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In October 1854, A government entomologist was inspecting farmland outside the city of Ottawa, in northern Illinois, when he came across a troubling scene in a cabbage field.
The big outside the leaves of the vegetables were "literally riddled with holes, more than half of their stuff being eaten". At each step, he circled the ravaged cabbages, tiny swarms of gray-ashen butterflies rising from the ground and moving on. This was apparently the first report in the United States of diamondback moths, an invasive pest which, in its larval form, is particularly indicative of cruciferous plants. In the late 19th century, butterflies chew through the leaves of cabbages, Brussels sprouts, kale and kale from Florida to Colorado.
To fight this invasion, farmers started bombing their fields with primitive pesticides. It worked. Or seemed. It killed most moths, but those who survived the poison have bred and the population has rebounded stronger than ever. For decades, one pesticide after another failed because butterflies evolved to support it. Even DDT, extremely toxic, could not compete with Diamondback. From the late 1950s, agricultural experts began to abandon the idea of eradication and adopted a new strategy. Farmers would leave moths alone until their numbers exceed a certain threshold, and only then would they use pesticides. Remarkably, it helped. Moths are not dead, but the pest could be managed and crop damage controlled.
When Robert Gatenby heard this story about diamondback moth in 2008, he immediately became involved. Gatenby is neither a farmer nor agronomist nor a lover of cruciferous vegetables. In fact, he deeply hates Brussels sprouts. He is a trained radiologist and directs the radiology department of the H. Lee Moffitt Cancer Center in Tampa, Florida. But unlike your usual doctor, he is also obsessed with the evolutionary principles put forward by Charles Darwin more than 150 years ago. The history of diamond moth moths appealed to Gatenby as a useful metaphor for his own project – a project that was not about crops but about cancer.
Like the cruciferous moth, cancer cells develop resistance to the powerful chemicals used to destroy them. Even though cancer treatments kill most of the cells they target, a small subset can survive, largely because of the genetic changes that make them resistant. In advanced cancers, it is usually necessary to know when, and not if, the surviving pugnacious cells will become an unstoppable force. Gatenby thought that this deadly issue could be avoided. His idea was to expose a tumor to medications intermittently, rather than in a constant badault, thus reducing the pressure on his cells for them to develop resistance.
Just as ecologists admit a manageable population of diamondback moth, 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 authorization in 2014 to conduct a clinical trial in patients with advanced prostate cancer at Moffitt. Patients had cancer that was no longer responding to treatment; their drug-resistant cells gained an evolutionary battle in the body, surviving an onslaught of toxic drugs where weaker cancer cells succumbed. The hope was that by using a precise drug dosing regimen developed using evolutionary principles, they could slow the rise of mutations that would give some cancer cells the ability to survive. Gatenby's name for this approach was adaptive therapy.
One of the patients of the trial was Robert Butler, a British engineer in oil exploration who had retired to Tampa. In 2007, he was diagnosed with prostate cancer and seven years later, after taking the drug Lupron and undergoing radiation, his prostate tumor had progressed to stage 4, advanced cancer. Butler did not give up, though. He tried a recently approved immunotherapy treatment. This involved sending blood cells to a facility outside Atlanta, where they were mixed with a molecule that activates the immune cells, and then returned to Florida for treatment. reinjected. The treatment was expensive – its sale price could reach $ 120,000 – but the threat of cancer progression persisted.
When Butler and his wife went to the office of his oncologist at the Moffitt Cancer Center in August 2014, they prepared for the events. they had heard of invasive treatments, such as radioactive implants. So they were intrigued when the doctor told them about Gatenby's lawsuit and asked if Butler wanted to participate. He would take a powerful and extremely expensive medicine called Zytiga, but not in the way of scorched earth and kill all the cells that is standard. Instead, he would only receive the amount of Zytiga needed to prevent the cancer from developing. The idea was radical and counter-intuitive. His last blow to escape the death of his cancer was to give up healing.
Knowing the modified Zytiga treatment regimen was not designed to rid him of his cancer, engineer Butler explained, about how doctors would measure the success of their new therapeutic approach. He asked, "How do we know this product works?" And one of his doctors replied, "Well, you will not be dead."
In the USA We use military metaphors when we talk about cancer. We fight and fight, and if we survive, we are victorious. This attitude dates back in part to 1969, when the Citizens Committee for the Conquest of Cancer published an announcement in The Washington Post and The New York Times imploring the President with the words "Mr. Nixon: You can cure cancer. The call to action helped trigger the "war on cancer" in the country, as it was determined that by using enough medical weapons, the evil enemy could be wiped out.
By the mid-1970s, however, signs were beginning to appear that some strategies for total eradication might turn against them. In this context, a cancer researcher, Peter Nowell, published a feature article in Science in 1976. Nowell hypothesized that the forces of evolution are pushing certain cell populations in tumors to become more and more malignant over time. The cells inside a tumor are competing, not only with the surrounding healthy cells, Butell explained, but also with each other. Nowell has suggested – and subsequent research has confirmed – that certain alterations in DNA confer on cancer cells resistance to chemotherapy or other treatments, allowing them to differentiate themselves from drug-sensitive cells by through a natural selection process.
Nowell pbaded on his ideas to his medical school students at the University of Pennsylvania, sometimes smoking a cigarette during his presentation. His theories were respected but slow to understand. He pointed out that tumors can become more deadly as they accumulate more genetic errors. It was an idea ahead of his time. Scientists of the time did not have the technical ability to measure all the changes in the vast genomes of tumor cells. Instead, they could only sequence small amounts of DNA at a time, and most scientists thought that cancers were the result of some genetic mutations.
One of the medical students who listened to the Nowell conference in the late 1970s was a young Bob Gatenby. But Nowell's ideas did not impress him very much, says Gatenby; Instead, what inspired him was what he saw in his early years of radiology on the front lines of the war on cancer.
"I did not understand why you would treat someone with a deadly disease and kill them with your treatment. It did not seem right to me. "
By the mid-1980s, Gatenby had landed a job at the Fox Chase Cancer Center in Philadelphia. In this hospital and in other laboratories across the country, clinical trials have treated bad cancer patients with extreme care: a combination of a potentially lethal dose of chemotherapy followed by a bone marrow transplant. The treatment was heartbreaking. The women had diarrhea and nausea, and some had so much lung damage that they had trouble breathing. Others had liver damage and a weakened immune system that made them vulnerable to serious infections. As a radiologist, Gatenby's job was to interpret X-rays and other patient examinations. He found the treatment failed. In the United States, of the more than 30,000 women with bad cancer who underwent the procedure between 1985 and 1998, 15% died as a result of the actual treatment. "What happened is that these women have suffered terribly and have not been healed," says Gatenby.
At about the same time as the bad cancer trials, a colleague of Gatenby's father went to the hospital to get his first aggressive chemotherapy for lung cancer. According to the colleague, her father arrived on a Friday without any apparent symptoms and died on Monday. "This event was very traumatic for me," Gatenby recalls, and the cause seemed obvious to him. "I did not understand why you would treat someone with a deadly disease and kill them with your treatment. It did not seem right to me. During this difficult period, Gatenby's own father died of esophageal cancer.
Gatenby felt that there must be a better way to treat cancer, to thwart it rather than to bomb it. He had studied physics at the university and thought that biologists could use the equations to capture the forces at the root of cancer in the same way that physicists use mathematics to describe phenomena such as gravity . While Nowell had advanced general theories about how cancer followed the principles of evolution, Gatenby went one step further: he wanted to find a way to describe the evolution of cancers at the same time. using mathematical formulas.
Robert Gatenby, a radiologist, has seen patients with intensive bad cancer treatments. He felt that there must be a better way to treat cancer, to thwart it rather than to bomb it.
Mark Sommerfeld
In 1989, Bob Gatenby was concerned with modeling the evolution of cancers. During the day, he was examining X-rays of cancer patients and, at night, after sleeping with his wife, he and his wife, he sat at the kitchen table in their home from Philadelphia to the suburbs and was reviewing medical journals. The patterns that he began to observe in the literature led him to ask himself a question: what would happen if the cancer cells outperformed the normal and healthy cells of the body in the same way that they did? an animal species surpbaded its competitors in the wild?
Gatenby recalled that ecologists had developed equations to describe the balance between predators and prey. As a student of Princeton University, he had learned the clbadic example of computation that showed how growing populations of snowshoe hares were strengthening the rise of the lynx that fed them. He began to dust old books and buy new ones to learn about the interactions between species.
For a year, Gatenby read and pondered. Then, in 1990, on a family trip to the Atlantic coast of Georgia, he found himself stuck in a hotel room one afternoon with his two sibling children. From nowhere, an idea has come up. He grabbed a piece of writing paper and a pen and began to scribble key phrases from the ecology of the people. These formulas, known as Lotka-Volterra equations, have been used since the 1920s to model predator-prey interactions and, later, the dynamics of competition among species, and were among those that he had recently refined. him. Gatenby thought that this set of formulas could also describe how tumor cells compete with healthy cells for energy resources such as the glucose that feeds them.
Back in Philadelphia, he spent the time he could on a typewriter to compose a document outlining this theoretical model. As soon as he finished, he showed it to 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 does not do justice to the way they were negative about it," he says. His peers felt that a brief set of formulas could not account for the seemingly infinite complexity of cancer.
Louis Weiner, who worked alongside Gatenby at the time, remembers that their colleagues perceived Gatenby's ideas as offbeat. "At that time, orthodox treatment favored high-intensity, high-dose treatments to eradicate all tumor cells from a cancer patient," said Weiner, who is now director of the Georgetown Lombardi Integral Cancer Center in Washington. . "Bob's point of view was the antithesis of these beliefs."
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But Gatenby insisted and managed to get acceptance of the paper, which is full of equations of Lotka-Volterra, accepted in the leading newspaper. Research against cancer in 1991.
Despite the publication of his theory, he still could not convince oncologists that his idea had merit. "I think they felt intimidated," says Gatenby. "Most doctors are mathematically illiterate." He found that the medical establishment was reluctant to publish much of its follow-up work.
In the years that followed, Gatenby rose through the ranks to head the Fox Chase Cancer Center's Department of Diagnostic Imaging. He was later named head of the Department of Radiology at the College of Medicine at the University of Arizona at Tucson. He continued to be recognized for his effective interpretation of scanners and to receive federal grants to study cancer.
Then, in 2007, the Moffitt Cancer Center offered Gatenby a position as Director of the Department of Radiology. He was suffering from an illness: he would come if the hospital created a division allowing him to look for the link between Darwin's principles and cancer. The department of integrated mathematical oncology, born from this negotiation, is the first mathematical department of a hospital specialized in cancer treatment, he said. Finally, Gatenby had a place where he could put his ideas to the test.
Gatenby arrives at his corner office in Moffitt almost every day at 7 o'clock. He is now 67 years old and his hair is gray at the temples, but his eyebrows are still brown. His children – those who were napping in this hotel room when he noted his Darwinian inspiration – now have their own children and he has the coffee cup "I ♥ Grandpa" to prove it. A hospital thong around his neck, he rolls up his flawless shirt sleeves and sits at his desk. Outside his office, some 30 scientists and doctoral students spend their days researching patterns of cancer growth using equations such as those describing population dynamics.
To Gatenby's knowledge, no one had attempted to exploit the cancer evolution as part of a clinical trial until he or she came up with his experience with prostate cancer. He chose prostate cancer to test this approach in part because, unlike other cancers, routine blood sampling for a molecule called prostate specific antigen (PSA) can provide an immediate indicator of progression. cancer.
To design a clinical trial, Gatenby and his Moffitt collaborators first had to explain their idea that tumor cells were competing for resources. They turned to game theory to plot this dynamic and integrated the numbers into the Lotka-Volterra equations. The computer simulations they performed with these equations made it possible to estimate the speed with which drug-resistant cells could replace other tumor cells when exposed to the continuous Zytiga baday generally administered to patients with cancer. advanced prostate.
In simulations, the typical drug administration led to the rapid proliferation of drug-resistant cancer cells. The treatment will fail each time. This dark result corresponds to the results of the hospital records. In contrast, computer simulations suggested that if Zytiga was given only when the tumor appeared to be developing, drug-resistant cells would take much longer to take sufficient advantage to overcome the cancer.
In 2014, the Moffitt team managed to launch the first small study testing this adaptive therapy approach, recruiting Robert Butler and a small group of other men with prostate cancer at a stage advanced. Butler's oncologist told him how it would work. He would stay on the Lupron he had been taking for years, and every month he went to the hospital to have his PSA test tested to determine if his prostate tumor was growing. Every three months, he underwent a CT scan and a whole body bone to monitor the spread of the disease. Whenever his PSA level was above his initial level at the start of the trial, he began to take the more powerful Zytiga. But when his PSA rate fell to less than half of the base, he could do without Zytiga. This is interesting because Zytiga and drugs like this can cause side effects such as hot flushes, muscle aches and high blood pressure.
The Moffitt approach also promised to be much cheaper than taking Zytiga on an ongoing basis. When purchased wholesale, a one – month supply costs almost $ 11,000. Butler had health insurance, but even so, the first month of his supplies would cost him $ 2,700 in his pocket, then $ 400 a month. Abandoning the treatment each time her PSA level was low would result in huge savings.
"Conceptually, it's a wonderfully simple approach. It makes cancer a chronic disease. "
Butler was participating in a so-called pilot trial, which was less rigorous than a large-scale clinical trial because he did not randomly badign patients to receive experimental or standard treatments. The study relied instead on a group of patients treated outside of the trial, as well as on the results of a 2013 article on Zytiga, in order to propose a benchmark on the way patients typically cope when they receive the drug continuously.
When the first results of their new test were presented, Moffitt's scientists were satisfied and relieved. Before the trial, "we were, to be honest, terrified," says Gatenby. The benefits of adaptive therapy seemed enormous. Of the 11 men in the study, one quit the test after the spread of his illness, but most lived longer than expected without progression of their cancer. Men taking a continuous dose of Zytiga have a median of 16.5 months before the cancer becomes resistant to the drug and spreads. In comparison, the median time to progression in men receiving adaptive therapy was at least 27 months. In addition, they used on average less than half of the standard amount of Zytiga. Joel Brown, an evolutionary ecologist and one of Gatenby's collaborators, said that the team felt morally compelled to spread the word: "The effect was so important that It would be unethical not to report it immediately, "he says.
They released a report in 2017, much earlier than expected, on a generally positive reaction from prostate experts, particularly because it suggested a way in which people with cancer could live longer with fewer drugs . "If you can reduce the side effects, I think it's fantastic," says Peter Nelson, an oncologist who studies prostate cancer at the Fred Hutchinson Cancer Research Center in Seattle. "Conceptually, it's a wonderfully simple approach." Jason Somarelli, a biologist at the Duke Cancer Institute, calls Gatenby a pioneer: "He turns cancer into a chronic disease."
Butler, 75, has spent long periods off Zytiga, with trips that can last up to five months. "I'm now the boy of the posters, they say," Butler said. He is one of the best speakers in the study.
Some doctors are already trying to adopt adaptive therapy in patients outside of clinical trials. In 2017, inspired by the Gatenby pilot study, an Oregon physician initiated a prostate cancer patient on a modified version of the approach when he declined standard continuous dosing. Since then, she has started treating 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 require government approval. The protocol uses already approved drugs and the US Food and Drug Administration does not control specific dosing schedules.
Experts call for caution, however. The study on prostate cancer was very small and without a randomly badigned control group, the results are not really reliable. Although the majority of men in the trial remain stable, four more have seen their cancer progress since the publication of the document. "This is an approach that must now be carefully studied in the context of prospective clinical trials before adopting it into clinical practice," states Richard L. Schilsky, medical director of the clinic. American Society of Clinical Oncology. Years could go by before a large scale adaptive therapy test takes place. Len Lichtenfeld, Acting Chief Medical Officer of the American Cancer Society, echoes Schilsky's concerns. "Is it intriguing? Yes, says Lichtenfeld. "But there is still a long way to go."
Gatenby agrees that adaptive therapy requires rigorous testing. It expresses a kind of humility that is not often observed in the higher spheres of medical science. He repeatedly told me that it was not an interesting topic on which to write and, more than once, I heard colleagues approaching him. the pronunciation of his name (which is pronounced GATE-en-bee); apparently, he had never corrected them. But when he believes in something, he does not back down. And he believes in adaptive therapy. "It looks like a teddy bear, but beneath that soft exterior, it's steel," said Athena Aktipis, who is studying theoretical biology and cancer at Arizona State University and collaborated with Gatenby.
At the end of last year, Gatenby presented his work at a meeting of prostate cancer specialists. During the Q & A session that followed, one participant shared his surprise at the results. "I guess what you are saying is that we have done badly all these years," said the man, according to Gatenby. "I stayed literally speechless for a few moments," admits Gatenby, "then I said," Well, yes, I guess that's what I'm saying. "He's still on the exchange and wants to be able to find the man and apologize, he does not pick up what he said, he thinks the profession can do better." But, he says, "I'm 39, should have been more diplomatic.
In 2016, a A dozen researchers gathered in a conference room in a state-of-the-art genetic sequencing center on the banks of the River Cam, 15 km from Cambridge, England. The meeting brought together experts to discuss how the principles of ecology might apply to cancer. When they took a break, their idea of the fun was to play a series of "Clone Games", in which a small group of scientists claimed to be cancer cells trying to persuade as many other researchers as possible. bouncing around the room to be their own cells. malignant clones.
During this meeting, a general theme emerged: evolution does not operate in the same way in all cancers. It is not even clear that Darwinian natural selection always determines the genetic mutations that abound within a tumor. A study of colon cancer samples led by one of the conference participants, Andrea Sottoriva of the Cancer Institute in London, and Christina Curtis, a computer scientist biologist at the University of Stanford, suggested a different scheme.
When colorectal tumors begin to form, there appears to be a "big bang" of mutations. This initial explosion of cell diversity in these colon cancers appears to be followed by a period during which random genetic changes occur and become more frequent by chance than by the fact that mutations provide a competitive advantage. It is still unclear whether adaptive therapy, based on the badumption of Darwinian competition between tumor cells, would be appropriate for cancers in which mutations occur continuously by chance.
Nevertheless, a kind of consensus emerged and, one year after the Cambridge meeting, the organizers issued a statement outlining how to better clbadify cancers. The paper was co-authored by twenty-two researchers, including some of the biggest names in the field of evolutionary oncology, including Gatenby.
An important factor in the clbadification scheme suggested by the group is the measure of how quickly a cancer is transformed. Over the last decade, faster DNA sequencing tools have shown that Nowell – Gatenby's former professor, a pioneer of smoking in the application of evolutionary thought to cancer – was premature: individual tumors bristle often rapid genetic changes. Rather than two or three initial errors triggering an uncontrolled growth chain, many tumors result from several sets of mutations. A significant experiment published in 2012, for example, revealed at least 128 different DNA mutations in various samples of kidney tumors from a patient. There is evidence that the more mutations there are, the more aggressive the cancer is, suggesting an increased risk that one of these DNA changes confers tumor cells the potential for drug resistance. Compte tenu des progrès technologiques, il n’est pas exagéré de penser qu’au cours de la prochaine décennie, les médecins mesureront systématiquement le nombre de mutations dans les tumeurs de leurs patients.
Aujourd'hui, la plupart des cancers sont évalués à l'aide d'un système datant des années 1940. Les médecins évaluent généralement des facteurs tels que le stade de développement d'un cancer jusqu'aux ganglions lymphatiques ou au-delà. Ces cancers déterminent son «stade». À une extrémité du spectre, les cancers de stade 1 sont relativement confinés, tandis que sont des cancers de stade 4, qui se sont largement répandus. De manière cruciale, ce système consistant à attribuer un stade au cancer ne prend pas formellement en compte les mutations génétiques d’un cancer.
Le système de catégorisation suggéré, issu de la réunion de Cambridge, examinerait le cancer d'une manière totalement nouvelle. Au lieu de quatre stades de cancer, les auteurs de la déclaration de consensus de 2017 proposent pas moins de 16 catégories différentes, par exemple, les tumeurs dont le renouvellement cellulaire est lent et le taux de mutations accumulées faible, ou les tumeurs qui sont un foyer de diversité génétique rapidement cellules de réplication en concurrence pour les ressources. Ce dernier type de tumeur pourrait être le plus susceptible de mettre au point un moyen de supplanter les cellules sensibles aux médicaments dans le corps et pourrait ainsi, dans certains cas, être le plus dangereux. Un cancer de ce type en évolution rapide pourrait également constituer le meilleur candidat pour une thérapie adaptative.
Au moment où la déclaration de consensus a été publiée, Gatenby et ses collaborateurs à Tampa travaillaient fort pour mener des expériences sur des cellules dans un laboratoire situé dans le hall de son bureau. L'objectif était de prouver un principe clé de la thérapie adaptative. L’approche de Gatenby suppose que lorsque le traitement est supprimé, les cellules cancéreuses résistantes aux médicaments se répliquent plus lentement que les cellules sensibles aux médicaments. La théorie repose sur l'hypothèse que ces cellules résistantes ont besoin de beaucoup d'énergie pour maintenir leur armure contre les médicaments destinés à les tuer. On pense que pendant les pauses de traitement, les cellules résistantes énergivores sont supplantées par les cellules sensibles aux médicaments, qui ont besoin de moins de ressources pour s'épanouir.
Pour rbadembler des preuves de cette idée, l’équipe de recherche de Gatenby a placé des cellules cancéreuses du sein humaines résistantes au doxorubicine dans une boîte de Pétri, aux côtés d’une population égale de cellules de cancer du sein sensibles à la doxorubicine et a regardé les deux groupes se battre pour obtenir des ressources. Au dixième jour, les cellules résistantes ne représentaient plus que 20% des cellules de la boîte et continuaient à diminuer lentement à partir de là. À la fin de l'expérience publiée l'année dernière, ces cellules résistantes avaient chuté pour représenter environ 10% de la population totale.
Certes, cette expérience s’est déroulée dans une boîte de Pétri, pas dans un corps humain, ni même dans le corps d’un rat de laboratoire. De grands spécialistes du cancer s'accordent avec Gatenby pour dire que les cellules résistantes aux médicaments sont probablement plus performantes que les autres lorsque le médicament anticancéreux est retiré. Mais, disent les autres, que se pbadera-t-il si Gatenby a tort? Que se pbade-t-il si les cellules résistantes se développent réellement pendant la période où le patient est retiré de la drogue? Les risques sont élevés. Personne ne veut hâter la mort.
Repenser le cancer en tant que une maladie chronique nécessite un changement de mentalité – un changement que d'autres changements dans le traitement du cancer pourraient être en train d'atténuer. Par exemple, il est courant de laisser les patients atteints de cancer prendre des «congés pour médicaments» sous la surveillance de leur médecin. Et nous avons déjà adapté notre pensée en matière de médecine. Les médecins pensaient autrefois que le stress était la principale cause des ulcères, mais les biologistes ont découvert qu'une bactérie en était la principale cause. Plus récemment, nous nous sommes habitués à l’idée étrange que des milliers de milliards de bactéries vivent dans notre microbiome intestinal.
Peut-être alors n’est-il pas difficile de penser que nous pourrions tolérer la coexistence de cellules cancéreuses tant que nous pourrons les empêcher de se développer sans contrôle. Alors que Darwin a avancé des idées sur ce que l’on appelle maintenant la macroévolution – l’ascension et la disparition d’espèces, qu’il s’agisse de coléoptères ou de pygargues à tête blanche – cette nouvelle conception du cancer pourrait être un exemple de ce que nous pourrions appeler «l’endo-évolution»: la sélection naturelle. jouer dans les propres tissus d'un organisme.
L'American Cancer Society reconnaît que certains cancers sont déjà gérés en tant que maladies chroniques. Dans certains cas, les médecins essaient simplement d'empêcher les tumeurs malignes de se propager avec de nouvelles séries de médicaments. La thérapie adaptative de Gatenby a pour but d’éliminer les incertitudes liées au traitement. De plus en plus d'essais chez Moffitt sont en cours de planification ou en cours pour les cancers du sein, de la peau et de la thyroïde, ainsi qu'un nouvel essai plus vaste chez les patients atteints du cancer de la prostate. Dans l’ensemble du pays, en Arizona, Athena Aktipis et son mari et collaborateur scientifique, Carlo Maley, ont obtenu une subvention pour commencer un essai sur le cancer du sein en utilisant un traitement adaptatif en collaboration avec une branche locale de la clinique Mayo.
Ce n’est pas très difficile de penser que nous pourrions tolérer la coexistence de cellules cancéreuses tant que nous pourrons les empêcher de se développer sans contrôle.
Mais l'idée du cancer en tant qu'ennemi implacable qui doit être annihilé est profonde. Même Gatenby le ressent, particulièrement en ce qui concerne les enfants. Quand sa fille était adolescente, l'un de ses camarades de clbade est décédé d'un cancer appelé rhabdomyosarcome. Il n'a jamais rencontré l'ami de sa fille mais a entendu parler de son déclin. Puis, l’année dernière, un oncologue pédiatrique de Moffitt l’a approché pour lui demander si une thérapie inspirée par la théorie de l’évolution pourrait aider à éliminer complètement le cancer chez les enfants nouvellement diagnostiqués de la même maladie. Dans le groupe à haut risque, ce cancer tue jusqu'à 80% des patients dans les cinq ans.
En octobre, ils se sont rencontrés pour commencer à concevoir une étude. Cet essai utilisera un modèle évolutif plus sophistiqué pour faire basculer les patients de plusieurs médicaments. L’espoir est de déployer les médicaments supplémentaires pour vaincre le cancer et le conduire ainsi à l’extinction. C’est un objectif ambitieux.
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 pbades 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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