What Is Cancer?
Siddhartha Mukherjee is the author of The Emperor of All Maladies: A Biography of Cancer, winner of the 2011 Pulitzer Prize in general nonfiction, and The Laws of Medicine. He is the editor of Best Science Writing 2013. Mukherjee is an assistant professor of medicine at Columbia University and a cancer physician and researcher. A Rhodes scholar, he graduated from Stanford University, University of Oxford, and Harvard Medical School. He has published articles in Nature, The New England Journal of Medicine, The New Yorker, The New York Times, and Cell. He lives in New York with his wife and daughters.
Dr. Siddhartha Mukherjee: The term cancer covers over 100 different diseases. Starting with the biological definition what is cancer, what characteristics do these diseases share, Harold?
Dr. Harold Varmus: Well cancer is indeed a disease that can arise in virtually any of our tissues and virtually every cancer that arises is somewhat different from another, but there are commonalities and the most obvious is the fact that cancer represents a derangement of growth. Cells grow too much and they grow in antisocial ways. They cross normal tissue boundaries. They invade. They can grow in other places where they shouldn’t be growing. They often fail to differentiate the way normal cells will. There are my characteristics of cancer cells that have been identified in different tissues in which cancers arise, but the basic finding is a derangement of growth and a derangement of the normal ability of cells to stay in the places where they should be growing.
Dr. Siddhartha Mukherjee: Recently there has been an enormous degree of research on cancer. Has this definition begun to change of what cancer is?
Dr. Harold Varmus: The definition hasn’t so much changed, but the- but we’ve enlarged our sense of what cancer is about and we understand a great deal more about the basic mechanism that drives cells to behave inappropriately, to grow too much, to fail to die, to fail to differentiate, to fail to respond to signals all around cells that normally tell them to restrict growth and we now understand that many of those failures that cells exhibit when they become cancerous can be traced to mutations or to changes in the way genes are expressed, so we’ve enlarged dramatically our sense of what cancers are and we’ve changed our means of defining a cancer. A cancer is not simply a lung cancer. It doesn’t simply have a certain kind of appearance under the microscope or a certain behavior, but it also has a set of changes in the genes or in the molecules that modify gene behavior that allows us to categorize cancers in ways that is very useful in thinking about new ways to control cancer by prevention and treatment.
Dr. Lewis Cantley: Yeah, I can expand a little bit on that. So we say there is a hundred different cancers. That is based on pathology, what you can see in a microscope and even back in the 60s pathologists began to do what we now call molecular pathology. They don’t just look- stay in the tissue and look at it by eye. They look at chromosomes for example and so leukemia has broke out from a single leukemia to dozens of leukemias that are defined differentially based on what chromosomal change can be seen in a microscope and so we’re now taking it to an even deeper level where we can go in and sequence the entire genome of the cancer and these mutations keep giving us more and more subtypes, so breast cancer is going to be hundreds if not thousands of subtypes of breast cancers once we get to the actual molecular events that are going on, so it’s I think in a way this is good. It’s bad, but it’s good and the good thing about it is it kind of explains why no one type of cancer gets completely cured by a given drug or it’s relatively rare. You have some cured, some are not. They probably don’t really have the exact same disease and our previous classifications were not really detailed enough, so we can use the approach of divide and conquer, but it also means we need many more therapies than we currently have.
Dr. Harold Varmus: It’s probably good to understand though that while the subdivision is absolutely correct and every cancer has its signature there are commonalities and in many cases you can say yes there are hundreds of different cancer types that look the same. They look different genetically, but frequently there are commonalities that can be points of attack, mutations that act as drivers of the cancer behavior.
Dr. Lewis Cantley: Yeah, so hopefully we won’t need a thousand treatments.
One in three Americans are diagnosed in their lifetime with cancer, a derangement of normal cell growth in which cells grow in antisocial ways, crossing natural tissue boundaries.
Dominique Crenn, the only female chef in America with three Michelin stars, joins Big Think Live this Thursday at 1pm ET.
Students who think the world is just cheat less, but they need to experience justice to feel that way.
- Students in German and Turkish universities who believed the world is just cheated less than their pessimistic peers.
- The tendency to think the world is just is related to the occurence of experiences of justice.
- The findings may prove useful in helping students adjust to college life.
The world is just? That’s news to a lot of people.<p>The study is the most recent addition to a long line of work focusing on the belief in justice, our behavior, and our reactions to evidence that might suggest injustice occasionally occurs. This study focuses on a personal belief in a just world, (PBJW) rather than a general belief in a just world (GBJW). The difference between them must be highlighted.</p><p>GBJW is the stance that justice prevails all over the world and that people tend to get what they deserve. PBJW is more focused on the individual's social environment and their belief that they tend to be treated justly. While several studies show PBJW correlates with a higher sense of well-being and a variety of other positive effects, a high GBJW is associated with less life satisfaction, negative behavior, and callousness towards the suffering of <a href="https://link.springer.com/book/10.1007%2F978-1-4939-3216-0" target="_blank">others</a>. This study controlled for GBJW, and focused on PBJW as much as possible. </p><p>To assure that culture was not a factor, the study included students at universities in both Germany and Turkey. </p><p>The researchers gave students at the four participating universities a series of questionnaires that asked if they ever cheated in class, if they perceived the world to be just, if they though that justice always prevailed everywhere, their tendencies towards socially appropriate behavior, their life satisfaction, and if they felt like they were treated justly by their teachers and fellow students. </p><p>The answers were statistically analyzed for relationships. While some of the connections seem trivially true, others were surprising. <strong></strong></p><p>PBJW turned out to only be an indirect predictor of if a student was likely to cheat. Both a belief in a just world and a lower likelihood of cheating were mediated by the justice experiences of the students, with more of these positive experiences lowering the rate of cheating and improving their belief in justice. This was also associated with higher levels of life satisfaction. </p><p>These effects existed across all demographics in both countries. </p>
What does this mean? Is a belief in justice a self-fulfilling prophecy?<iframe width="730" height="430" src="https://www.youtube.com/embed/6oMv-azHNCA" frameborder="0" allow="accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture" allowfullscreen></iframe><p>In a way, it seems to be. People who have reason to think the world is just to them tend to interpret events in a way to sustain that belief and behave in a just manner. In a larger sense, the take away from this study is that experiences of justice, both from peers and instructors, is vital to student's wellbeing and understanding that the rules that exist about cheating are part of a larger, legitimate, system. </p><p>The researchers, citing previous studies on the perception of justice, note that "justice experiences (1) signal that university students are esteemed members of their social group, which in turn conveys feelings of belonging and social inclusion and (2) motivate them to accept and observe university rules and norms. These cognitive processes may thus strengthen their well-being and decrease the likelihood that they cheat."</p><p>The authors also suggest that if you want people (not only students) to act justly; consider treating them with "civility, respect, and dignity."</p><p>Sometimes, all it can take to help somebody act virtuously is to treat them well. Likewise, people treated harshly can rarely find reason to play by rules that don't protect them. The findings of this study will certainly add to the literature on how we perceive justice in the world around us, but might also help us remember that there are real consequences to our actions which can be much larger than we imagine. <strong></strong></p>
This could change how researchers approach vaccine development.
- The reason children suffer less from the novel coronavirus has remained mysterious.
- Researchers identified a cytokine, IL-17A, which appears to protect children from the ravages of COVID-19.
- This cytokine response could change how researchers approach vaccine development.
A member of staff wearing personal protective equipment (PPE) takes a child's temperature at the Harris Academy's Shortland's school on June 04, 2020 in London, England.
Photo by Dan Kitwood/Getty Images<p>Experts don't want to place kids at the back of the line, regardless of how strong their immune systems appear. At least one company, Moderna, <a href="https://www.businessinsider.com/coronavirus-vaccine-for-kids-moderna-plans-pediatric-trial-2020-9" target="_blank">hopes to begin testing</a> vaccines in pediatric volunteers by year's end.</p><p>Innate immune response is especially high during childhood (compared to adaptive immunity). This makes evolutionary sense: nature wants an animal to survive until its ready to procreate. Turns out the children in the study possessed high levels of cytokines that boost their immune response. The biggest impact is made by IL-17A, which appears to protect the youngest cohort from the ravages of the coronavirus. </p><p>While both age groups produced antibodies to fight off the infamous spike protein, adults that produce neutralizing antibodies actually suffer a <em>worse</em> fate. Herold says this "over-vigorous adaptive immune response" might promote inflammation, triggering acute respiratory distress syndrome (ARDS). </p><p>This matters for vaccine development. As Herold says, </p><p style="margin-left: 20px;">"Our adult COVID-19 patients who fared poorly had high levels of neutralizing antibodies, suggesting that convalescent plasma—which is rich in neutralizing antibodies—may not help adults who have already developed signs of ARDS. By contrast, therapies that boost innate immune responses early in the course of the disease may be especially beneficial."</p><p>Herold says current vaccine trials are focused on boosting neutralizing-antibody levels. With this new information, researchers may want to work on vaccines that boost the innate immune response instead. </p><p>With <a href="https://www.nytimes.com/interactive/2020/science/coronavirus-vaccine-tracker.html" target="_blank">at least 55 vaccine trials</a> underway, every piece of data matters. </p><p>--</p><p><em>Stay in touch with Derek on <a href="http://www.twitter.com/derekberes" target="_blank">Twitter</a>, <a href="https://www.facebook.com/DerekBeresdotcom" target="_blank">Facebook</a> and <a href="https://derekberes.substack.com/" target="_blank" rel="noopener noreferrer">Substack</a>. His next book is</em> "<em>Hero's Dose: The Case For Psychedelics in Ritual and Therapy."</em></p>
Astronomers spot an object heading into Earth orbit.
Minimoons<p>Scientists have confirmed just two prior minimoons. One was <a href="https://en.wikipedia.org/wiki/2006_RH120" target="_blank">2006 RH120</a>, which orbited us from September 2006 to June 2007. The other was <a href="https://en.wikipedia.org/wiki/2020_CD3" target="_blank">2020 CD3</a>, which got stuck in the 2015–2016 timeframe, and is believed to gotten away in May 2020.</p><p>2020 SO, the new kid on the block, is expected to arrive in October 2020 and pop out of orbit in May 2021.</p><div id="37962" class="rm-shortcode" data-rm-shortcode-id="f4c0fc8a2cba6536ea4cd960ebed3e6e"><blockquote class="twitter-tweet twitter-custom-tweet" data-twitter-tweet-id="1307729521869611008" data-partner="rebelmouse"><div style="margin:1em 0">Asteroid 2020 SO may get captured by Earth from Oct 2020 - May 2021. Current nominal trajectory shows shows capture… https://t.co/F5utxRvN6Z</div> — Tony Dunn (@Tony Dunn)<a href="https://twitter.com/tony873004/statuses/1307729521869611008">1600621989.0</a></blockquote></div>
Identifying 2020 SO<p>The first clue 2020 SO isn't your ordinary asteroid is its exceptionally low velocity. It's traveling much more slowly that a typical asteroid — their <a href="https://www.lpi.usra.edu/exploration/training/illustrations/craterMechanics/" target="_blank">average rate of travel</a> <a href="https://www.lpi.usra.edu/exploration/training/illustrations/craterMechanics/" target="_blank" rel="noopener noreferrer"></a>is 18 kilometers (58,000 feet) per second. Even <a href="https://en.wikipedia.org/wiki/Moon_rock" target="_blank">moon rocks</a> sent careening into Earth orbit by impacts on the lunar surface outpace pokey 2020 SO.</p><p>For another thing, 2020 SO has an orbital path very similar to Earth's, lasting about one Earth year. It's also just slightly less circular than our own orbit, from which it's barely tilted off-axis.</p><p>So, what is it? <a href="https://cneos.jpl.nasa.gov/ca/" target="_blank">NASA estimates</a> that the object has dimensions very reminiscent of a discarded Centaur rocket stage from the <a href="https://en.wikipedia.org/wiki/Surveyor_2" target="_blank" rel="noopener noreferrer">Surveyor 2 mission</a> that landed an unmanned craft on the moon. Back in the day, rocket stages were jettisoned as craft were aimed toward their desired position. This stuff, if released high enough, remains in space. It appears that this Centaur rocket, launched in September 1966, is now making its way back homeward, at least for a little bit.</p><p>When 2020 SO arrives at its closest point in December, the rocket is expected to be about 50,000 kilometers from Earth. Its next closest approach is much further: 220,000 kilometers, in February 2010.</p><img type="lazy-image" data-runner-src="https://assets.rebelmouse.io/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yNDQzMDk3NC9vcmlnaW4uanBnIiwiZXhwaXJlc19hdCI6MTYyODg1MTQ1MX0.HGknDwqp0GmeuczKY_AS7vrPG7KMFUc_XO95tNoI2xo/img.jpg?width=980" id="e5cda" class="rm-shortcode" data-rm-shortcode-id="85eb1f790d8c3ee5b261f7ba13eaa5e1" data-rm-shortcode-name="rebelmouse-image" alt="Centaur rocket stage" />
Centaur rocket stage
What we may be able to learn<p>Earthly space programs being as young as they are, scientists would love to know what's happened to our rocket during a half century in space.</p><p>While 2020 SO won't get close enough to drop into our atmosphere, its slow progress has scientists hopeful that they'll still get some kind of a decent look at it.</p><p>Spectroscopy may be able to reveal what the rocket's surface is like now — has any of its paint survived, for example? Of course, being out in space, it's likely to have been hit by lots of dust and micrometeorites, so the current state of its surfaces is also of interest. Experts are curious to know how reflective the rocket is at this point, valuable information that can help planners of future long-term missions anticipate how well a craft out in space for extended periods will remain able to reflect sunlight.</p>
Researchers from the University of Toronto published a new map of cancer cells' genetic defenses against treatment.
A moving target<img type="lazy-image" data-runner-src="https://assets.rebelmouse.io/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yNDQzNjQ2Ny9vcmlnaW4uanBnIiwiZXhwaXJlc19hdCI6MTY1MDM3OTA0N30.z4u2eaulqRu8cslqqny8t9G7iaHr_DarbDJSFKLdDwI/img.jpg?width=980" id="21b22" class="rm-shortcode" data-rm-shortcode-id="aefbbccdf3bb0d25bf14268ab87a821f" data-rm-shortcode-name="rebelmouse-image" alt="IV drip" />
Credit: Marcelo Leal/Unsplash<p>Speaking to <a href="https://www.utoronto.ca/news/u-t-researchers-identify-genes-enable-cancer-evade-immune-system" target="_blank" rel="noopener noreferrer">U of T News</a>, lead author of the study molecular geneticist <a href="http://www.moleculargenetics.utoronto.ca/faculty/2014/9/30/jason-moffat" target="_blank" rel="noopener noreferrer">Jason Moffat</a> of the university's <a href="https://ccbr.utoronto.ca/donnelly-centre-cellular-and-biomolecular-research" target="_blank" rel="noopener noreferrer">Donnelly Centre for Cellular and Biomolecular Research</a> says, "Over the last decade, different forms of immunotherapy have emerged as really potent cancer treatments, but the reality is that they only generate durable responses in a fraction of patients and not for all tumor types."</p><p>There can be a significant degree of heterogeneity between cancer cells from human to human, and even within the same person, making the development of therapies maddeningly difficult. Attempting to address potential cancer-cell vulnerabilities across these variations is a life-or-death game of whack-a-mole.</p><p>"It's an ongoing battle between the immune system and cancer, where the immune system is trying to find and kill the cancer whereas the cancer's job is to evade that killing," says Moffat.</p>
Mapping the mechanisms<img type="lazy-image" data-runner-src="https://assets.rebelmouse.io/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yNDQzNjQ3Ni9vcmlnaW4uanBnIiwiZXhwaXJlc19hdCI6MTYyMjQ1OTM0MX0.HNtivrlU9VBYxcG9JaWKvPJ5RrBsgqd8Fw6ohfSpfh0/img.jpg?width=980" id="0faa6" class="rm-shortcode" data-rm-shortcode-id="7687cdc5abe93503764c1c0401b65fd4" data-rm-shortcode-name="rebelmouse-image" />
Illustration: genes (red, green, and blue spots within the nuclei of HeLa cells) artificially superimposed on images of multi-well plates.
Credit: National Cancer Institute/Unsplash<p>Moffat and his colleagues decided to investigate and identify genes within cancer cells that help them defeat treatment. Co-lead author Keith Lawson of Moffat's lab explains that "it's important to not just find genes that can regulate immune evasion in one model of cancer, but what you really want are to find those genes that you can manipulate in cancer cells across many models because those are going to make the best therapeutic targets."</p><p>To accomplish this, the researchers, working with scientists at <a href="https://www.agios.com" target="_blank">Agios Pharmaceuticals</a> in Cambridge, Massachusetts, first exposed cells from breast, colon, kidney and skin cancer tumors to T cells in lab dishes. This established a baseline of their responses to treatment. Next, using CRISPR, the scientists went through the cells, exhaustively turning off one gene at a time to determine its role in immunotherapy resistance by comparing the cells' response to the T cells compared to their original baseline response.</p><p>The team identified 182 "core cancer intrinsic immune evasion genes" that affected the cells' response to T cells. The fact that some of the identified genes were already known to be involved in resistance provided the researchers with some confidence that they were on the right track.</p><p>Still, many of the genes they ID'ed had not been previously implicated. "That was really exciting to see because it means that our dataset was very rich in new biological information," says Lawson.</p>