The Big Outer Leaves The vegetables were "literally riddled with holes, more than half of its substance was eaten away." With each step he took around the devastated cabbage, tiny swarms of small ash-gray moths emerged Ground and fluttered away. It was, it seems, the first record of the Diamond-tailed Moth in the United States, an invasive pest that shows a predilection for cruciferous vegetables in its larval form. Towards the end of the 1
To combat this invasion, farmers began to bombard their fields with primitive pesticides. That worked. Or seemed to. It killed most of the moths, but those who survived the poison multiplied, and the population recovered more than ever. For decades, one pesticide failed after another as the moths evolved. Even the badly toxic DDT was no match for the Diamondback. In the late 1950s, agricultural experts began to abandon the idea of extermination and adopted a new strategy. Farmers left the moths alone until their numbers exceeded a certain threshold, and only then would they use pesticides. Remarkably, this has helped. The moths did not die out, but the pest could be kept under control and crop damage kept in check.
When Robert Gatenby heard this story of the Rhododendrons in 2008, he immediately locked them up. Gatenby is neither a farmer nor an agronomist and a fan of cruciferous vegetables – he hates Brussels sprouts. He is a trained radiologist and directs the Department of Radiology at the H. Lee Moffitt Cancer Center, Tampa, Florida. However, unlike your typical physician, he is also obsessed with the evolutionary principles that Charles Darwin set up over 150 years ago. The story of the Rhomboid Butterfly appealed to Gatenby as a useful metaphor for his own project – one that dealt not with grain but with cancer.
Like the moth moth, cancer cells develop resistance to the powerful chemicals used to destroy them. Even if cancer therapies kill most target cells, a small subgroup can survive, mainly thanks to genetic changes that make them resistant. In advanced cancer, it is usually a question of when, if not, militant surviving cells become an unstoppable force. Gatenby thought that this deadly result could be prevented. His idea was to intermittently expose a tumor to drugs instead of suppressing it in a constant attack, reducing the pressure on his cells to develop resistance.
Just as ecologists permit a manageable population of diamond tail moths, Gatenby's method would allow cancer to remain in the body as long as it does not spread further. To test this idea, Gatenby obtained permission in 2014 to conduct a study of advanced prostate cancer patients in Moffitt. The patients had cancer that did not respond to the treatment; Their drug-resistant cells gained an evolutionary struggle within the body and survived a rush of toxic drugs that killed weaker cancer cells. The hope was to slow down the increase in mutations that would give some cancer cells survivability with a precise drug-delivery regimen developed according to evolutionary principles. Gatenby's name for this approach was adaptive therapy.
One of the patients in the study was Robert Butler, a British oil exploration engineer who retired in Tampa. He was diagnosed with prostate cancer in 2007, and seven years later, after taking Lupron and receiving radiation, his prostate tumor had progressed to stage 4 advanced cancer. Butler did not give up. He tried a newly approved immunotherapy, where cells from his blood were sent by a courier to a facility outside of Atlanta, where they were mixed with a molecule that activates immune cells, and then sent back to Florida to be injected into it to become. The treatment was expensive – the price of a sticker can reach up to $ 120,000 – but the risk of the cancer progressing remains.
When Butler and his wife came to his oncology office in Moffitt Cancer Center in August 2014, they got ready for what would come next; They had heard of invasive treatments, such as radioactive seed implants. They were intrigued when the doctor told them about Gatenby's trial and asked if Butler wanted to attend. He would take a powerful and very expensive drug called Zytiga, but not in the scorched earth, which would kill all cells, which is standard. Instead, he would only receive as much Zytiga as was needed to prevent the growth of the cancer. The idea was radical and not intuitive. His last chance to avoid death from cancer was the best way to heal him.
The knowledge of the modified Zytiga regime was not intended to free him from cancer, and left engineer Butler with a question as to how the doctors would measure him the success of her new approach to treatment. He asked, "How do we know this stuff works?" And one of his doctors replied, "Well, you will not be dead."
In the United States we use military metaphors when we talk about cancer. We fight and we fight, and if we survive we are victorious. The stance dates back in part to the year 1969, when the Citizens Committee for the Conquest of Cancer The Washington Post and The New York Times issued an ad in which he quoted the president as saying "Mr. Nixon: You Can Cure Cancer." The call to action triggered the country's "war on cancer," noting that the evil enemy could be wiped out with sufficient medical weapons.
Mid-1970s, however Signs It became apparent that certain strategies aimed at complete extermination could backfire, and in this context, a cancer researcher named Peter Nowell published a seminal paper in Science in 1976. Nowell suspected that the evolutionary Influences of certain cell populations in tumors become progressively more malignant over time.The cells in a tumor not only compete closely with each other Healthy cells, Nowell argued, but also with each other. Nowell suggested – and later research confirmed – that certain DNA changes confer cancer cell resistance to chemotherapy or other treatments, causing them to knock out drug-sensitive cells through a process of natural selection.
Nowell transmitted his ideas to his students at the University of Pennsylvania School of Medicine, sometimes smoking a cigarette while teaching. His theories were respected, but only slowly enforced. He emphasized that tumors can become deadlier as they accumulate more genetic defects. It was an idea that was ahead of its time. At that time, scientists did not have the technical ability to measure all changes in the huge genomes of tumor cells. Instead, they could only sequence small tidbits of DNA, and most scientists saw cancer as the result of a few genetic mutations.
One of the medical students who heard the Nowell lecture in the late 1970s happened to be a young man, Bob Gatenby. But Nowell's ideas did not make a strong impression on him, says Gatenby. What inspired him was what he experienced during his first years as a practicing radiologist on the bloody fronts of the war against cancer.
"I could not understand why you treat someone with a deadly disease and thereby kill your therapy. It just did not feel right for me. "
In the mid-eighties, Gatenby had received a job at the Fox Chase Cancer Center in Philadelphia. In that hospital and other hospitals in the country, clinical trials have undergone extreme treatment, a combination of potentially fatal chemotherapy followed by bone marrow transplantation. The treatment was staggering. The women had diarrhea and nausea, and some had so much lung damage that they had difficulty breathing. Others experienced liver damage and a weakened immune system that made them susceptible to serious infections. As a radiologist, Gatenby had the task of interpreting radiographs and other patient images, and he saw that the treatment failed. Of more than 30,000 women with breast cancer in the US who had undergone the procedure between 1985 and 1998, 15 percent died from the treatment. "What happened were these women who suffered terribly, and they were not healed," says Gatenby.
Approximately at the same time as the breast cancer studies, the father of a colleague from Gatenby came to the hospital for a first aggressive action to receive round chemo in lung cancer. According to the colleague, her father had arrived on a Friday with no apparent symptoms and was dead on Monday. "This event was very traumatic for me," recalls Gatenby, and the cause for him seemed to be obvious. "I could not understand why you treat someone with a deadly disease and kill him with your therapy. It just did not feel right for me. "In this difficult time, Gatenby's own father died of esophageal cancer."
Gatenby believed that there had to be a better way to treat cancer – instead of outwitting him with carpet bombs – he had studied physics at the University and believed that biologists equations To grasp the forces that affect cancer in the same way that physicists use mathematics to describe phenomena such as gravity, while Nowell's general theories about how cancers followed evolutionary principles, Gatenby took another step: He wanted to find a way to describe the development of cancer based on mathematical formulas.
Until 1989, Bob Gatenby was engaged in modeling the development of cancer. During the day, he examined x-rays of cancer patients, and at night, after he and his wife had put their young children to bed, he sat at the kitchen table in their Philadelphia suburb and pore on medical journals. The patterns he began to see in the literature led him to ask a question: what if cancer cells defeated normal, healthy cells in the body in the same way that a species excludes its competitors in nature?
using equations to describe the balance between predators and prey. As a student at Princeton University, he had learned the classic example of mathematics, which showed how growing populations of snowshoe hares promote the ascent of the lynx that feeds on them. He began to wipe old books and buy new ones to learn about species interactions.
For a year, Gatenby read and thought. In 1990, he found himself on a family trip on the Georgian Atlantic coast one afternoon with his two sleeping children in a hotel room. From nowhere an idea presented itself. He grabbed a writing utensil and a pen and began to write down some important formulas from population ecology. These formulas, referred to as Lotka-Volterra equations, have been used since the 1920s to model predator-prey interactions and later inter-species competitive dynamics, and were among those he had recently worked up at home. Gatenby believed that this set of formulas could also describe how tumor cells compete with healthy cells for energy sources such as glucose that drives them.
When he returned to Philadelphia, he spent a lot of time writing a typewriter, a work laid out authoring this theoretical model. As soon as he finished, he showed it to some colleagues. He did not get the answer he was hoping for: they found it ridiculous to use ecological equations to model cancer. "To say that they hated it would not do justice to how negative they were," he says. His colleagues believed that a short series of formulas can not capture the seemingly infinite complexities of cancer.
Louis Weiner, who worked with Gatenby at the time, recalls that her colleagues regarded Gatenby's ideas as unusual. "Orthodoxy preferred high-intensity, dose-tight treatments aimed at eradicating every last tumor cell in a cancer patient," says Weiner, who is now director of the Georgetown Lombardi Comprehensive Cancer Center in Washington, DC. "Bob's perspective was contrary to those beliefs."
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But Gatenby pushed on and managed to get the newspaper packed with Lotka. Volterra equations, accepted in 1991 by the prestigious journal Cancer Research .
Despite the publication of his theory, he still could not convince oncologists that his idea was of practical value. "I think they felt intimidated," says Gatenby. "Most doctors are mathematically illiterate." He noted that the medical facility did not want to publish much of his follow-up work.
In the following years, Gatenby joined the head of the diagnostic imaging department at Fox Chase Cancer Center. Later, he was appointed head of the Department of Radiology at the University of Arizona College of Medicine in Tucson, and continued to receive recognition for his trained interpretation of scans and received government grants to study cancer.
Then in 2007. The Moffitt Cancer Center offered Gatenby a position as chair of radiology. He had one condition: He would come if the hospital had created a department where he could seriously build the link between Darwin's principles and cancer. The Department of Integrated Mathematical Oncology, which emerged from this trial, is the first mathematics department in a cancer hospital, he says. Finally, Gatenby had a place where he could put his ideas to the test.
Gatenby arrives at his corner office in Moffitt most days at 7 o'clock. He is now 67 and his hair is gray at the temples, but his eyebrows are still brown. His children – those who slept in this hotel room when he wrote down his Darwinian inspiration – now have their own children, and he has the coffee cup "I ♥ Grandpa" to prove it. A hospital neck strap around his neck, he rolls up the crisp shirt sleeves and sits down at his desk. Outside his office, some 30 scientists and doctoral students spend their days studying patterns of cancer growth using equations describing population dynamics.
According to Gatenby's knowledge, no one had tried to exploit the evolution against cancer in a clinical trial until he developed his own prostate cancer experiment. He chose prostate cancer to test this approach, in part because, unlike other cancers, routine blood sampling of a prostate-specific antigen (PSA) molecule provides a direct replacement for the progression of the cancer.
To design a clinical study, Gatenby and his Moffitt staff first had to explain their idea that tumor cells are fighting for resources. They turned to game theory to record this momentum and put the numbers in the Lotka-Volterra equations. The computer simulations they performed using these equations estimated how fast drug-resistant cells would outperform other tumor cells with a continuous dosage of cytiga normally administered to advanced stage patients of prostate cancer.
In the simulations, the drug's typical administration resulted in drug-resistant cancer cells that quickly became overwhelming. The treatment would ultimately fail each time. This bleak result was consistent with the results found in the medical records. In contrast, the computer simulations indicated that if Zytiga was administered only when the tumor appeared to be growing, the drug-resistant cells would take much longer to out-pass the cancer.
In 2014, the Moffitt team got the first small trial to test this adaptive therapy approach by recruiting Robert Butler and a small group of other men with advanced prostate cancer. Butler's oncologist explained how it would work. He would stay on the Lupron he had taken for years, and every month he went to the hospital to test his PSA level to see if his prostate tumor was growing. Every three months, he received a CT scan and a whole body bone scan to monitor the spread of the disease. Whenever his PSA level was higher than he was at the trial, he started to take the stronger Zytiga. However, when his PSA level fell below half the baseline, he could do without Zytiga. This is attractive because Zytiga and similar medicines can cause side effects such as hot flashes, muscle aches and high blood pressure.
Moffitt's approach also promised to be much cheaper than taking Zytiga continuously. At wholesale price, a one-month offer costs nearly $ 11,000. Butler was covered by health insurance, but his first month's supply each year would pay him $ 2,700 in self-pay and $ 400 a month thereafter. If the PSA level was low, this would lead to significant cost savings.
"Conceptually, this is a very simple approach. He makes cancer a chronic disease. "
Butler participated in a so-called pilot study, which was less stringent than a large clinical study because it does not arbitrarily assign patients to experimental or standard treatment. Rather, the study relied on a group of patients treated outside the study and on results from a 2013 Zytiga study to benchmark how patients normally recover from continued drug dosing.
The Moffitt scientists were pleased with their new study and were relieved. Before the trial, "we were, frankly, scared," says Gatenby. The benefits of adaptive therapy seemed enormous. Of the eleven men in the study, one left the study after his illness had spread, but most lived longer than expected without the cancer progressing. Men who receive a sustained dose of Zytiga achieve an average of 16.5 months before the cancer becomes resistant to the drug and spreads. In comparison, the mean time to progression of men who received adaptive therapy was at least 27 months. In addition, they consumed on average less than half the standard amount of cytiga. Joel Brown, an evolutionary ecologist and one of Gatenby's co-workers, said the team felt morally obliged to spread the word: "The effect was so great that it would be unethical not to report it immediately," he says.
In 2017, he published a report on a generally positive reaction from prostate experts much earlier than expected, particularly because he suggested that people with cancer could live longer with fewer medicines. "If you can reduce side effects, I think that's fantastic," says Peter Nelson, an oncologist who studies prostate cancer at the Fred Hutchinson Cancer Research Center in Seattle. "Conceptually, it's a beautifully simple approach." Jason Somarelli, a biologist at the Duke Cancer Institute, describes Gatenby as a pioneer: "He makes cancer a chronic disease."
The 75-year-old Butler has long been out of action Zytiga – with runs that last up to five months. "I'm the figurehead now," she says. He is one of the best responders in the study.
Some physicians are already seeking adaptive therapy in patients outside of clinical trials. In 2017, a doctor in Oregon, inspired by Gatenby's pilot study, started a prostate cancer patient with a modified version of the approach, rejecting the standard continuous dosing. Since then she has started to treat a second man with adaptive therapy. Other oncologists could do the same. It is almost impossible to know for sure because adaptive therapy does not have to be approved by the government. The protocol uses already approved drugs, and the US Food and Drug Administration does not monitor any specific dosage plans.
However, experts are pushing for caution. The prostate cancer study was very small and without a randomly assigned control group, the results are not really reliable. While the majority of men in the study remained stable, four other cancers have been recorded since the newspaper was published. "This is an approach that must now be carefully considered in prospective clinical trials before it is adopted into clinical practice," says Richard L. Schilsky, chief physician of the American Society of Clinical Oncology. It could take years for a comprehensive adaptive therapy test to take place. Len Lichtenfeld, Interim Chief Medical Officer of the American Cancer Society, expresses Schilsky's concerns. "Is it fascinating? Yes, "says Lichtenfeld. "But there is still a long way to go."
Gatenby agrees that adaptive therapy requires rigorous testing. He conveys a kind of humility that is not often seen in the upper reaches of medicine. He has told me on several occasions that he is not an interesting subject to write about, and more than once I have heard that close colleagues are belittling the pronunciation of his name (pronounced GATE-en-bee); he had apparently never corrected her. But if he believes in something, he does not give in. And he believes in adaptive therapy. "He's like a teddy bear, but under that soft outside he's made of steel," says Athena Aktipis, who studied theory and cancer biology at Arizona State University and worked with Gatenby.
Late last year, Gatenby put his work to a meeting of prostate cancer specialists. In the subsequent question and answer session, one participant shared his surprise about the results. "I think what you're saying is that we've done it wrong all these years," the man mused, according to Gatenby. "I was literally speechless for a few moments," Gatenby admits, "and then I said," Well, I think that's what I'm saying. "He is still busy with the exchange and wishes he could somehow find that man and apologize. He does not take back what he said. He believes the profession can do better. But he says, "I should have been more diplomatic."
In 2016, a dozen researchers (19459006) gathered in a conference room in an ultramodern genetic sequencing center on the banks of the River Cam, 9 miles outside Cambridge, England. The gathering brought together experts to discuss how the principles of ecology can be applied to cancer. When they paused, they had the idea of playing a game of clones game in which a small group of scientists pretended to be cancer cells trying to convince the maximum number of other researchers hopping around in the room malicious clones.
During this meeting, an overarching theme kept popping up: evolution does not work the same way for all cancers. It is not even clear that Darwin's natural selection always determines the genetic mutations that occur within a tumor. A study of bowel cancer specimens performed by one of the conference participants, Andrea Sottoriva of the Institute of Cancer Research in London, and Christina Curtis, a computer biologist at Stanford University, suggested a different pattern.
When colorectal tumors begin to form, there appears to be a "big bang" of mutations. This initial explosion of cellular diversity in these colon cancers seems to follow a period when random genetic alterations occur for purely random reasons and occur more frequently than because the mutations bring some sort of competitive advantage. It is still unclear whether adaptive therapy, which assumes that there is Darwinian competition between the tumor cells, would be well suited for cancers in which the mutations occur by chance continuously.
Nonetheless, a kind of consensus emerged, and a year after Cambridge At this conference, the organizers issued a statement outlining how cancer could be better classified. Twenty-two researchers – some of the biggest names in the field of evolutionary oncology, including Gatenby – co-authored the document.
An important factor in the classification scheme proposed by the group is a measure of how rapidly a cancer mutates. In the last decade, faster DNA sequencing tools have shown that Nowell-Gatenby's old professor, the pioneer of cigarette smoking in the application of evolutionary thinking to cancer, was proactive: single tumors often struggle with rapid genetic changes. Instead of two or three initial defects that trigger a chain of uncontrolled growth, many tumors are the result of multiple mutational series. For example, a major experiment published in 2012 found at least 128 different DNA mutations in one patient in different kidney tumor samples. There is some evidence that the more mutations there are, the more aggressive a cancer is, suggesting a greater chance that one of these DNA alterations will give rise to tumor cells with the potential for drug resistance. In the light of technological advances, it is not too far-fetched to believe that doctors will routinely measure the number of mutations in their patients' tumors over the next ten years.
Today, most cancers are valued with a system dating back to the 1940s. Physicians typically evaluate factors such as the spread of cancer to or beyond the lymph nodes and use these characteristics to determine their "stage". At one end of the spectrum are stage 1 cancers, which are relatively limited, while at the other end are stage 4 cancers that have become prevalent. Crucially, this system of assigning cancer at one stage does not formally account for the genetic mutations of cancer.
The proposed categorization system that emerged from the Cambridge meeting would look at cancer in a completely new way. Instead of four stages of cancer, the authors of the 2017 Consensus Statement propose no fewer than 16 different categories – for example, tumors that have slow cell turnover and a low rate of mutations, or tumors that are a hotbed of genetic diversity, replicating rapidly Cells that compete for resources. This latter type of tumor could most likely help outsmart drug-sensitive cells in the body, and in some cases could be the most dangerous. A rapidly developing cancer of this kind could also be the best candidate for adaptive therapy.
Als die Konsenserklärung herauskam, arbeiteten Gatenby und seine Mitarbeiter in Tampa hart daran, Zellexperimente in einem Labor in der Halle durchzuführen sein Büro. Ziel war es, einen Schlüsselbegriff der adaptiven Therapie zu beweisen. Der Ansatz von Gatenby geht davon aus, dass sich medikamentenresistente Krebszellen langsamer replizieren als medikamentenempfindliche Zellen, wenn die Behandlung entfernt wird. Die Theorie beruht auf der Annahme, dass diese resistenten Zellen viel Energie benötigen, um ihre Rüstung gegen die Medikamente aufrechtzuerhalten, die dazu gedacht sind, sie zu töten. Während der Behandlungspausen, so der Gedanke, werden die brennstoffhungrigen resistenten Zellen von medikamentenempfindlichen Zellen, die weniger Ressourcen zum Gedeihen benötigen, überboten.
Um Beweise für diese Idee zu sammeln, setzte Gatenbys Forscherteam humane Brustkrebszellen mit einer Resistenz gegen das Medikament Doxorubicin in einer Petrischale zusammen mit einer gleichgroßen Population von Doxorubicin-empfindlichen Brustkrebszellen und beobachtete, wie die beiden Gruppen um Ressourcen kämpften. Am Tag 10 machten die resistenten Zellen nur 20 Prozent der Zellen in der Schale aus und gingen von dort aus langsam zurück. Am Ende des im letzten Jahr veröffentlichten Experiments waren diese resistenten Zellen auf etwa 10 Prozent der Gesamtbevölkerung gesunken.
Zugegeben, dieses Experiment fand in einer Petrischale statt und nicht in einem menschlichen Körper – oder sogar in einem Laboratorium Ratte. Einige führende Krebsspezialisten stimmen mit Gatenby darin überein, dass arzneimittelresistente Zellen wahrscheinlich von anderen Zellen übertroffen werden, wenn die Krebsmedikation abgesetzt wird. Aber sagen Sie andere, was ist, wenn Gatenby falsch liegt? Was ist, wenn resistente Zellen tatsächlich während der Zeit gedeihen, in der der Patient von Medikamenten genommen wird? Die Risiken sind hoch. Niemand will den Tod beschleunigen.
Krebs neu denken, da eine chronische Erkrankung eine mentale Verschiebung erfordert – eine Verschiebung, die möglicherweise durch andere Änderungen in der Krebstherapie gelindert wird. Es ist üblich, Krebspatienten von ihren Medikamenten beispielsweise ärztlich betreuten "Drogenurlaub" nehmen zu lassen. Und wir haben unser Denken in Sachen Medizin bereits angepasst. Ärzte dachten einmal, dass Stress die Hauptursache für Geschwüre sei, aber Biologen entdeckten ein Bakterium als Hauptursache. In letzter Zeit haben wir uns an die seltsame Vorstellung gewöhnt, dass Billionen von Bakterien in unserem Darmmikrobiom leben.
Vielleicht ist es keine große Frage zu glauben, dass wir das Zusammenleben mit Krebszellen tolerieren könnten, solange wir dies verhindern können sie wuchsen unkontrolliert. Während Darwin Ideen über das, was als Makroevolution bekannt wurde, zum Aufstieg und Fall von Arten, ob Käfer oder Weißkopfseeadler, brachte, könnte diese neue Sichtweise des Krebs ein Beispiel für das sein, was wir als "Endoevolution" bezeichnen könnten: natürliche Auslese in den eigenen Geweben eines Organismus zu spielen.
Die American Cancer Society räumt ein, dass einige Krebsarten bereits als chronische Krankheiten behandelt werden. In bestimmten Fällen versuchen Ärzte einfach zu verhindern, dass sich die Malignome mit neuen Medikamentenrunden verbreiten. Gatenbys adaptive Therapie zielt darauf ab, die Vermutung der Behandlung zu reduzieren. Weitere Studien bei Moffitt sind in Planung oder in Vorbereitung auf Krebserkrankungen an Brust, Haut und Schilddrüse sowie eine neue, größere Studie bei Patienten mit Prostatakrebs. Im ganzen Land, in Arizona, haben Athena Aktipis und ihr Ehemann und wissenschaftlicher Mitarbeiter, Carlo Maley, ein Stipendium erhalten, um eine Brustkrebsstudie mit adaptiver Therapie in Verbindung mit einem lokalen Zweig der Mayo Clinic zu beginnen.
Dies ist nicht der Fall ein gewaltiger Gedanke, dass wir mit Krebszellen koexistieren könnten, solange wir verhindern können, dass sie unkontrolliert wachsen.
Aber die Vorstellung von Krebs als unerbittlichem Feind, der vernichtet werden muss, ist tief verwurzelt. Sogar Gatenby spürt es, besonders wenn es um Kinder geht. Als seine Tochter ein Teenager war, starb eine ihrer Klassenkameraden an einer Krebserkrankung namens Rhabdomyosarkom. He never met his daughter’s friend but heard about his decline. Then, last year, a pediatric oncologist at Moffitt approached him to see if therapy inspired by evolutionary theory might work to fully weed out cancer from children newly diagnosed with that same disease. In the highest-risk group, that cancer kills as many as 80 percent of patients within five years.
In October, they met to begin designing a study. This trial will use a more sophisticated evolutionary model to cycle patients on and off of several drugs. The hope is to deploy the additional drugs to kick the cancer while it’s down, and thereby drive it to extinction. It’s an ambitious goal.
For now, Gatenby is most focused on managing advanced cancers in adults, and doing so as a chronic disease. In that sense, he’s challenging the words emblazoned on the outside wall of the Moffitt Cancer Center: “To contribute to the prevention and cure of cancer.” Robert Butler has pondered these words too, which he passes when walking into the building for checkups and treatments. “Certainly, in my case there’s no intention of cure. What we’re doing is control. So that’s not really the correct logo anymore, is it?” he says. Butler tells me about a time when he and some of the Moffitt researchers brainstormed alternative slogans. “We finally came up with ‘Our aim is to make you die of something else’—which I thought was lovely,” he adds. “It’s more true.”
Robert Gatenby photographed at Everson Museum of Art
Roxanne Khamsi (@rkhamsi) is a science writer living in New York and chief news editor of Nature Medicine.
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