged 18-59, was:

• 42.5 percent in the total population,
• 45.2 percent among men,
• 39.9 percent among women.

High-risk genital HPV prevalence was:

• 22.7 percent in the total population,
• 25.1 percent among men,
• 20.4 percent among women.

In the U.S., the CDC estimates 31,000 women and men are diagnosed with a cancer caused by HPV infection. Cervical cancer accounts for 1 in 3 cancers caused by HPV infection. While there is screening for cervical cancer, there is no routine screening for the other 20,000 cancers caused by HPV infections each year. Often these cancers — such as cancers of the back of the throat (oropharynx) and cancers of the anus/rectum — aren’t detected until later stages when they are difficult to treat.

• Cervical cancer deadlier than revealed

Most cervical cancer cases are seen in women under the age of 50. Women of African ancestry have a higher risk factor than caucasian women.

The Washington Post reported that lingering misconceptions and fears are among the reasons for the lower use of HPV vaccination, according to Electra Paskett, a cancer control researcher at Ohio State University's Comprehensive Cancer Center. Some people still think vaccination encourages youth to become promiscuous. “The way [the vaccine] was introduced in Australia and the United Kingdom was as a cancer vaccine, which is truly what it is. It is a cancer vaccine,” Paskett said.

Data from the National Health and Nutrition Examination Survey from 2011-14 were used for these analyses. NHANES is a program of studies designed to assess the health and nutritional status of adults and children in the U.S. The survey is unique in that it combines interviews and physical examinations.

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Researchers followed 86,206 women from 1980 to 2012 and 43,977 men from 1986 to 2012. Baseline aspirin use was recorded and then researchers followed up on use every two years after that. Participants with a history of cancer, heart disease, or stroke were excluded.

Long-term follow of clinical trials of aspirin for the prevention of cardiovascular disease have shown that aspirin may be associated with a reduced risk of death from cancer, including colorectal, esophageal, and lung cancer, and possibly breast and prostate cancer.

• Long-term aspirin use and total and cancer-specific mortality

Researchers were from Massachusetts General Hospital, Harvard Medical School, Harvard T.H. Chan School of Public Health, Brigham and Women’s Hospital, and Dana Farber Cancer Institute.

“Evidence suggests that aspirin not only reduces the risk of developing cancer, but may also play a strong role in reducing death from cancer,” said Yin Cao, lead author of the study and an instructor in Medicine, Clinical, and Translational Epidemiology Unit at Massachusetts General Hospital and Harvard Medical School.

Overall mortality risk rates among aspirin users compared to those who did not were 11 percent (men) and 7 percent (women) lower. Mortality risk from cancer was 7 percent lower for women and 15 percent lower for men who used aspirin compared to those who did not.

During the study timeframe, 22,094 women and 14,749 men died. Among those, 8,271 women and 4,591 men died of cancer, the study found.

The largest reduction in mortality risk was for colorectal cancer — 31 percent reduction for women and 30 percent for men who regularly took aspirin. Women who took aspirin were also at a 11 percent lower risk of dying from breast cancer. Men who took aspirin had a 23 percent lower risk of dying from prostate cancer, the result showed.

The study noted that the potential benefits of aspirin use, at a range of doses and duration of use, on total and cancer-specific mortality have not been examined in large prospective cohort studies with long-term follow-up.

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According to the CBC report, the country’s marijuana supply and license producers will be legislated by lawmakers in Ottawa. The national age limit to purchase the drug will be set at 18, but provinces will be able to set it higher. Provinces also will control price, along with how marijuana is bought and sold.

Also, Canadians who wish to grow their own marijuana would be limited to four plants per household.

Marijuana legalization was a high-profile campaign promise for Prime Minister Justin Trudeau.

Speaking with the Toronto Star’s editorial board in December, Trudeau stressed that marijuana remains illegal until legislation passes. The prime minister also condemned the rise of illegal storefront dispensaries. “People are right now breaking the law,” Trudeau said.

“We haven’t changed the laws. We haven’t legalized it yet. Yes, we got a clear mandate to do that. We’ve said we will. We’ve said we’re going to do it to protect our kids and to keep the money out of the pockets of criminals.”

The new rules generally follow the recommendations of a federal task force chaired by Anne McLellan, a former justice minister. The task force delivered a 106-page report in December with 80 recommendations.

Marijuana has health benefits for cancer patients, including:

• CBD, a compound within marijuana, has the potential to halt the spread of cancer by switching off a gene called Id-1;
• It can provide immense relief to those undergoing chemotherapy, by reducing nausea, while relieving pain.

Mark Pedersen of the eCS Therapies Center, an organization which concentrates on cannabis education, told Cancer Tutor, “The effects of THC are felt when that chemical makes its way to those receptors within the brain, according to Pedersen. “The euphoria we experience is basically identical to the experience we have, what people call ‘runner's high'.”

“Basically, that happens whenever anandamide is released into your bloodstream because you've exerted yourself and because one of the responsibilities of your endocannabinoid system is modulating the chemicals that repair our cells and strip away the waste and deal with the cells like cancer cells.”

Cannabis can not only be an effective, valid cancer treatment, but also a first-line preventative measure, according to Pedersen.

“Cannabis affects a weakened and/or damaged endocannabinoid system, essentially supercharging it,” Pedersen explained. “The endocannabinoid system is responsible for dealing  with cancerous tumors, as well as basic cell health. Cannabis has actually been found to stimulate the production of endocannabinoids.

“Because it works with this endogenous system, it is effective in treating all forms of cancer — albeit, with varying levels of success based on the condition of the patient's heath, current damage from the cancer and conventional treatments, age, etc. Of course, cannabis oil is an excellent preventative treatment.”

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However, exploitation of these discoveries has been slow because of the lack of a test to easily measure functional levels of AMACR. [1]

Now a simple color-changing test to help scientists investigate potential cancer drugs has been developed by University of Bath scientists, allowing research to progress at a much greater speed than has been possible.

Scientists from the Department of Pharmacy & Pharmacology have created a simple and cheap test that turns a clear liquid bright yellow in the presence of the functional protein, within minutes. The research is published in the journal Chemical Communications. [2]

Lead author Dr. Matthew Lloyd, from the University of Bath Department of Pharmacy & Pharmacology, said: “The research suggests new ways of treating cancer can be developed based on reducing AMACR function, which is exciting, but progress has been extremely limited because of the technical difficulties in measuring function.

“One of the important things about our test is that we can now quickly analyze samples and start investigating the development of new treatments based on reducing AMACR function. It will also allow investigation of the underlying biology, which is currently poorly understood. There is also potential for developing the method into a new way of monitoring the cancer. This is an extremely significant step forwards in the field.”

Using the new test many samples can be analyzed quickly and at the same time, and the functional level of AMACR can be measured much more accurately than by previous methods.

“The development of new treatments to halt the spread of prostate cancer is crucial if we are to stop thousands of men dying from the disease every year,” said Dr. Iain Frame, Director of Research at Prostate Cancer UK. “It has been known for some time that a protein called AMACR is involved in prostate cancer development. This makes it an exciting drug target, but until now, it has been difficult to test the effectiveness of potential new drugs on blocking the protein.”

The post Color-change test may advance AMACR, cancer research appeared first on Cancer Tutor.

The program works by looking for specific molecular patterns in cancer DNA that are free flowing in the patients' blood and comparing the patterns against a database of tumor epigenetics, from different cancer types, collated by the authors. DNA from tumor cells is known to end up in the bloodstream in the earliest stages of cancer so offers a unique target for early detection of the disease.

“In general, the higher the fraction of tumor DNAs in blood, the more accurate the program was at producing a diagnostic result,” said UCLA Professor Jasmine Zhou, co-lead author of the paper. “Therefore, tumors in well­-circulated organs, such as the liver or lungs, are easier to diagnose early using this approach than in less­-circulated organs such as the breast.”

In the study, the new computer program and two other methods — Random Forest and Support Vector Machine — were tested with blood samples from 29 liver cancer patients, 12 lung cancer patients and 5 breast cancer patients. Tests were run 10 times on each sample to validate the results. The Random Forest and Support Vector Machine methods had an overall error rate (the chance that the test produces a false positive) of 0.646 and 0.604 respectively, while the new program obtained a lower error rate of 0.265. [1]

Twenty-five out of the 29 liver cancer patients and 5 out of 12 lung cancer patients tested in this study had early stage cancers, which the program was able to detect in 80 percent of cases. Although the level of tumor DNA present in the blood is much lower during the early stages of these cancers, the program was still able to make a diagnosis demonstrating the potential of this method for the early detection of cancer, according to the researchers.

Similarly, Zhou and her colleagues tested CancerLocator on real data from breast, liver, and lung cancer patients — though their model was developed to distinguish between those and non-cancer as well as colon and kidney tumors — and compared it to random forest and support vector machine approaches. Again they found that their approach outperformed the others, with an error rate of 0.265.

The research results were published in Genome Biology.

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From The New York Times:

The youngest of six siblings, David Rockefeller was born in Manhattan on June 12, 1915. His father, John D. Rockefeller Jr., the only son of the oil titan, devoted his life to philanthropy. His mother, Abby Aldrich Rockefeller, was the daughter of Nelson Aldrich, a wealthy senator from Rhode Island.

Besides Nelson, born in 1908, the other children were Abby, who was born in 1903 and died in 1976 after leading a private life; John D. Rockefeller III, who was born in 1906 and immersed himself in philanthropy until his death in an automobile accident in 1978; Laurance, born in 1910, who was an environmentalist and died in 2004; and Winthrop, born in 1912, who was governor of Arkansas and died in 1973.

David, the youngest, grew up in a mansion at 10 West 54th Street, the largest private residence in the city at the time. It bustled with valets, parlor maids, nurses, and chambermaids. For dinner every night his father dressed in black tie and his mother in a formal gown. [1]

These were the spoils of the family that derailed natural medicine and built what became Big Pharma by usurping the teachings of medical schools in the wake of the Flexner Report.

John D. Rockefeller founded Standard Oil Company in 1870. His fortune made him the first billionaire in the United States.

In the early half of the 20th century, the petrochemical giants organized a coup on the medical research establishments, hospitals and universities. The Rockefellers did this by sponsoring research and donating monetary gifts to U.S. universities and medical schools where research was drug based and further extended this policy to foreign medical establishments via their International Education Board. Those who were not drug based were refused funding and were soon dissolved in favor of the more lucrative pharmaceutical-based projects. [2]

• The Flexner Report

The obituary of David Rockefeller noted, “As an octogenarian, Mr. Rockefeller, whose fortune was estimated in 2012 at $2.7 billion, increasingly devoted himself to philanthropy, donating tens of millions of dollars in particular to Harvard, the Museum of Modern Art and the Rockefeller University, which John D. Rockefeller Sr. founded in 1901.” [3]

However, many on social media did not cast a favorable light on David Rockefeller:

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“Cancer, above all other diseases, has countless secondary causes. But, even for cancer, there is only one prime cause,” Warburg said. “Summarized in a few words, the prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar.”

Cancer cells are low in oxygen primarily because they have changed from taking in and utilizing oxygen for respiration to a more primitive form of respiration which utilizes sugar instead of oxygen. It is the cancer process itself which causes most of the lack of oxygen, not the lack of oxygen which causes the cancer process. [1]

Led by Iñigo San-Millán, director of the Sports Performance Department and physiology laboratory at the University of Colorado's Sports Medicine and Performance Center, researchers have examined the role of lactate in angiogenesis (the process by which new blood vessels form inside the tumors), immune escape (the cancer cells' ability to elude the body's immune response), and cell migration, as well as in metastasis and self-sufficient metabolism. [2]

“We still do not know the ‘why’ or the ‘purpose’ of the Warburg Effect, its role in cancer growth and carcinogenesis, or how to halt or reverse metabolic dysregulation in cancer cells,” San-Millán said.

The researchers noted despite lactate being the end product of the Warburg Effect, lactate does not just “sit around;” lactate turnover is significant in resting individuals and very high during exercise far exceeding the glucose turnover rate.

“In cancer, it seems plausible to think that many of, or all the highly orchestrated oncogene and tumor suppressor mutations promoting glycolysis, lactate formation and distribution, while at the same time suppressing oxidative disposal of lactate, are all actors in the same play, the subtitle of which is ‘The Warburg Effect,’ ” San-Millán notes. “In other words, we posit that lactagenesis for carcinogenesis is the purpose of the Warburg Effect in cancer cells and tumors.”

• What is lactagenesis?

The research was published in the journal Carcinogenesis. [3]

The post Lactate for carcinogenesis may explain ‘Warburg Effect’ appeared first on Cancer Tutor.

The finding provides more evidence for how long non-coding RNAs, which were once thought to be a type of “junk DNA” of no particular value or function, may instead play a critical role in triggering cells to become malignant and spread.

Evidence shows that lncRNAs have a major role in cell biology and development, often by controlling what genes are turned on, or “expressed” to carry out their genetic function. Scientists now believe that when these lncRNAs are dysregulated they can contribute to multiple disease processes, including cancer.

“This could be a turning point in our understanding of how cancer may be triggered and spreads,” said Emily Ho, director of the Moore Family Center for Whole Grain Foods, Nutrition and Preventive Health at OSU. The findings were published in the Journal of Nutritional Biochemistry. [1]

The lncRNAs are of special interest, researchers say, because they are so highly cell- and tissue-specific. Unlike many chemotherapeutic drugs that affect healthy cells as well as malignant ones and can cause undesired side effects, the control of lncRNAs may offer a new way to specifically prevent or slow the progression of malignant cells.

“It’s obviously of interest that this dietary compound, found at some of its highest levels in broccoli, can affect lncRNAs,” said Ho, who also is the principal investigator with the Linus Pauling Institute. “This could open the door to a whole range of new dietary strategies, foods or drugs that might play a role in cancer suppression or therapeutic control.”

In particular, this research showed that one lncRNA, called LINC01116, is upregulated in a human cell line of prostate cancer, but can be decreased by treatment with sulforaphane. The data “reinforce the idea that lncRNAs are an exciting new avenue for chemoprevention research, and chemicals derived from diet can alter their expression,” the scientists wrote in their study.

The impact of diet on lncRNA expression has been largely unknown until now, the researchers said. In this study, they identified a four-fold decrease in the ability of prostate cancer cells to form colonies when LINC01116 was disrupted.

That same lncRNA, they noted, is also overexpressed in studies of several other types of cancer, including brain, lung and colon cancer. Some other lncRNAs have been found at higher levels in breast, stomach, lung, prostate cancer and chronic lymphocytic leukemia.

“We showed that treatment with sulforaphane could normalize the levels of this lncRNA,” said Laura Beaver, a research associate in the Linus Pauling Institute and College of Public Health and Human Sciences, and lead author on the study. “This may relate to more than just cancer prevention. It would be of significant value if we could develop methods to greatly slow the progress of cancer, help keep it from becoming invasive.”

Among men, prostate cancer is the second most frequently diagnosed cancer globally, and the second leading cause of cancer-related deaths in the United States. Worth noting, the researchers said, is that an increased consumption of cruciferous vegetables such as broccoli, which are high in sulforaphane, appears to be associated with a lower risk of developing prostate cancer.

The post Broccoli may be a ‘turning point’ in understanding cancer appeared first on Cancer Tutor.

Jess Rowland, the EPA official, is at the center of more than 20 lawsuits that accuse Monsanto of failing to warn consumers and regulators of the risk Roundup can cause non-Hodgkin’s lymphoma. Rowland was a manager in the EPA’s pesticide division.

“[Monsanto] cannot say that Roundup does not cause cancer. We have not done the carcinogenicity studies with Roundup.”

Donna Farmer

Monsanto toxicologist

Monsanto sought Rowland’s help stop a probe of glyphosate by the Agency for Toxic Substances and Disease Registry, a part of the U.S. Health and Human Service Department. “If I can kill this I should get a medal,” Rowland told a Monsanto regulatory affairs manager who recounted the conversation in an email to his colleagues, according to a court filing. [1]

After the phone conversation with Rowland, the Monsanto head of U.S. regulatory affairs, Daniel Jenkins, cautioned his colleagues not to “get your hopes up,” according to an email.

“I doubt EPA and Jess can kill this,” Jenkins wrote. However, another internal Monsanto memorandum unsealed on Tuesday said the ATSDR, as the federal toxics agency is known, “agreed, for now, to take direction from EPA.”

Contrary conclusions on glyphosate

Farmers like Roundup because many crops, including corn, soybeans, and cotton, have been genetically modified to tolerate glyphosate. Farmers can spray it across fields to kill weeds while their crops survive.

Two years ago, a U.N.-sponsored scientific agency declared that glyphosate probably causes cancer. That finding from the International Agency for Research on Cancer caused an international uproar. Monsanto unleashed a fierce campaign to discredit the IARC's conclusions.

Evaluation of Five Organophosphate Insecticides and Herbicides

Since that announcement, however, others have looked at the same collection of data and come to contrary conclusions. The European Food Safety Agency convened a group of experts who concluded that glyphosate probably does not cause cancer. So did the UN's Food and Agriculture Organization.

Joint FAO/WHO Meeting on Pesticide Residues

Tim Litzenburg, one of the lawyers suing Monsanto, said the cache of unsealed documents “represents a huge development in public health.”

California lists glyphosate in Prop 65

Superior Court Judge Kristi Culver Kapetan ruled California can require Monsanto to label Roundup as a possible cancer threat. Thhe state will list glyphosate in Proposition 65 — a list of chemicals known to cause cancer — but if the IARC’s findings are disproved, court documents indicate glyphosate can be removed from Proposition 65. [2]

“If the glyphosate listing under Proposition 65 is invalidated, it will immediately remove the protection that the State considers necessary to public health and welfare,” the court documents state.

Monsanto, of course, defended the chemical. “The allegation that glyphosate can cause cancer in humans is inconsistent with decades of comprehensive safety reviews by the leading regulatory authorities around the world,” Monsanto said in a statement.

However, Donna Farmer, Monsanto’s lead toxicologist, admitted in her deposition that she “cannot say that Roundup does not cause cancer” because “We [Monsanto] have not done the carcinogenicity studies with Roundup.” [3]

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As a cancerous tumor progresses, it takes over parts of the body. It battles “regular” cells for space as well as nutrients. The tumor kills these cells. Upon death, such cells release DNA in the blood. This DNA impacts the affected tissue.

However, the results don’t indicate where the tumor resides.

Now, bioengineers at the University of California-San Diego have developed a blood test that could detect cancer — and locate where in the body the tumor is growing. “Knowing the tumor’s location is critical for effective early detection,” said Kun Zhang, a bioengineering professor at the UC San Diego Jacobs School of Engineering and senior author of the study.

The study could provide a way to diagnose cancer early on without having to do invasive surgical procedures like biopsies. Researchers published their findings in Nature Genetics.

Zhang and his team discovered a new clue in blood that could both detect tumor cells and identify where they are. When a tumor starts to take over a part of the body, it competes with normal cells for nutrients and space, killing them off in the process. As normal cells die, they release their DNA into the bloodstream — and that DNA could identify the affected tissue.

The method screens for a particular DNA signature called CpG methylation haplotypes, which are the addition of methyl groups to multiple adjacent CG sequences in a DNA molecule. Each tissue in the body can be identified by its unique signature of methylation haplotypes.

“We made this discovery by accident. Initially, we were taking the conventional approach and just looking for cancer cell signals and trying to find out where they were coming from. But we were also seeing signals from other cells and realized that if we integrate both sets of signals together, we could actually determine the presence or absence of a tumor, and where the tumor is growing,” Zhang said.

To develop their new method, the researchers put together a database of the complete CpG methylation patterns of 10 different normal tissues (liver, intestine, colon, lung, brain, kidney, pancreas, spleen, stomach and blood). They also analyzed tumor samples and blood samples from cancer patients at the UC San Diego Moores Cancer Center to put together a database of cancer-specific genetic markers.

Zhang and his team then screened blood samples from individuals with and without tumors. They looked for signals of the cancer markers and the tissue-specific methylation patterns. The test works like a dual authentication process — the combination of both signals, above a statistical cutoff, is required to assign a positive match.

“This a proof of concept. To move this research to the clinical stage, we need to work with oncologists to further optimize and refine this method,” Zhang said.

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