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10 new things we’ve learned about cancer
Cancer's sweet tooth. Turning cancer cells into fat. Unveiling genetic secrets. Scientists are learning about cancer every day.
- Cancer is a leading cause of death among Americans, second only to heart disease.
- Researchers are unearthing cancer's genetic secrets and, with it, potential new treatments.
- Their efforts have seen the cancer death rate for men, women, and children fall year after year between 1999 and 2016.
The 21st century has been, and will continue to be, shaped by cancer. Although heart disease remains the United States' number one killer, cancer is quickly closing the gap and may soon surpass it. Some oncologists claim a cure is five, 10, certainly no more than 20 years away. Others aren't so sure because, in a way, cancer is the price we pay for evolutionary success.
"It is no coincidence that the very genes that allow our embryos to grow — our hands to grow, our feet to grow — if you mutate them in inappropriate contexts, [they] will ultimately release the disease that kills us," said oncologist Siddhartha Mukherjee, who dubbed cancer the Emperor of All Maladies, also the title of his Pulitzer Prize-winning book.
Whether for five years or forever, cancer won't be going anywhere any time soon. Yet, the more doctors and scientists discover about it, the better we can learn to live with it.
A love-hate relationship: Cancer and antioxidants
Contrary to what many believe, cancer enjoys a nutrient-rich diet as much as the next cell because it helps it grow, even those legendary antioxidants.
In two independent studies published in Cell, Swedish and American research teams found that lung cancer utilizes antioxidants to activate a protein called BACH1. This protein stimulates the cancer cells to metabolize glucose and accelerate metastasis. Even without a ready supply of dietary antioxidants available, the tumor would simply produce its own.
Professor Martin Bergo, who led the Swedish study, hopes this research will help develop new treatments. "We now have important new information on lung cancer metastasis, making it possible for us to develop new treatments, such as ones based on inhibiting BACH1," he said in a release.
Does this mean you should abstain from antioxidant-rich foods? Not at all. Antioxidants do neutralize the free radicals that cause oxidative stress on cells. Preventing such cell damage can help prevent cancer.
However, it's best to avoid antioxidant supplements unless prescribed by a doctor. As reported by the National Cancer Institute, of nine randomized-controlled clinical trials, none provided evidence that such supplements lower cancer risks. A few even found that beta-carotene supplements increased the risk of lung cancer so severely that the trials had to be ended prematurely.
Get your antioxidants from fruits, veggies, and beans instead. Research suggests that these antioxidants work in combination with additional molecules found in the whole foods. It's this tag-team effect that ultimately give antioxidants their salubrious power.
Cancer costs (in more ways than one)
It goes without saying that cancer is costly. The physical strain of treatment. The potential loss of life, whether one's own or the life of a loved one. And even if one survives, there's the emotional cost of the ordeal.
But the toll imposed by cancer is more than physical or psychological. A study released last year found "that 42 percent of patients deplete their life savings during the first two years of treatment." Of the 9.5 million newly diagnosed cancer patients surveyed, the study calculated average losses at $92,098.
Its authors dubbed the effect "financial toxicity" and concluded: "As large financial burdens have been found to adversely affect access to care and outcomes, the active development of approaches to mitigate these effects among already vulnerable groups remains of key importance."
Cancer's sweet tooth
A recent study found a positive association between a daily sugary drink and an increased risk of cancer.
Researchers asked more than 100,000 people to complete surveys looking at their usual consumption of 3,300 foods and beverages. The results? A positive association between daily consumption of a sugary beverage and an increased risk of cancer. The sugary drinks not only included soda but also 100 percent fruit juice and artificially sweetened drinks.
"These data support the relevance of existing nutritional recommendations to limit sugary drink consumption, including 100% fruit juice, as well as policy actions, such as taxation and marketing restrictions targeting sugary drinks, which might potentially contribute to the reduction of cancer incidence," the researchers stated in a release.
Don't go trashing the OJ just yet, though. As an observational study, the data could not establish a cause-effect relationship, and the researchers note the results are only preliminary. Additionally, the results hinge on the memories of the participants. (What exactly did you eat for breakfast the Monday before last?)
But the study helps stress the American Institute for Cancer Research's (AICR) suggestion to limit sugary beverages. Try to remove soda from your diet. Drink 100 percent fruit juices with no added sugar sparingly. And of course, enjoy an active, healthy lifestyle.
Cancer on the grill
It's a summer tradition to throw some meat on the grill alongside a good beer. But grilled meats hide a few furtive carcinogens: polycyclic aromatic hydrocarbons and heterocyclic aromatic amines.
The hydrocarbons are carried in the smoke after fat burns on the flame, while the heterocyclic amines form when sugars, amino acids, and creatine react at high heats. Neither has been proven to cause cancer, but they are known mutagens that can damage DNA after being metabolized.
"Research shows that diets high in red and processed meat increase risk for colon cancer," said Alice Bender, AIRC Senior Director of Nutrition Programs. "And grilling meat, red or white, at high temperatures forms potent cancer-causing substances."
Like sugary drinks, however, you don't have to forever hang up your "Kiss the Cook" apron. The institute has several suggestions for safe summer grilling, such as limiting red meat, marinating foods beforehand, keeping a low flame, and throwing more vegetables into the mix.
A unified theory of leukemia
Acute lymphoblastic leukemia (ALL) afflicts about one in 2,000 children, and Mel Greaves, at the Institute of Cancer Research, London, believes he's found the cause. Researching 30 years of data and medical literature on childhood leukemia, he argues the "delayed infection" is the culprit.
According to this theory, children develop a pre-leukemia mutation in utero. The mutation remains inert until later in life when the child encounters a common infection. The microbes then trigger secondary genetic changes that led to overt leukemia.
Does this mean children are safe only in cleanrooms? Strike that, reverse it. Greaves believes exposure to germs in the first year of life is proactive. It trains the immune system to deal with pathogens, therefore preventing the secondary mutation from triggering.
"Childhood ALL can be viewed as a paradoxical consequence of progress in modern societies, where behavioral changes have restrained early microbial exposure," Greaves writes. "This engenders an evolutionary mismatch between historical adaptations of the immune system and contemporary lifestyles. Childhood ALL may be a preventable cancer."
The future of cancer treatment is genetic
A major stride toward our understanding of cancer came with the Human Genome Project. Why? At its core, cancer is a genetic disease.
Our ability to sequence and read cancerous genomes will be a major step toward cancer treatments. As Eric Green, director of the National Human Genome Research Institute, told Big Think:
"[The] standard of care for many types of cancer is going to be: Get that tumor, read out its DNA, sequence its genome and based on what you've seen what's wrong with that tumor -- not by looking at it under a microscope only or by looking at it in a sort of a gross fashion but actually looking inside its blueprint -- you will be able to have a much better way of deciding what types of treatments to pursue and have a much better idea about what's wrong in that kind of tumor."
A future treatment? The "cancer vaccine"
An airman receives a vaccine. Could the future of cancer treatment be as easy as a shot?
Rather than using chemotherapy to combat cancer with the subtlety of an atomic bomb, immunotherapies aim to uncloak cancer cells, so the body's immune system can go on the offensive
One example of an immunotherapeutic approach is the so-called "cancer vaccine." During its clinical trial, 11 patients had a tumor injected with a steroid to bolster the site's dendritic cells — immune system cells that specialize in processing antigens.
Following a light dose of radiation and a stimulant, the patients' dendritic cells directed T-cells to attack the cancer cells. Once the T-cells could recognize the tumor, they became able to locate cancer cells throughout the body.
Of the 11 patients, three saw their cancer go into regression or remission. Six others had their cancer stymied for at least three months.
"It's really promising, and the fact you get not only responses in treated areas, but areas outside the field [of treatment with radiation] is really significant," Dr. Silvia Formenti, chairwoman of radiation oncology at Weill Cornell Medicine and New York Presbyterian, told CNBC. (Dr. Formenti was not involved in the study.)
Turning tumors into fat
Cancer cells spreading to other parts of the body through the circulatory system.
A deadly tool in cancer's arsenal is cell plasticity, a cell's ability to alter its physiological characteristics. It is one of the reasons cancers can metastasize throughout the body, and it helps the disease resist treatments.
Researchers at the University of Basel, Switzerland, have hijacked this ability and turned it against cancer. Using a drug therapy that combined an anti-diabetic drug and MEK inhibitors, they attacked cancer cells and turned them into adipocytes (a.k.a. fat cells).
While this did not remove the tumor, it did make the cells post-miotic, meaning they could no longer divide. This inhibited the cancer's ability to spread.
"In future, this innovative therapeutic approach could be used in combination with conventional chemotherapy to suppress both primary tumor growth and the formation of deadly metastases," senior study author Gerhard Christofori told Medical News Today.
An image of the E. coli bacteria. Will these become the next breakthrough in cancer therapies?
Another advancement in cancer treatment is synthetic biology, a field in which scientists use the principals of engineering to redesign biological systems. In one example, researchers genetically programmed a non-pathogenic E. coli strain to attack tumors in lab mice.
Once injected, the rewired bacteria took refuge in the tumor, where they self-destructed. These dead bacteria leaked from the tumor, and thanks to encoded nanobodies, drew the attention of T-cells which devoured the bacteria and tumor alike.
Of course, lab tests in mice do not guarantee a successful transition to human patients, but it remains a promising avenue for treatment.
"At some point in the future, we will use programmable bacteria for treatment," Michael Dougan, an immunologist at Massachusetts General Hospital, told the New York Times. "I think there's just too much potential."
A new attitude toward cancer
Medical professionals originally viewed cancer as a disease to be destroyed with extreme prejudice; the treatment was only better than the disease because the disease ended in death.
But as David Agus, professor of medicine and engineering at USC, told us, there are better ways to approach cancer:
"Well, to me cancer is a verb and not a noun. You're cancering, it's something the body does and not that the body gets. And so that philosophy needs a very different way of approaching disease, and it means changing the system in addition to trying to target the cancer."
One way is to approach treatment holistically. Agus points to a trial that gave premenopausal women with breast cancer a bone-building drug. The drug didn't target the cancer, yet it reduced recurrence by 40 percent because breast cancer metastasizes in bone.
Another method is psychosocial oncology. In this relatively new field, the practitioners' goal is to enhance the quality of life for cancer patients through mental health care as a part of physical care.
Living with cancer
Cancer death rates in the United States by cancer type, male and female, age standardized.
Scientists have learned a lot about cancer, but there remains much we don't know. Does that mean we should despair for the future? Quite the contrary. Thanks to the knowledge accumulated by scientists, we have much to be hopeful for.
Headlines are correct that the total number of new cancer cases and deaths continue to increase. However, the rates of cancer diagnoses and death have declined year after year. This is because absolute numbers don't account for metrics like population growth and increased life expectancy. In fact, the Annual Report to the Nation on the Status of Cancer found that the cancer death rate for men, women, and children fell year after year between 1999 and 2016, as did cancer incident rates.
"Death in old age is inevitable. The job of science is to prevent unanticipated deaths in unanticipated times. I find that is a perfectly reasonable goal," said Mukerjee. "If you're saying to me that we will have a more profound, more proximal reconciliation with cancer in the next few decades, I think the answer is absolutely yes."
We may not be able to eradicate cancer as we did with diseases like smallpox and polio. But we're learning how to live with it more and more every day.
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Andy Samberg and Cristin Milioti get stuck in an infinite wedding time loop.
- Two wedding guests discover they're trapped in an infinite time loop, waking up in Palm Springs over and over and over.
- As the reality of their situation sets in, Nyles and Sarah decide to enjoy the repetitive awakenings.
- The film is perfectly timed for a world sheltering at home during a pandemic.
Richard Feynman once asked a silly question. Two MIT students just answered it.
Here's a fun experiment to try. Go to your pantry and see if you have a box of spaghetti. If you do, take out a noodle. Grab both ends of it and bend it until it breaks in half. How many pieces did it break into? If you got two large pieces and at least one small piece you're not alone.
But science loves a good challenge<p>The mystery remained unsolved until 2005, when French scientists <a href="http://www.lmm.jussieu.fr/~audoly/" target="_blank">Basile Audoly</a> and <a href="http://www.lmm.jussieu.fr/~neukirch/" target="_blank">Sebastien Neukirch </a>won an <a href="https://www.improbable.com/ig/" target="_blank">Ig Nobel Prize</a>, an award given to scientists for real work which is of a less serious nature than the discoveries that win Nobel prizes, for finally determining why this happens. <a href="http://www.lmm.jussieu.fr/spaghetti/audoly_neukirch_fragmentation.pdf" target="_blank">Their paper describing the effect is wonderfully funny to read</a>, as it takes such a banal issue so seriously. </p><p>They demonstrated that when a rod is bent past a certain point, such as when spaghetti is snapped in half by bending it at the ends, a "snapback effect" is created. This causes energy to reverberate from the initial break to other parts of the rod, often leading to a second break elsewhere.</p><p>While this settled the issue of <em>why </em>spaghetti noodles break into three or more pieces, it didn't establish if they always had to break this way. The question of if the snapback could be regulated remained unsettled.</p>
Physicists, being themselves, immediately wanted to try and break pasta into two pieces using this info<p><a href="https://roheiss.wordpress.com/fun/" target="_blank">Ronald Heisser</a> and <a href="https://math.mit.edu/directory/profile.php?pid=1787" target="_blank">Vishal Patil</a>, two graduate students currently at Cornell and MIT respectively, read about Feynman's night of noodle snapping in class and were inspired to try and find what could be done to make sure the pasta always broke in two.</p><p><a href="http://news.mit.edu/2018/mit-mathematicians-solve-age-old-spaghetti-mystery-0813" target="_blank">By placing the noodles in a special machine</a> built for the task and recording the bending with a high-powered camera, the young scientists were able to observe in extreme detail exactly what each change in their snapping method did to the pasta. After breaking more than 500 noodles, they found the solution.</p>
The apparatus the MIT researchers built specifically for the task of snapping hundreds of spaghetti sticks.
(Courtesy of the researchers)
What possible application could this have?<p>The snapback effect is not limited to uncooked pasta noodles and can be applied to rods of all sorts. The discovery of how to cleanly break them in two could be applied to future engineering projects.</p><p>Likewise, knowing how things fragment and fail is always handy to know when you're trying to build things. Carbon Nanotubes, <a href="https://bigthink.com/ideafeed/carbon-nanotube-space-elevator" target="_self">super strong cylinders often hailed as the building material of the future</a>, are also rods which can be better understood thanks to this odd experiment.</p><p>Sometimes big discoveries can be inspired by silly questions. If it hadn't been for Richard Feynman bending noodles seventy years ago, we wouldn't know what we know now about how energy is dispersed through rods and how to control their fracturing. While not all silly questions will lead to such a significant discovery, they can all help us learn.</p>
The multifaceted cerebellum is large — it's just tightly folded.
- A powerful MRI combined with modeling software results in a totally new view of the human cerebellum.
- The so-called 'little brain' is nearly 80% the size of the cerebral cortex when it's unfolded.
- This part of the brain is associated with a lot of things, and a new virtual map is suitably chaotic and complex.
Just under our brain's cortex and close to our brain stem sits the cerebellum, also known as the "little brain." It's an organ many animals have, and we're still learning what it does in humans. It's long been thought to be involved in sensory input and motor control, but recent studies suggests it also plays a role in a lot of other things, including emotion, thought, and pain. After all, about half of the brain's neurons reside there. But it's so small. Except it's not, according to a new study from San Diego State University (SDSU) published in PNAS (Proceedings of the National Academy of Sciences).
A neural crêpe
A new imaging study led by psychology professor and cognitive neuroscientist Martin Sereno of the SDSU MRI Imaging Center reveals that the cerebellum is actually an intricately folded organ that has a surface area equal in size to 78 percent of the cerebral cortex. Sereno, a pioneer in MRI brain imaging, collaborated with other experts from the U.K., Canada, and the Netherlands.
So what does it look like? Unfolded, the cerebellum is reminiscent of a crêpe, according to Sereno, about four inches wide and three feet long.
The team didn't physically unfold a cerebellum in their research. Instead, they worked with brain scans from a 9.4 Tesla MRI machine, and virtually unfolded and mapped the organ. Custom software was developed for the project, based on the open-source FreeSurfer app developed by Sereno and others. Their model allowed the scientists to unpack the virtual cerebellum down to each individual fold, or "folia."
Study's cross-sections of a folded cerebellum
Image source: Sereno, et al.
A complicated map
Sereno tells SDSU NewsCenter that "Until now we only had crude models of what it looked like. We now have a complete map or surface representation of the cerebellum, much like cities, counties, and states."
That map is a bit surprising, too, in that regions associated with different functions are scattered across the organ in peculiar ways, unlike the cortex where it's all pretty orderly. "You get a little chunk of the lip, next to a chunk of the shoulder or face, like jumbled puzzle pieces," says Sereno. This may have to do with the fact that when the cerebellum is folded, its elements line up differently than they do when the organ is unfolded.
It seems the folded structure of the cerebellum is a configuration that facilitates access to information coming from places all over the body. Sereno says, "Now that we have the first high resolution base map of the human cerebellum, there are many possibilities for researchers to start filling in what is certain to be a complex quilt of inputs, from many different parts of the cerebral cortex in more detail than ever before."
This makes sense if the cerebellum is involved in highly complex, advanced cognitive functions, such as handling language or performing abstract reasoning as scientists suspect. "When you think of the cognition required to write a scientific paper or explain a concept," says Sereno, "you have to pull in information from many different sources. And that's just how the cerebellum is set up."
Bigger and bigger
The study also suggests that the large size of their virtual human cerebellum is likely to be related to the sheer number of tasks with which the organ is involved in the complex human brain. The macaque cerebellum that the team analyzed, for example, amounts to just 30 percent the size of the animal's cortex.
"The fact that [the cerebellum] has such a large surface area speaks to the evolution of distinctively human behaviors and cognition," says Sereno. "It has expanded so much that the folding patterns are very complex."
As the study says, "Rather than coordinating sensory signals to execute expert physical movements, parts of the cerebellum may have been extended in humans to help coordinate fictive 'conceptual movements,' such as rapidly mentally rearranging a movement plan — or, in the fullness of time, perhaps even a mathematical equation."
Sereno concludes, "The 'little brain' is quite the jack of all trades. Mapping the cerebellum will be an interesting new frontier for the next decade."
What happens if we consider welfare programs as investments?
- A recently published study suggests that some welfare programs more than pay for themselves.
- It is one of the first major reviews of welfare programs to measure so many by a single metric.
- The findings will likely inform future welfare reform and encourage debate on how to grade success.
Welfare as an investment<p>The <a href="https://scholar.harvard.edu/files/hendren/files/welfare_vnber.pdf" target="_blank">study</a>, carried out by Nathaniel Hendren and Ben Sprung-Keyser of Harvard University, reviews 133 welfare programs through a single lens. The authors measured these programs' "Marginal Value of Public Funds" (MVPF), which is defined as the ratio of the recipients' willingness to pay for a program over its cost.</p><p>A program with an MVPF of one provides precisely as much in net benefits as it costs to deliver those benefits. For an illustration, imagine a program that hands someone a dollar. If getting that dollar doesn't alter their behavior, then the MVPF of that program is one. If it discourages them from working, then the program's cost goes up, as the program causes government tax revenues to fall in addition to costing money upfront. The MVPF goes below one in this case. <br> <br> Lastly, it is possible that getting the dollar causes the recipient to further their education and get a job that pays more taxes in the future, lowering the cost of the program in the long run and raising the MVPF. The value ratio can even hit infinity when a program fully "pays for itself."</p><p> While these are only a few examples, many others exist, and they do work to show you that a high MVPF means that a program "pays for itself," a value of one indicates a program "breaks even," and a value below one shows a program costs more money than the direct cost of the benefits would suggest.</p> After determining the programs' costs using existing literature and the willingness to pay through statistical analysis, 133 programs focusing on social insurance, education and job training, tax and cash transfers, and in-kind transfers were analyzed. The results show that some programs turn a "profit" for the government, mainly when they are focused on children:
This figure shows the MVPF for a variety of polices alongside the typical age of the beneficiaries. Clearly, programs targeted at children have a higher payoff.
Nathaniel Hendren and Ben Sprung-Keyser<p>Programs like child health services and K-12 education spending have infinite MVPF values. The authors argue this is because the programs allow children to live healthier, more productive lives and earn more money, which enables them to pay more taxes later. Programs like the preschool initiatives examined don't manage to do this as well and have a lower "profit" rate despite having decent MVPF ratios.</p><p>On the other hand, things like tuition deductions for older adults don't make back the money they cost. This is likely for several reasons, not the least of which is that there is less time for the benefactor to pay the government back in taxes. Disability insurance was likewise "unprofitable," as those collecting it have a reduced need to work and pay less back in taxes. </p>