For some people, it's Christmas. For others, it's the languid days of summer. Still others prefer the crisp promise of fall's fresh start. Not me. For me, it's all about asparagus season. I await the early wisps of spring with intensity, eager to get my hands on those sweet, vegetal stalks. The window for the best of the bunch is short (March through June with a peak in April), so get in early and stay late. If it's still a bit too chilly for asparagus in your neck of the woods, then go ahead and bookmark these recipes and whip them out when the time is right — you won't regret it.
Descubren un nuevo órgano humano que ayudaría al cáncer a propagarse
El intersticio es una red de canales llenos de líquido que tiene una función protectora, y también es capaz de transportar células tumorales por el cuerpo.
La biología humana en sí misma sigue manteniendo misterios para la ciencia. Un equipo de científicos ha descubierto una red de canales llenos de líquido en el organismo, en lo que parece tratarse de un nuevo ‘órgano humano’: el intersticio.
Ya se tenía constancia de que existía un espacio entre las células, llamado espacio intersticial, pero una nueva investigación le ha dado la categoría de órgano.
Esta red de canales tendría una función protectora, pero además permitiría transportar células cancerosas de un lugar a otro del cuerpo, tal y como se detalla en la investigación, publicada en la revista Scientific Reports.
A través de una endoscopio de rutina, los científicos observaron por casualidad que el conducto biliar estaba rodeado por patrones extraños inexplicables en su tejido, en lugar de una pared dura y densa, como esperaban.
Investigaciones adicionales en otros tejidos del cuerpo han aportado más datos: sugieren que estos patrones son en realidad canales, que estarían en todas partes del cuerpo, llenos de líquido. El equipo estima que el órgano contiene alrededor de un quinto del volumen total de líquido del cuerpo humano.
¿Cómo es que no se ha descubierto antes?
Si efectivamente estamos ante un nuevo órgano humano, ¿cómo es que no se ha descubierto antes? Los investigadores creen que, dado que los enfoques estándar para procesar y visualizar el tejido humano hacen que los canales se drenen, las fibras de colágeno que le dan a la red su estructura se colapsan sobre sí mismas. Esto habría hecho que los canales parecieran una pared dura de tejido protector denso, en lugar de una especie de bolsa llena de líquido.
“Creemos que funciona como amortiguador”, dicen los científicos. Es decir, que esta red tiene una función protectora.
Ayudaría a propagar el cáncer
Pero además de proteger los órganos, la red también contribuiría a la propagación del cáncer, según las observaciones de los científicos.
Cuando el equipo analizó muestras tomadas de personas con cánceres invasivos, encontraron evidencias de que las células cancerosas que habían salido de sus tejidos originales habían sido transportadas a través de estos canales, que los llevaron directamente al sistema linfático.
"Tenemos ante nosotros una nueva ventana hacia el mecanismo de diseminación tumoral", enfatizan los investigadores.
El siguiente paso es comprobar si analizar el líquido en estos canales recientemente descubiertos podría conducir a un diagnóstico más temprano del cáncer. Es más, los científicos creen que el nuevo órgano también podría estar involucrado en otros problemas, como los edemas, una rara enfermedad hepática y otros trastornos inflamatorios.
While significant progress has been made in halting the spread of communicable diseases in Africa, rates of non-communicable illnesses, especially cancers, are rising. With just 5% of global funding for cancer prevention spent in Africa, a new global strategy is needed to help manage a looming health crisis.
CHICAGO – One of the most pressing public-health challenges in Africa today is also one of the least reported: cancer, a leading cause of death worldwide. Every year, some 650,000 Africans are diagnosed with cancer, and more than a half-million die from the disease. Within the next five years, there could be more than one million cancer deaths annually in Africa, a surge in mortality that would make cancer one of the continent’s top killers.
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Throughout Sub-Saharan Africa, tremendous progress has been made in combating deadly infectious diseases. In recent decades, international and local cooperation have reduced Africa’s malaria deaths by 60% , pushed polio to the brink of eradication, and extended the lives of millions of Africans infected with HIV/AIDS.
Unfortunately, similar gains have not been made in the fight against non-communicable diseases (NCDs), including cancer. Today, cancer kills more people in developing countries than AIDS, malaria, and tuberculosis combined. But, with Africa receiving only 5% of global funding for cancer prevention and control, the disease is outpacing efforts to contain it. Just as the world united to help Africa beat infectious disease outbreaks, a similar collaborative approach is needed to halt the cancer crisis.
Surviving cancer requires many things, but timely access to specialists, laboratories, and second opinions are among the most basic. Yet, in much of Africa, a lack of affordable medications, and a dearth of trained doctors and nurses, means that patients rarely receive the care they need. On average, African countries have fewer than one trained pathologist for every million people, meaning that most diagnoses come too late for treatment. According to University of Chicago oncologist Olufunmilayo Olopade, a diagnosis of cancer in Africa is “nearly always fatal.”
Building health-care systems that are capable of managing infectious diseases, while also providing quality cancer care, requires a significant investment in time, money, and expertise. Fortunately, Africa already has a head start. Past initiatives – like the Global Fund to Fight AIDS, Tuberculosis, and Malaria, the US President’s Emergency Plan for AIDS Relief, and the World Bank’s East Africa Public Health Laboratory Networking Project – have greatly expanded the continent’s medical infrastructure. National efforts are also strengthening pharmaceutical supply chains, improving medical training, and increasing the quality of diagnostic networks.
Still, Africans cannot face down this threat alone. That is why the American Society for Clinical Pathology, where I work, is cooperating with other global health-care innovators to attack the region’s growing cancer crisis. We have teamed up with the American Cancer Society (ACS) and the pharmaceutical company Novartis to support cancer treatment and testing efforts in four countries: Ethiopia, Rwanda, Tanzania, and Uganda. Together, we have brought immunohistochemistry, a key diagnostic tool, to seven regional laboratories, an effort we hope lead to more timely cancer diagnoses and greatly improve the quality of care.
To complement these technical efforts, the ACS is also training African health-care professionals how to carry out biopsies and deliver chemotherapy. That initiative, funded by Novartis, is viewed as a pilot program that could expand to other regional countries.
Finally, our organizations are advocating for enhanced cancer-treatment guidelines in national health-care planning efforts, protocols that we believe are essential to improving health outcomes. These initiatives are in conjunction with other undertakings, such as a joint ACS-Clinton Health Access Initiative program to broaden access to cancer medications.
When the world took notice that infectious diseases like HIV/AIDS, polio, and malaria were ravaging Africa, action plans were drawn up and solutions were delivered. Today, a similar global effort is needed to ensure that every African with a cancer diagnosis can get the treatment they need. Now, as then, success depends on coordination among African governments, health-service providers, drug makers, and non-governmental organizations.
There is no place on Earth that is immune from the dread of a cancer diagnosis; wherever the news is delivered, it is often devastating to recipients and their families. But geography should never be the deciding factor in patients’ fight to survive the disease. Cancer has been Africa’s silent killer for far too long, and the global health community must no longer remain quiet in the face of this crisis.
Greenway told mySA.com she started the diary as a way to avoid constant conversation about her skin cancer.
The face is the most common place on the body for skin cancers to form—but people tend to miss spots on their face when they apply sunscreen, according to new research
Media: Time
"People are always asking 'how are you doing,' 'are you alright,'" Greenway said. "I just want to be able to be present. Enjoy the life that I have instead of constantly rehashing the crap that I've had to go through."
The public album is there for her friends and family to see what's happening, instead of having to ask. Plus, it's a way for her to cope, she said.
"It's really strange to have your face change so much," Greenway said.
But as of late the public album has been drawing attention from others too.
The Austin mother was diagnosed with skin cancer August of last year after investigating what looked like a "big liver spot" on her forehead following her second pregnancy.
Her dermatologist initially dismissed the spot, but fear crept back into Greenway's mind after developing a mole in that area nine months later.
Una característica de este padecimiento es precisamente que en un inicio no presenta síntomas. Esto vuelve al cáncer de estómago más difícil de identificar.
Según las estadísticas el cáncer de estómago no es un cáncer muy común, llegando a padecerla 1 de cada 111 adultos y siendo más freciemte en hombres adultos.
Para identificar esta enfermedad hay señales que se presentan en algunos pacientes, y aunque podrían indicar otro padecimiento es importante prestarles atención y buscar ayuda médica para descartar o detectar a tiempo el cáncer de estómago.
1.- Reflujo y agruras que no desaparecen
Este síntoma puede indicar otras enfermedades como gastritis, pero acompañada de otras señales requiere atención médica.
2.- Pérdida de peso inexplicable
Perder peso de manera inexplicable, es decir sin estar sometido a una dieta o plan de ejercicio puede ser señal de enfermedades como la Diabetes y el cáncer. Esta pérdida de peso puede ser gradual, no completamente repentina.
3.- Apetito cambiante
Las personas que presentan este padecimiento por lo regular aseguran perder el apetito de un momento a otro, a esto se le llama ‘saciedad temprana’ y es otra característica que podría indicar cáncer de estómago.
4.- Dolor
Aunque en la mayoría de los casos el dolor de estómago es el resultado de otros problemas intestinales, puede ser una señal de cáncer si este se presenta persistente en medio del estómago.
5.- Sangre en heces o en vómito
Si el sangrado está relacionado con esta enfermedad lo más seguro es que las heces presentan un color vino o negro. Si la sangre se presenta en el vómito será de un color rojo brillante y con una textura de ‘granos de café.’
6.- Inflamación, diarrea y estreñimiento
El cáncer provoca inflamación y un funcionamiento negativo de los intestinos, por lo que estas molestias se pueden presentar también.
Los síntomas por sí solos no son peligrosos, pero si van acompañados de otros requieren de atención médica. Enfermedades como el cáncer pueden ser curables si se detectan a tiempo.
Cancer cells outcompete normal cooperative cells, and evolution takes it from there.
iStock
This article is part of Future Tense, a collaboration among Arizona State University, New America, and Slate. On Thursday, April 27, at noon, Future Tense will host an event in Washington called “Do We Need to Stop Talking About ‘Curing’ Cancer?” For more information and to RSVP, visit the New America website.
If your life has been touched by it, cancer can seem like the least normal thing imaginable. It disrupts all aspects of life, threatens many things we hold dear, and baffles us with its mysterious ways. It seems possessed with an uncanny ability to evade our treatments, rise from the dead when we think it’s finally gone, and even hijack our bodies’ resource-delivery systems to feed its growth. But cancer has been with us since the beginning of multicellular life, and it’s not going anywhere. It has been a supporting character throughout humanity’s story. In fact, it predates us.
About a billion years ago, multicellularity began. Single-celled organisms started forming groups and using cellular teamwork to get an evolutionary leg up on their less social competition. This transition to multicellular living—from a solitary to a social lifestyle—had many benefits for cells, but it also had some costs. Cells in multicellular bodies had to give up much of the freedom of the unicellular lifestyle. Multicellularity meant several things, including cells not dividing so fast, reining in resource use, taking care of the extracellular environment, and sometimes even making the ultimate sacrifice: cellular suicide.
We descended from the cells that chose this path. Our bodies are made of highly cooperative cells that make trillions of sacrifices every second for the well-being of our entire organism. We are, in many ways, the most complex cooperative system known to humankind, though we rarely pause to think about the feat of cellular cooperation occurring within ourselves.
Our bodies are made of 30 trillion cells (that’s 500 times as many humans are on Earth) that achieve cooperation on a massive scale. But cooperation is not so easy, as anybody who has been on a team project knows. Even a small-scale cooperative venture is vulnerable to failure, whether through a lack of coordination, breakdown of division of labor, or—perhaps most relevant to cancer—exploitation by cheaters. The problem of cellular cheating in our bodies is the exact same problem that plagues cooperative systems everywhere. Cancer cells consume resources faster than normal cells, divide more quickly than they should, and literally leave a trail of acid in their wake. This is the cellular version of the tragedy of the commons: Our bodies are the commons, and cancer is the tragedy.
Cooperation poses an evolutionary conundrum because individuals can benefit from cheating and taking advantage of others’ altruistic behaviors. If evolution favors those strategies that garner the most benefits, then how could cooperation possibly evolve? Decades of research in evolutionary biology have led to two classic solutions to this problem. One is reciprocity: when cooperators get some future benefit from helping. The other is genetic relatedness: when the cooperative acts benefit kin who share genes coding for that cooperative behavior. In the case of the cellular cooperation going on inside our bodies, it is the genetic relatedness of our cells that made cooperation viable. Cooperation makes evolutionary sense for large multicellular organisms like us because the cells in our bodies are highly related to one another. A cell’s self-sacrifice ultimately benefits those that share its genes.
For example, consider a liver cell working hard to detoxify the wine you had with dinner last night. If you are more likely to survive and reproduce as a result of this effort, the genes coding for hardworking liver cells will get passed along to your offspring. If, on the other hand, your liver cells cheat—by shirking their duties, overconsuming resources, and dividing out of control—the genes coding for that cellular bad behavior won’t get passed to the next generation.
The same is true of the systems for policing cellular cheaters. If you have a well-functioning cheater policing systems (including immune system and cell division controls), you are more likely to survive to reproductive age and pass the genes coding for these systems along to the next generation.
But even the most cooperative bodies cannot completely control and suppress cellular cheating. Our bodies are like a massive public goods game with the highest possible stakes. Cells within us are constantly dividing, growing, using resources, and surviving or dying within us. Every time a cell in your body divides, there is some chance that a mutation will happen in the genes that code for multicellular cooperation. And those mutated cells can cheat in the rules that make multicellularity work: monopolizing resources, proliferating out of turn, and trashing the environment that they share with other cells.
When the cells in our bodies start to cheat in the foundations of multicellular cooperation, this creates an ecological problem within our bodies. Resources (like glucose and oxygen) get depleted, cells get overcrowded, the environment gets trashed by acid and other cellular waste. This is the cellular equivalent of the tragedy of the commons. Our immune systems are constantly policing the body, looking for and eliminating cells that are overconsuming, overproliferating, and generating too much cellular waste. But they can’t stop every wayward cell from exploiting the environment of the body. And if this ecological problem persists, then it can escalate into an evolutionary problem: a tragic game in which cellular cheaters win out in the evolutionary race to proliferate, acquire resources, and survive.
This evolutionary problem is the reason that we get cancer. In fact, we could say that this evolutionary problem is cancer. Once cancer cells gain the abilities to exploit the resources of the body and proliferate without the usual controls, then cellular evolution just happens and doesn’t stop, even though it may be racing toward the ultimate evolutionary dead end: host death. This harkens back to the problem of how cooperation can be viable in the first place. If cheaters can do better than cooperators in a population, they will expand in that population. This is exactly what happens in cancer. Cancer cells outcompete normal cooperative cells, and evolution takes it from there.
As cancer progresses, the evolutionary and ecological dynamics interact, making treatment and clinical management extremely complex and challenging. Take, for example, drug resistance. A tumor is a population of diverse cells living in a very complex ecological environment in our bodies. Some cancer cells live nearer to blood vessels that deliver resources; some cells live in regions with high acidity and cellular waste products. This means that when a drug is administered through the bloodstream, some cells will experience high doses while others get lower doses. And since cancer cells can be highly mutated and the population sizes of even small tumors are huge (in the millions), it is highly likely that somewhere in the tumor there will be at least a few cells that can survive in the presence of the drug. Those cancer cells that do survive will then have an open field upon which to grow back, with little competition from other cancer cells. In ecology, this process is called competitive release.
So every time a tumor is treated with a medication, that drug can become less effective. The mere act of administering the drug actually selects for cells that are resistant to it. One way to get around this problem is to use lower doses of drugs and treat the tumor only when it is growing. This approach, called adaptive therapy, is currently in clinical trials at Moffitt Cancer Center in Tampa, Florida, and early results are promising. (I collaborate with Robert Gatenby at Moffitt on modeling adaptive therapy but am not involved with the clinical trials.)
Metastasis is another problem rooted in ecological and evolutionary dynamics. As cells evolve to monopolize resources and overproliferate, they create a less favorable environment, which then selects for cells that can move and find a new, less exploited environment. Metastasis happens when cells leave the primary site of the tumor and colonize new areas of body, usually in large clumps or colonies of cells. We still don’t quite understand exactly how they do this, but research suggests that the cells in these metastatic colonies might actually be cooperating with one another to better exploit our bodies. Signaling for blood vessels, avoiding the immune system, and detoxification are all complex cellular behaviors that can be better accomplished by groups of cells than by individual cells. To what extent cells in metastatic colonies cooperate is an open question—but it’s perhaps the most exciting one in cancer research right now. If cooperation is required for successful metastasis, it opens up a new opportunity for treatment: targeting and interfering with cancer cells cooperating with one another.
One of the reasons that we get cancer is because our natural cheater detection systems sometimes fail. Our cells have internal checks to make sure they don’t proliferate with mutations, but the genes coding for these internal checks can themselves mutate. Our bodies have other backup systems, including a vast network of immune cells that constantly police for cells that are behaving inappropriately. But the policing that the immune system becomes less effective over time because cancer cells evolve to be able to be better at hiding from immune cells, just like prey evolve to be more successful at evading predators. Restoring the immune system’s ability to detect these cellular cheaters has been an effective approach to treatment. The immunotherapies that block the ability of cancer cells to hide from the immune system (called immune checkpoint blockade therapies) can be very effective in previously intractable forms of cancer, including melanoma and lung cancer.
Cancer is a normal part of being a large and complex multicellular organism. But that does not mean it’s inevitable. Evolutionary and ecological approaches to cancer point to many things we can do to reduce our risk. For example, we can slow down the mutation rates in our bodies by reducing inflammation. (Studies have shown that nonsteroidal anti-inflammatory drugs like Aspirin reduce mutation rates and progression to cancer.) We can also keep the ecological conditions in our body more stable by exercising, eating well, and sleeping well, making it less likely that a boom-and-bust evolutionary process will select for opportunistic cells that rapidly proliferate and consume resources.
But there may be many more opportunities to reduce our cancer risk that researchers haven’t yet considered. As we look to the future of cancer, we should be asking: What we can do to fortify the cooperation our multicellular bodies are built on? How we can support our natural cheater detection systems like our immune system? And can we interfere with cancer cells ability to cooperate with one another to reduce metastasis?
We are all vulnerable to cancer. It appears across the tree of life in almost every multicellular organism that has been studied, from humans to elephants to cacti. We will never be able to completely eliminate it. Susceptibility to cancer is simply the price we pay for being a complex and highly cooperative cellular society. Given how successful multicellular life has been on this planet, it must be an evolutionary price worth paying. But we can work to reduce our vulnerability to cancer by slowing down evolution among our cells, creating a stable ecological environment in our bodies, and supporting the cellular cooperation that defines us.
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THE YEAR AHEAD 2018
The world’s leading thinkers and policymakers examine what’s come apart in the past year, and anticipate what will define the year ahead.