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Healthy Living Greatly Reduces Likelihood of Dying from Cancer

Posted on May 28, 2016  Comments (1)

Lifestyle choices can greatly reduce the incidence and death rates from cancer. 4 factors can reduce the incidence of cancer by up to 40% and death rate by 50%: don’t smoke, don’t drink alcohol in excess, maintain a BMI between 18.5 and 27.5, and exercising at a moderate intensity for at least 150 minutes or at a vigorous intensity for at least 75 minutes every week.

Preventable Incidence and Mortality of Carcinoma Associated With Lifestyle Factors Among White Adults in the United States

A substantial cancer burden may be prevented through lifestyle modification. Primary prevention should remain a priority for cancer control.

Cancer is the second leading cause of death in the United States, with 1.6 million new cancer cases and 0.6 million cancer deaths projected to occur in 2016.1 The cancer mortality rate, age-standardized to the 2000 US standard population, decreased from 199 to 163 per 100”¯000 between 1969 and 2013.2 However, this decline (17.9%) has been modest compared with the dramatic decrease in heart disease mortality (67.5%) during the same period, highlighting the need for further efforts in cancer prevention and treatment.

The study reviewed previous studies and the makeup of the previous studies and available statistics. As they state in the paper: “Because our cohorts’ participants were predominantly whites, to avoid any influence of different racial distributions on the comparison with the general population, we only included whites in the analysis.” They also excluded about 10% of cancers that are believed to have strong environmental factors.

Table Showing a Comparison of Lifestyle Factors in the Low- and High-Risk Groups

In the 2 cohort studies of US white individuals, we found that overall, 20% to 40% of carcinoma cases and about half of carcinoma deaths can be potentially prevented through lifestyle modification. Not surprisingly, these figures increased to 40% to 70% when assessed with regard to the broader US population of whites, which has a much worse lifestyle pattern than our cohorts.

Notably, approximately 80% to 90% of lung cancer deaths could be avoided if Americans adopted the lifestyle of the low-risk group, mainly by quitting smoking. For other cancers, from 10% to 70% of deaths could be prevented. These results provide strong support for the importance of environmental factors in cancer risk and reinforce the enormous potential of primary prevention for cancer control.

Related: A Healthy Lifestyle is More About Health Care than the Sickness Management That We Call Health Care Is – Better Health Through: Exercise, Not Smoking, Low Weight, Healthy Diet and Low Alcohol Intake (2013) – Exercise Is Really Really Good for You – Physical Activity for Adults: Inactivity Leads to 5.3 Million Early Deaths a Year (2012)

$1 Device To Give Throat Cancer Patients Their Voice Again

Posted on January 2, 2016  Comments (1)

Bengaluru Doctor Invents a Rs. 50 Device To Give Throat Cancer Patients Their Voice Again

Dr. Vishal Rao, a Bangalore based oncologist, has developed a voice prosthesis that can help throat cancer patients speak after surgery. And unlike the extremely expensive ones available in the market today, this device will cost just Rs. 50. [$US 1]

We need to keep developing cost effective solutions to provide for the needs of billions of people around the world. It is great to see appropriate technology solutions at work making people’s lives better.

Related: Appropriate Technology Health Care Solution Could Save 72,000 Lives a Year – Manufacturing Biological Sensors Using Silk and Looms – Pedal Powered Washing Machine – Appropriate Technology: Self Adjusting Glasses

Using Diatom Algae to Deliver Chemotherapy Drugs Directly to Cancer Cells

Posted on November 26, 2015  Comments (2)

I am thankful for scientists doing the time consuming and important research to find new ways to fight disease. Here is an interesting webcast discussing how chemotherapy is used to fight cancer and how scientists are looking to algae to deliver the chemotherapy drugs to better target cancer cells (while not savaging our health cells).

I am also thankful to the funding sources that pay for this research (and for cool explanations of science, like SciShow).

Read more about the genetically engineered algae kills 90% of cancer cells without harming healthy ones. The algae are a diatom and many diatoms look very cool.

Sadly the actual research paper (by government funded university professors) is published by a closed science publisher (when are we finally going to stop this practice that was outdated over a decade ago?). Thankfully those responsible for SciShow are much more interested in promoting science than maintaining outdated business models (in direct contrast to so many science journal publishers).

Related post on cool delivery methods for life saving drugs: Using Bacteria to Carry Nanoparticles Into Cells – Self-Assembling Cubes Could Deliver Medicine (2006) – Nanoparticles With Scorpion Venom Slow Cancer Spread – NASA Biocapsules Deliver Medical Interventions Based Upon What They Detect in the Body

Cancer Rates Consistent Across Species Instead of Increasing Due to Body Mass

Posted on October 12, 2015  Comments (1)

It would seem sensible to think cancer should be more prevalent in species with a huge number of cells, and thus more cells to become cancerous. But cancer risk doesn’t increase in this way. This interesting, open source paper, sheds some light on what is behind this.

Solutions to Peto’s paradox revealed by mathematical modelling and cross-species cancer gene analysis

Whales have 1000-fold more cells than humans and mice have 1000-fold fewer; however, cancer risk across species does not increase with the number of somatic cells and the lifespan of the organism. This observation is known as Peto’s paradox. How much would evolution have to change the parameters of somatic evolution in order to equalize the cancer risk between species that differ by orders of magnitude in size? Analysis of previously published models of colorectal cancer suggests that a two- to three-fold decrease in the mutation rate or stem cell division rate is enough to reduce a whale’s cancer risk to that of a human. Similarly, the addition of one to two required tumour-suppressor gene mutations would also be sufficient.

We surveyed mammalian genomes and did not find a positive correlation of tumour-suppressor genes with increasing body mass and longevity. However, we found evidence of the amplification of TP53 in elephants, MAL in horses and FBXO31 in microbats, which might explain Peto’s paradox in those species. Exploring parameters that evolution may have fine-tuned in large, long-lived organisms will help guide future experiments to reveal the underlying biology responsible for Peto’s paradox and guide cancer prevention in humans.

Elephants in Kenya

Elephants in Kenya by John Hunter. See more photos from my trip to Kenya.

In another way it would make sense that large animals would have hugely increased risks of cancer. As they evolved, extremely high cancer rates would be a much bigger problem for them. Therefore it wouldn’t be surprising to find they have evolved a way of reducing cancer risks.

Despite these limitations, we found genes that have been dramatically amplified in specific mammalian genomes, the most interesting of which is the discovery of 12 TP53 copies in the genome of the African elephant. We subsequently cloned those genes and identified 19 distinct copies of TP53 in African elephants and 15–20 in Asian elephants [1]. Another potential lead for solving Peto’s paradox is MAL, which is found to have eight copies in the horse genome and two in microbat. This could be an example of convergent evolution where a large animal (horse) and a small, long-lived animal (microbat) both evolved extra copies of the same gene to overcome their increased risk of cancer. Further analysis and experimentation would need to be performed to determine the function of these copies and whether or not they provide enhanced suppression of carcinogenesis.

The researchers have found an interesting potential explanation for how that has been accomplished.

Related: The Only Known Cancerless Animal (the naked mole rat) – Webcast of a T-cell Killing a Cancerous Cell – Researchers Find Switch That Allows Cancer Cells to Spread – Cancer Vaccines

Starting a Career in Science to Fight Cancer

Posted on June 14, 2014  Comments (1)

Keven Stonewall Preventing Colon Cancer from VNM USA on Vimeo.

Keven Stonewall is a student at the University of Wisconsin – Madison working to prevent colon cancer.

Related: I Always Wanted to be Some Sort of Scientist – High School Student Creates Test That is Much More Accurate and 26,000 Times Cheaper Than Existing Pancreatic Cancer Tests – Webcast of a T-cell Killing a Cancerous Cell

Massive Blast of Measles Vaccine Wiped Out Cancer In Study

Posted on May 31, 2014  Comments (0)

Unfortunately these stories are not uncommon but the hoped for follow through of practical solutions that work at all are rare. But we keep learning and while the breakthroughs based on these news stories is rare we do keep finding new and better methods to cope with health issues.

Mayo Clinic trial: Massive blast of measles vaccine wipes out cancer

Stacy Erholtz was out of conventional treatment options for blood cancer last June when she underwent an experimental trial at the Mayo Clinic that injected her with enough measles vaccine to inoculate 10 million people.

The 50-year-old Pequot Lakes mother is now part of medical history.

The cancer, which had spread widely through her body, went into complete remission and was undetectable in Erholtz’s body after just one dose of the measles vaccine, which has an uncanny affinity for certain kinds of tumors.

Erholtz was one of just two subjects in the experiment and the only one to achieve complete remission. But the experiment provides the “proof of concept” that a single, massive dose of intravenous viral therapy can kill cancer by overwhelming its natural defenses, according to Dr. Stephen Russell, a professor of molecular medicine who spearheaded the research at Mayo.
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Researchers have known for decades that viruses can be used to destroy cancer. They bind to tumors and use them as hosts to replicate their own genetic material; the cancer cells eventually explode and release the virus. Antiviral vaccines that have been rendered safe can produce the same effects and can also be modified to carry radioactive molecules to help destroy cancer cells without causing widespread damage to healthy cells around the tumors. The body’s immune system then attacks any remaining cancer that carries remnants of the vaccine’s genetic imprint.
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Mayo started out giving patients 1 million infectious units and gradually cranked up the dosage — but it didn’t work until Erholtz and another patient were injected with 100 billion infectious units, he said.

While the treatment worked in Erholtz, whose tumors were primarily in her bone marrow, the results weren’t sustained in the second patient, whose tumors were largely confined to her leg muscles. Russell said researchers need to study how the nature of the tumor affects the lethality of the virus.

One challenge of health research on fatal health conditions is that the experimentation with people is usually limited to people that have no available options left from the approved treatments. So, in general they are very sick. And the great complexity of dealing with human immune systems, the variation in the disease and in people create a very difficult research environment. Thankfully we have many great scientists dedicated to finding new treatments.

Related: Virus Kills Breast Cancer Cells in Laboratory – Virus Engineered To Kill Deadly Brain Tumors – Using Bacteria to Carry Nanoparticles Into Cells – Webcast of a T-cell Killing a Cancerous Cell

Outdoor Air Pollution Resulted in 223,000 Cancer Deaths in 2010

Posted on October 19, 2013  Comments (7)

The specialized cancer agency of the World Health Organization, the International Agency for Research on Cancer (IARC), announced today that it has classified outdoor air pollution as carcinogenic to humans.

After thoroughly reviewing the latest available scientific literature, the world’s leading experts convened by the IARC Monographs Programme concluded that there is sufficient evidence that exposure to outdoor air pollution causes lung cancer. They also noted a positive association with an increased risk of bladder cancer.

Particulate matter, a major component of outdoor air pollution, was evaluated separately and was also classified as carcinogenic to humans.

The IARC evaluation showed an increasing risk of lung cancer with increasing levels of exposure to particulate matter and air pollution. Although the composition of air pollution and levels of exposure can vary dramatically between locations, the conclusions of the Working Group apply to all regions of the world.

Air pollution is already known to increase risks for a wide range of diseases, such as respiratory and heart diseases. Studies indicate that in recent years exposure levels have increased significantly in some parts of the world, particularly in rapidly industrializing countries with large populations. The most recent data indicate that in 2010, 223,000 deaths from lung cancer worldwide resulted from air pollution.

“The air we breathe has become polluted with a mixture of cancer-causing substances,” says Dr Kurt Straif.

The stories of amazingly high (and persistent) air pollution levels in China have been continuing for years. But, while China, likely represents several of the worst existing air pollution conditions hundreds of thousands have died outside China due to air pollution just in the last 5 years.

Continue reading →

Cell Aging and Limits Due to Telomeres

Posted on March 17, 2013  Comments (2)

When cells divide the process fails to copy DNA all the way to the end. Telomeres are are the end of DNA strands, as essentially a buffer of material that won’t cause information to be lost when part of the telomere isn’t copied. As DNA is copied, as new cells are created, the length of telomeres at the end is reduced. Once the telomeres are gone the cell will no longer divide.

The 2009 Nobel Prize in Physiology or Medicine went to 3 scientists for discovering how the chromosomes can be copied in a complete way during cell divisions and how they are protected against degradation. The Nobel Laureates have shown that the solution is to be found in the ends of the chromosomes – the telomeres – and in an enzyme that forms them – telomerase.

There is some debate over the benefit of the mechanism of cells not dividing do to lack of telomere. This can prevent cancerous cells from replicating (once they replicate to the extent that the necessary telomere buffer is gone). It is also seen that as telomeres get shorter the cells become more likely to become cancerous.

Cancer also can stimulate the production of telomerase which can stop telomeres from getting shorter as cells divide and thus allow the cancer cells to keep dividing (thus producing more cancer cell and increasing the amount of cancerous cells). Using telomerase to allow health cells to avoid the limits of division is being researched.

Are Telomeres the Key to Aging and Cancer? (University of Utah)

An enzyme named telomerase adds bases to the ends of telomeres. In young cells, telomerase keeps telomeres from wearing down too much. But as cells divide repeatedly, there is not enough telomerase, so the telomeres grow shorter and the cells age.
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Cells normally can divide only about 50 to 70 times, with telomeres getting progressively shorter until the cells become senescent, die or sustain genetic damage that can cause cancer.
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shorter telomeres are associated with shorter lives. Among people older than 60, those with shorter telomeres were three times more likely to die from heart disease and eight times more likely to die from infectious disease.

While telomere shortening has been linked to the aging process, it is not yet known whether shorter telomeres are just a sign of aging – like gray hair – or actually contribute to aging.

Related: The Naked Mole Rat is the Only Known Cancerless Animal – Webcast of a T-cell Killing a Cancerous Cell – RNA interference webcast

Cancer Cells in Blind Mole Rats ‘commit suicide’

Posted on November 6, 2012  Comments (3)

Cancer cells in blind mole rats ‘commit suicide’

Blind mole rats don’t get cancer, and geneticists have worked out why — their cells kill themselves with a poisonous protein when they multiply too much.

Blind mole rats, which live in underground burrows throughout Southern and Eastern Africa, and the Middle East, are fascinating creatures. The naked mole rat, in particular, is the only cold-blooded mammal known to man, doesn’t experience pain, and is also arguably the only mammal (along with the Damaraland mole rat) to demonstrate eusociality — that is, they live in large hierarchical communities with a queen and workers, like ants or bees.

They’re also cancer-proof, which was found in 2011 to be down to a gene that stops cancerous cells from forming. The same team thought that two other cancer-proof mole rat species might have similar genes, but instead it turns out that they do develop cancerous cells — it’s just that those cells are programmed to destroy themselves if they become dangerous.

Very interesting research. The results of evolution are amazing. And while turning the medical research discoveries into workable treatments for people is very difficult the continued increase in our knowledge helps us find treatments that work.

Related: Webcast of a T-cell Killing a Cancerous Cell – Synthetic Biologists Design a Gene that Forces Cancer Cells to Commit Suicide

Key Indicator for Malignant Melanoma Found

Posted on September 20, 2012  Comments (2)

Skin cancer detection breakthrough

The researchers found that certain biochemical elements in the DNA of normal pigment-producing skin cells and benign mole cells are absent in melanoma cells. Loss of these methyl groups — known as 5-hmC — in skin cells serves as a key indicator for malignant melanoma. Loss corresponded to more-advanced stages of melanoma as well as clinical outcome.

Strikingly, researchers were able to reverse melanoma growth in preclinical studies. When the researchers introduced enzymes responsible for 5-hmC formation to melanoma cells lacking the biochemical element, they saw that the cells stopped growing.

“It is difficult to repair the mutations in the actual DNA sequence that are believed to cause cancer,” said Christine Lian, a physician-scientist in the Department of Pathology at BWH and one of the lead authors. “So having discovered that we can reverse tumor cell growth by potentially repairing a biochemical defect that exists — not within the sequence but just outside of it on the DNA structure — provides a promising new melanoma treatment approach for the medical community to explore.”

Because cancer is traditionally regarded as a genetic disease involving permanent defects that directly affect the DNA sequence, this new finding of a potentially reversible abnormality that surrounds the DNA (thus termed “epigenetic”) is a hot topic in cancer research, according to the researchers.

In the United States, melanoma is the fifth most common type of new cancer diagnosis in men and the seventh most common type in women. The National Cancer Institute estimates that in 2012 there will be 76,250 new cases and 9,180 deaths in the United States owing to melanoma.

Thankfully scientists keep making great progress in understanding and finding potential clues to treating cancer. And big gains have been made in treating some cancers over the last few decades. But the research successes remain difficult to turn into effective solutions in treating patients.

I am thankful we have so many scientists doing good work in this difficult and important area (cancer).

Related: Webcast of a T-cell Killing a Cancerous Cell – Nanoparticles With Scorpion Venom Slow Cancer Spread – DNA Passed to Descendants Changed by Your Life – Researchers Find Switch That Allows Cancer Cells to Spread

Virus Kills Breast Cancer Cells in Laboratory

Posted on August 5, 2012  Comments (2)

Some very exciting and good news from Penn State. Researchers have found a virus that kills breast cancer cells. It is great to read about research breakthroughs like this. Of course, most of these announcements never become practical solutions, unfortunately. And if they do it is many many years later and almost always in much less exciting ways than the headlines. Still, the percentage that do make it through the process into workable solutions provide us great benefits.

Virus kills breast cancer cells in laboratory

Adeno-associated virus type 2 (AAV2) is a virus that regularly infects humans but causes no disease. Past studies by the same researchers show that it promotes tumor cell death in cervical cancer cells infected with human papillomavirus. Researchers used an unaltered, naturally occurring version of AAV2 on human breast cancer cells.

“Breast cancer is the most prevalent cancer in the world and is the leading cause of cancer-related death in women,” said Samina Alam, research associate in microbiology and immunology. “It is also complex to treat.”
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“We can see the virus is killing the cancer cells, but how is it doing it?” Alam said. “If we can determine which viral genes are being used, we may be able to introduce those genes into a therapeutic. If we can determine which pathways the virus is triggering, we can then screen new drugs that target those pathways. Or we may simply be able to use the virus itself.”
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AAV2 does not affect healthy cells. However, if AAV2 were used in humans, the potential exists that the body’s immune system would fight to remove it from the body. Therefore, by learning how AAV2 targets the death pathways, researchers potentially can find ways to treat the cancer without using the actual virus.

In ongoing studies, the Penn State researchers also have shown AAV2 can kill cells derived from prostate cancer, mesothelioma, squamous cell carcinoma, and melanoma. A fourth line of breast cancer cells — representing the most aggressive form of the disease — also was studied in a mouse breast tumor model, followed by treatment with AAV2. Preliminary results show the destruction of the tumors in the mice, and researchers will report the findings of those mouse studies soon.

The fight against cancer has many promising breakthroughs. We have made some great progress. Still the fight is extremely difficult and we have many more frustrations than successes.

Related: Webcast of a T-cell Killing a Cancerous Cell – Synthetic Biologists Design a Gene that Forces Cancer Cells to Commit Suicide – Researchers Find Switch That Allows Cancer Cells to Spread