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Las disparidades de salud son las diferencias en la incidencia, la prevalencia, la mortalidad y la carga de una enfermedad y sus efectos adversos en la salud entre grupos específicos de la población. Las disparidades afectan a muchas poblaciones, incluidas las minorías raciales y étnicas, los habitantes de las zonas rurales, mujeres, niños y adolescentes, los ancianos y las personas con discapacidades. Según la Oficina de Salud de las Minorías y Disparidades de Salud, la expectativa de vida y de salud en general de la mayoría de la población estadounidense han mejorado en los últimos años, pero no todos los estadounidenses se han beneficiado por igual. Los CDC y sus socios monitorean las tendencias en la incidencia (diagnósticos) y mortalidad (defunciones) vinculadas al cáncer para identificar qué grupos de la población se ven afectados de manera desproporcionada. Para reducir la desigualdad del cáncer en grupos de mayor riesgo, debemos: mejorar y aumentar la detección temprana del cáncer, promover estilos de vida saludables y ampliar el acceso una mejor atención sanitaria. Tasas de cáncer por raza y grupo étnicoPara todos los tipos de cáncer en los hombres estadounidenses:
Para todos los tipos de cáncer en las mujeres estadounidenses:
*El origen hispano no es mutuamente excluyente de la raza blanca, negra, asiática/nativa de las Islas del Pacífico e indoamericana/nativa de Alaska. Qué están haciendo los CDCInvestigacionesLos investigadores de los CDC han estudiado cuáles son los grupos de personas que no se han beneficiado por igual de las recientes mejoras en la atención de la salud. La División de Prevención y Control del Cáncer de los CDC patrocinó una edición complementaria de la revista American Journal of Public Health sobre las principales causas de muerte en los indoamericanos y nativos de Alaska. Los autores son expertos de muchos campos de especialización diferentes.AMIGAS(http://www.cdc.gov/spanish/cancer/gynecologic/what_cdc_is_doing/amigas.htm)El acrónimo AMIGAS significa ‘Ayudando a las Mujeres con Información, Guía y Amor para su Salud’. AMIGAS es un programa de intervención comunitario educativo y bilingüe, que fue diseñado con el fin de ayudar tanto a las promotoras (las trabajadoras de salud comunitaria) como a otros educadores de salud no profesionales a aumentar las pruebas de detección del cáncer de cuello uterino entre las hispanas que rara vez o nunca se habían hecho una prueba de Papanicoláu. Campaña de los medios de comunicación dirigida a las mujeres afroamericanas(http://www.cdc.gov/spanish/cancer/breast/what_cdc_is_doing/aamm.htm)La campaña utiliza la radio y la prensa escrita para lograr una mayor concientización de las mujeres sobre la importancia de realizarse las mamografías para detectar el cáncer de mama en las etapas iniciales. La campaña también busca aumentar el uso de los servicios de detección del Programa Nacional de Detección Temprana del Cáncer de Mama y de Cuello Uterino en las mujeres afroamericanas de 40 a 64 años de edad. El programa piloto de la campaña se está llevando a cabo en Savannah y Macon, Georgia. Actividades de concientización
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quinta-feira, 23 de abril de 2015
Disparidades de salud vinculadas al cáncer
terça-feira, 14 de abril de 2015
Recruiting the entire immune system to attack cancer
Tue, 04/14/2015 - 11:30am
Anne Trafton, MIT News Office
The human immune system is poised to spring into action at the first sign of a foreign invader, but it often fails to eliminate tumors that arise from the body’s own cells. Cancer biologists hope to harness that untapped power using an approach known as cancer immunotherapy.
Orchestrating a successful immune attack against tumors has proven difficult so far, but a new study from Massachusetts Institute of Technology (MIT) suggests that such therapies could be improved by simultaneously activating both arms of the immune system. Until now, most researchers have focused on one of two strategies: attacking tumors with antibodies, which activate the innate immune system, or stimulating T cells, which form the backbone of the adaptive immune system.
By combining these approaches, the MIT team was able to halt the growth of a very aggressive form of melanoma in mice.
“An anti-tumor antibody can improve adoptive T-cell therapy to a surprising extent,” says Dane Wittrup, the Carbon P. Dubbs Professor in Chemical Engineering at MIT. “These two different parts of the immune therapy are interdependent and synergistic.”
Wittrup, an associate director of MIT’s Koch Institute for Integrative Cancer Research and also a faculty member in the Department of Biological Engineering, is the senior author of a paper describing the work in Cancer Cell. Lead authors are graduate students Eric Zhu and Cary Opel and recent PhD recipient Shuning Gai.
Enlisting the immune system
Antibody drugs for cancer, which include rituximab and Herceptin, are believed to work by binding to cancer proteins and blocking the signals that tell cancer cells to divide uncontrollably. They may also draw the attention of cells belonging to the innate immune system, such as natural killer cells, which can destroy tumor cells.
Adoptive T cell therapy, on the other hand, enlists the body’s T cells to attack tumors. Billions of T cells flow through the average person’s bloodstream at any given time, each specialized to recognize different molecules. However, many tumor proteins do not provoke T cells to attack, so T cells must be removed from the patient and programmed to attack a specific tumor molecule.
Wittrup and his colleagues made the discovery that they could generate both types of immune responses while they were experimenting with improving antibody drug performance with a signaling molecule called IL-2, which helps boost immune responses.
Scientists have tried this strategy before, and about a dozen such therapies have gone through phase I clinical trials. However, most of these efforts failed, even though the antibody-IL-2 combination usually works very well against cancer cells grown in a lab dish.
The MIT team realized that this failure might be caused by the timing of IL-2 delivery. When delivered to cells in a dish, IL-2 sticks around for a long time, amplifying the response of natural killer cells against cancer cells. However, when IL-2 is injected into a patient’s bloodstream, the kidneys filter it out within an hour.
Wittrup and his colleagues overcame this by fusing IL-2 to part of an antibody molecule, which allows it to circulate in the bloodstream for much longer. In tests in mice with a very aggressive form of melanoma, the researchers found they could stop tumor growth by delivering this engineered form of IL-2, along with antibody drugs, once a week.
Immune synergy
To their surprise, the researchers found that T cells were the most important component of the anti-tumor response induced by the antibody-IL-2 combination. They believe that the synergy of IL-2-induced cells and cytokines, and the antibody treatment, creates an environment that lets T cells attack more effectively.
“The antibody-driven innate response creates an environment such that when the T cells come in, they can kill the tumor. In its absence, the tumor cells establish an environment where the T cells don’t work very well,” Wittrup says.
Cells called neutrophils, which are considered the immune system’s “first line of defense” because they react strongly to foreign invaders that enter the skin through a cut or other injury, were also surprisingly important.
“They’re a really powerful force in your immune system, but people in immunotherapy don’t usually focus on neutrophils. They don’t really consider them as a viable tool,” Zhu says. “It pointed us to the idea that although T cells and natural killer cells are important, maybe we’re forgetting about a part of the immune system that is also really important and could help us achieve our goals of ultimately curing the tumors.”
The researchers also found that when they delivered an antibody, IL-2, and T cells targeted to the tumor, the adoptively transferred T cells killed cancer cells much more successfully than when only T cells were delivered. In 80 to 90% of the mice, tumors disappeared completely; even when tumor cells were re-injected into the mice months after the original treatment, their immune systems destroyed the cells, preventing new tumors from forming
In a related paper that appeared recently in the Proceedings of the National Academy of Science, the MIT team also found that delivering IL-2 bound to any kind of antibody, even if the antibody did not target a protein on the tumor cell surface, would halt or slow tumor growth, especially if additional doses of the antibody alone were also given. Graduate student Alice Tzeng was the lead author of that study.
The researchers are now exploring additional proteins that could be added to the IL-2 and antibody combination to make immunotherapy more effective. In the meantime, simply giving patients more prolonged exposure to IL-2 could improve the effectiveness of existing antibody drugs, Wittrup says.
Source: Massachusetts Institute of Technology
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sexta-feira, 20 de fevereiro de 2015
Olive oil ingredient leads cancer cells to their death
| A compound in extra-virgin olive oil has been found to destroy cancer cells without harming healthy cells (Photo: Shutterstock) An ingredient found in extra-virgin olive oil called oleocanthal has been known as a compound capable of killing a variety of human cancer cells, but how this process actually played out was not understood. Now, a team of researchers has uncovered not only how oleocanthal destroys cancer cells, but that it is able to do so while leaving healthy cells unharmed. Paul Breslin, a professor of nutritional sciences at Rutgers University, had thought that oleocanthal killed the cancer cells by targeting a key protein in cancer cells that triggers apoptosis, a process that sees dangerous or damaged cells self-destruct by upsetting the balance of ions in the cell membranes. In investigating this theory, he teamed up with David Foster and Onica LeGendre, two cancer biologists from New York City's Hunter College to more closely examine the process. "We needed to determine if oleocanthal was targeting that protein and causing the cells to die," says Breslin. What first surprised the scientists was how quickly the oleocanthal destroyed the cancer cells. While apoptosis requires between 16 and 24 hours to take effect, the oleocanthal was killing off the cancer cells within 30 minutes to one hour. This led the team to believe that there were some other factors at play. What they discovered was that the oleocanthal was piercing the cancer cell's vesicles, the containers that store the cell's waste. By puncturing these "dumpsters," as Breslin describes them, it creates an outpouring of enzymes that then cause the cell to die. "Once you open one of those things, all hell breaks loose," says Breslin. And when it came to the healthy cells, the researchers found that they remain completely unharmed. While the application of oleocanthal caused a temporary halt in their life cycles, after 24 hours they returned to normal. With the testing thus far carried out in the lab, the researchers say that they will now look to establish the effects of oleocanthal on cancer cells in living animals. The findings were published in the journal Molecular and Cellular Oncology. Source: Rutgers University
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segunda-feira, 2 de fevereiro de 2015
Supercomputing reveals genetic code of cancer
| "This charting may help tailor the treatment to each patient," says Associate Professor Rolf Skotheim, who is affiliated with the Centre for Cancer Biomedicine and the Research Group for Biomedical Informatics at the University of Oslo in Norway, as well as the Department of Molecular Oncology at Radiumhospitalet, Oslo University Hospital. His research group is working to identify the genes that cause bowel and prostate cancer, which are both common diseases. There are 4,000 new cases of bowel cancer in Norway every year. Only six out of ten patients survive the first five years. Prostate cancer affects 5,000 Norwegians every year. Nine out of ten survive. Comparisons between healthy and diseased cells In order to identify the genes that lead to cancer, Skotheim and his research group are comparing the genetic material in tumours with the genetic material in healthy cells. In order to understand this process, a fast introduction to our genetic material is needed. Our genetic material consists of just over 20,000 genes. Each gene consists of thousands of base pairs, represented by a specific sequence of the four building blocks adenine, thymine, guanine, and cytosine, popularly abbreviated to A, T, G, and C. The sequence of these building blocks is the very recipe for the gene. Our whole DNA consists of some six billion base pairs. The DNA strand carries the molecular instructions for activity in the cells. In other words, DNA contains the recipe for proteins, which perform the tasks in the cells. DNA, nevertheless, does not actually produce proteins. First a copy of DNA is made. This transcript is called RNA, and it is this molecule that is read when proteins are produced. RNA is only a small component of DNA, and is made up of its active constituents. Most of DNA is inactive. Only 1-2 % of the DNA strand is active. In cancer cells, something goes wrong with the RNA-transcription. There is either too much RNA, which means that far too many proteins of a specific type are formed, or the composition of base pairs in RNA is wrong. The latter is precisely the area being studied by the UiO researchers. Wrong combinatorics All genes can be divided into active and inactive parts. A single gene may consist of tens of active stretches of nucleotides (exons). "RNA is a copy of a specific combination of the exons from a specific gene in DNA." There are many possible combinations, and it is precisely this search for all of the possible combinations that is new in cancer research. Different cells can combine the nucleotides in a single gene in different ways. A cancer cell can create a combination that should not exist in healthy cells. And as if that didn't make things complicated enough, sometimes RNA can be made up of stretches of nucleotides from different genes in DNA. These special, complex genes are called fusion genes. In other words, researchers must look for errors both inside genes and between the different genes. "Fusion genes are usually found in cancer cells, but some of them are also found in healthy cells." In patients with prostate cancer, researchers have found some fusion genes that are only created in diseased cells. These fusion genes may then be used as a starting-point in the detection of and fight against cancer. The researchers have also found fusion genes in bowel cells, but they were not cancer-specific. "For some reason, these fusion genes can also be found in healthy cells. This discovery was a let-down." Can improve treatment There are different RNA errors in the various cancer diseases. The researchers must therefore analyse the RNA errors of each disease. Among other things, the researchers are comparing RNA in diseased and healthy tissue from 550 patients with prostate cancer. The patients that make up the study do not receive any direct benefits from the results themselves. However, the research is important in order to be able to help future patients. "We want to find the typical defects associated with prostate cancer. This will make it easier to understand what goes wrong with healthy cells, and to understand the mechanisms that develop cancer. Once we have found the cancer-specific molecules, they can be used as biomarkers. In some cases, the biomarkers can be used to find cancer, determine the level of severity of the cancer, the risk of spreading, and whether the patient should be given a more aggressive treatment. Even though the researchers find deviations in the RNA, there is no guarantee that there is appropriate, targeted medicine available. "The point of our research is to figure out more of the big picture. If we identify a fusion gene that is only found in cancer cells, the discovery will be so important in itself that other research groups around the world will want to begin working on this straight away. If a cure is found that counteracts the fusion genes, this may have enormous consequences for the cancer treatment." Laborious work Recreating RNA is laborious work. The set of RNA molecules consists of about 100 million bases, divided into a few thousand bases from each gene. The laboratory machine reads millions of small nucleotides. Each one is only one hundred base pairs long. In order for the researchers to be able to place them in the right location, they must run large statistical analyses. The RNA analysis of a single patient can take a few days. All of the nucleotides must be matched with the DNA strand. Unfortunately the researchers do not have the DNA strands of each patient. In order to learn where the base pairs come from in the DNA strand, they must therefore use the reference genome of the human species. "This is not ideal, because there are individual differences." The future potentially lies in fully sequencing the DNA of each patient when conducting medical experiments. Supercomputing There is no way the research can be carried out using pen and paper. "We need powerful computers to crunch the enormous amounts of raw data. Even if you spent your whole life on this task, you would not be able to find the location of a single nucleotide. This is a matter of millions of nucleotides that must be mapped correctly in the system of coordinates of the genetic material. Once we have managed to find the RNA versions that are only found in cancer cells, we will have made significant progress. However, the work to get that far requires advanced statistical analyses and supercomputing," says Rolf Skotheim to the reserach magazine Apollon. The analyses are so demanding that the researchers must use the University's supercomputer, which was ranked as one of the world's fastest computers a few years ago. It is 10,000 times faster than a regular computer. "With the ability to run heavy analyses on such large amounts of data, we have an enormous advantage not available to other cancer researchers. Many medical researchers would definitely benefit from this possibility. This is why they should spend more time with biostatisticians and informaticians. RNA samples are taken from the patients only once. The types of analyses that can be run are only limited by the imagination." "We need to be smart in order to analyse the raw data. There are enormous amounts of data here that can be interpreted in many different ways. We have just got started. There is lots of useful information that we have not seen yet. Asking the right questions is the key. Most cancer researchers are not used to working with enormous amounts of data, and how to best analyse vast data sets. Once researchers have found a possible answer, they must determine whether the answer is chance or if it is a real finding. The solution is to find out whether they get the same answers from independent data sets from other parts of the world." |
terça-feira, 21 de outubro de 2014
Digest this: Cure for cancer may live in our intestines
The discovery of Robo1 protein in the intestinal stem cells (depicted in yellow) leads to tolerance of higher doses of chemoradiation for cancer patients.
Treating a cancerous tumor is like watering a houseplant with a fire hose -- too much water kills the plant, just as too much chemotherapy and radiation kills the patient before it kills the tumor.
However, if the patient's gastrointestinal tract remains healthy and functioning, the patient's chances of survival increase exponentially, said Jian-Guo Geng, associate professor at the University of Michigan School of Dentistry. Recently, Geng's lab discovered a biological mechanism that preserves the gastrointestinal tracts in mice who were delivered lethal doses of chemotherapy.
The findings, which will appear in the journal Nature, could revolutionize cancer therapy, Geng said.
"It's our belief that this could eventually cure later-staged metastasized cancer. People will not die from cancer, if our prediction is true," said Geng, who emphasized that the findings had not yet been proven in humans. "All tumors from different tissues and organs can be killed by high doses of chemotherapy and radiation, but the current challenge for treating the later-staged metastasized cancer is that you actually kill the patient before you kill the tumor.
"Now you have a way to make a patient tolerate to lethal doses of chemotherapy and radiotherapy. In this way, the later-staged, metastasized cancer can be eradicated by increased doses of chemotherapy and radiation."
Geng's lab found that when certain proteins bind with a specific molecule on intestinal stem cells, it revs intestinal stem cells into overdrive for intestinal regeneration and repair. Stem cells naturally heal damaged organs and tissues, but so-called "normal" amounts of stem cells in the intestine simply cannot keep up with the wreckage left behind by the lethal doses of chemotherapy and radiation required to successfully treat late-stage tumors.
However, the phalanx of extra stem cells protect the intestine and gastrointestinal tract, which means the patient can ingest nutrients, the body can perform other critical functions and the bacterial toxins in the intestine are prevented from entering the blood circulation, Geng said.
These factors could give the patient just enough of an extra edge to survive the stronger doses of chemotherapy and radiation, until the tumor or tumors are eradicated.
In the study, 50-to-75 percent of the mice treated with the molecule survived otherwise lethal doses of chemotherapy. All of the mice that did not receive the molecule died, Geng said.
"If you can keep the gut going, you can keep the patient going longer," Geng said. "Now we have found a way to protect the intestine. The next step is to aim for a 100-percent survival rate in mice who are injected with the molecules and receive lethal doses of chemotherapy and radiation."
Geng's lab has worked with these molecules, called R-spondin1 and Slit2, for more than a decade. These molecules repair tissue in combination with intestinal stem cells residing in the adult intestine.
Story Source:
The above story is based on materials provided by University of Michigan. Note: Materials may be edited for content and length.
Journal Reference:
- Wei-Jie Zhou, Zhen H. Geng, Jason R. Spence & Jian-Guo Geng. Induction of intestinal stem cells by R-spondin 1 and Slit2 augments chemoradioprotection. Nature, 2013 DOI: 10.1038/nature12416
sexta-feira, 17 de outubro de 2014
Modeling tumor dormancy: What makes a tumor switch from dormant to malignant?
Here are snapshots of a simulated noninvasive tumor growing in the extracellular matrix.
Cancer constantly wages war on the human body. Battles are won, lost or sometimes end in a stalemate. In pancreatic cancer, this stalemate -- known as tumor dormancy -- can last up to 25 years before becoming aggressively malignant, a phenomena that is poorly understood.
A new computational model developed in the laboratory of Salvatore Torquato, a Professor of Chemistry at Princeton University, may help illuminate the conditions surrounding tumor dormancy and the switch to a malignant state. Published today in PLOS ONE, the so-called cellular automaton model simulated various scenarios of tumor growth leading to tumor suppression, dormancy or proliferation.
"The power of the model is that it lets people to test medically realistic scenarios," Torquato said. In future collaborations, these scenarios could be engineered in laboratory experiments and the observed outcomes could be used to calibrate the model.
For each scenario, a set of rules is imposed on the virtual cell population. Rules are possible interactions, such as neighboring cell death or immune system suppression, that dictate cell division through probabilities derived from past experimental data. Once the researchers programmed the rules, they watched as the simulated competition unfolded between the tumor and the environmental factors that may suppress its growth.
"We were very surprised to observe this phenomena where the tumor all of a sudden began to rapidly divide," said Duyu Chen, graduate student in the Torquato lab and lead author on the article. This was the first time that the emergent switch behavior, which has been observed clinically, occurred spontaneously in a model, Chen said.
The researchers evaluated a number of factors that could affect tumor cell growth including phenotypic changes, mechanical properties and the rate and strength of suppression factors such as the immune system. One of the model's findings was the likely suppression of tumors in harsh environments, characterized by high density and pressure.
The research team also predicted that if the number of actively dividing cells within the proliferative rim reached a certain critical level, the tumor was very likely to begin rapidly growing. This result could provide insight into early cancer treatment, Chen said.
Story Source:
The above story is based on materials provided by Princeton University. Note: Materials may be edited for content and length.
Journal Reference:
- Chen, Yang Jiao, Salvatore Torquato. A Cellular Automaton Model for Tumor Dormancy: Emergence of a Proliferative Switch Duyu. PLOS ONE, October 2014 DOI: 10.1371/journal.pone.0109934
quarta-feira, 8 de outubro de 2014
'Cyberwar' against cancer gets a boost from intelligent nanocarriers
Two years ago, Prof. Eshel Ben-Jacob of Tel Aviv University's School of Physics and Astronomy and Rice University's Center for Theoretical Biological Physics made the startling discovery that cancer, like an enemy hacker in cyberspace, targets the body's communication network to inflict widespread damage on the entire system. Cancer, he found, possessed special traits for cooperative behavior and used intricate communication to distribute tasks, share resources, and make decisions.
In research published in the Early Edition of the Proceedings of the National Academy of Sciences, Prof. Ben-Jacob and researchers from Rice University and the University of Texas M.D. Anderson Cancer Center, the leading cancer treatment center in the U.S., offer new insight into the lethal interaction between cancer cells and the immune system's communications network. Prof. Ben-Jacob and the study co-authors developed a computer program that models a specific channel of cell-to-cell communication involving exosomes (nanocarriers with crucial cellular "intelligence") that both cancer and immune cells harness to communicate with other cells.
"Recent research has found that cancer is already adept at using a kind of 'cyberwarfare' against the immune system. We studied the interplay between cancer and the immune system to see how we might be able to shift the balance against cancer," said Prof. Ben-Jacob, noting a difference between the innate and the adaptive qualities of the immune system. "In the beginning, cancer is inhibited by the body's innate immunity. But once cancer escapes the immunity, there is a race between the progression of cancer and the ability of the adaptive immune system to recognize and act against it."
Cyberwarfare of the body
"What we are dealing with is cyberwarfare, pure and simple. Cancer uses the immune systems' own communications network to attack not the soldiers but the generals that are coordinating the body's defense," said Prof. Ben-Jacob.
To better understand the role of exosome-mediated cell-to-cell communication in the battle between cancer and the immune system, the researchers created a computer model that captured the exosomal exchange between cancer cells, dendritic cells, and the other cells in the immune system.
The new model is based on earlier research, which showed that dendritic cells, mediators between the body's innate and adaptive immune systems (the former protects against all threats at all times and the latter guards more efficiently against specific, established dangers), employed exosomes to fulfil their task. The researchers discovered that, overtaken by cancer, these nanocarriers, which contain such vital components as signaling proteins, RNA snippets, and microRNAs, can command cells to change their tasks, placing the entire system at risk.
Finding a better balance between the strong and the weak
According to the new research, three possible cancer states can exist: strong, intermediary, and weak. The intermediary state -- in which cancer is neither strong nor weak and in which the immune system is on high alert -- could be the key to a new therapeutic approach with reduced side effects. Prof. Ben-Jacob believes it is possible to force cancer from a strong to moderate state, and then from a moderate to weak state, by alternating cycles of radiation or chemotherapy with immune-boosting treatments.
"Our first important discovery is that this situation is due to the exosome-based cyberwar between cancer and the immune system," said Prof. Ben-Jacob. "Without exosomes, the two possible states are only strong-weak and weak-strong. With exosomes, an intermediary state opens a new way to treat cancer using very a different approach."
Prof. Ben-Jacob likened the exchange to a tug-of-war between cancer and the immune system. "The challenge is to be familiar with the battlefield so that we can manipulate cancer therapies to change the balance in favor of the immune system. When cancer is detected, it is almost always in the context of a cancer-immunity competition," said Prof. Ben-Jacob. "We showed that the way to stop and reverse tumor progression without causing strong side effects is an individualized approach of mixed treatments -- i.e., four days of radiation followed by a few days of immune system boosting, followed again by four days of radiation, and so on. If provided in the right order, the treatments could indeed shift the balance toward the immune system's 'victory' in reducing the cancer to the moderate-strong state."
Story Source:
The above story is based on materials provided by American Friends of Tel Aviv University. Note: Materials may be edited for content and length.
Journal Reference:
- B. A. Camley, Y. Zhang, Y. Zhao, B. Li, E. Ben-Jacob, H. Levine, W.-J. Rappel. Polarity mechanisms such as contact inhibition of locomotion regulate persistent rotational motion of mammalian cells on micropatterns. Proceedings of the National Academy of Sciences, 2014; DOI: 10.1073/pnas.1414498111
segunda-feira, 6 de outubro de 2014
Seis em cada dez homens com câncer têm mais de 60 anos
Idosos são 50% dos atendidos no Instituto do Câncer de SP; doença ocupa 2º lugar como causa de morte nessa faixa etária
DO IG SAÚDE
No Dia Mundial do Idoso, pesquisa inédita realizada pelo Instituto do Câncer do Estado de São Paulo (Icesp), ligado a Secretaria de Estado da Saúde e à Faculdade de Medicina da USP, maior centro de oncologia da América Latina aponta que os idosos representam 50% dos pacientes em tratamento na unidade.
Os homens são maioria, 61% no total, e entre os tipos de tumores mais comuns nesta faixa etária estão os dos órgãos genitais (próstata, pênis e testículos), órgãos digestivos (estômago, esôfago, intestino, cólon e reto) e aparelho respiratório.
Cenário: 'O Brasil está às vésperas de uma epidemia de câncer'
Já entre as mulheres – 39% no total –, o câncer nos órgãos digestivos vem na frente, seguido de tumores na mama e nos órgãos genitais. O levantamento ainda mostra que os pacientes com mais de 60 anos respondem por 54% das cirurgias.
“A parcela da população brasileira que mais cresce é a de idosos e o câncer já ocupa o segundo lugar como causa de morte entre essa faixa etária. É de extrema importância, portanto, estarmos preparados para oferecer um acompanhamento geriátrico completo, que, aliado as novas técnicas cirúrgicas e as drogas modernas, proporcione mais possibilidades de tratamento e, principalmente, qualidade de vida aos pacientes maduros”, destaca o oncologista Paulo Hoff, diretor geral do Icesp.
Muitas pessoas ainda acreditam que o principal fator para o surgimento do câncer é o genético, mas apenas 10% dos tumores têm esta correlação. Por isso é fundamental que homens e mulheres acima dos 50 anos realizem, anualmente, check-up para detectar o câncer no início, como o exame físico da próstata (toque retal), a mamografia e o papanicolau, por exemplo.
Veja alimentos que ajudam na prevenção do câncer:
Abacate: rico em ácidos-graxos poli-insaturados e em vitaminas do grupo B, essenciais no combate ao câncer .
Além disso, existem outros cuidados importantes que valem ser seguidos por toda a população. Manter uma dieta equilibrada, evitando o consumo excessivo de carnes vermelhas e bebidas alcoólicas, não fumar e praticar exercícios físicos – pelo menos 30 minutos diários – são atitudes que ajudam no combate a doença.
Exposição
Para homenagear os idosos, o Instituto promove durante todo o mês de outubro a exposição “Retratos da Maturidade”. Quem passar pelo hall de entrada vai se deparar com uma seleção de 25 fotos de pacientes e familiares, registradas em diversos locais e situações distintas. “Nós percebemos que os idosos costumam lidar melhor com o diagnóstico de câncer, uma vez que a maturidade traz mudanças positivas como o alinhamento de expectativas e prioridades, além de maior controle emocional. As imagens selecionadas para a exposição conseguem, justamente, demonstrar esses sentimentos”, explica a coordenadora de humanização Maria Helena Sponton.
quinta-feira, 28 de agosto de 2014
Three-quarters of depressed cancer patients do not receive treatment for depression; new approach could transform care.
Major depression in cancer patients
Three papers reveal that around three-quarters of cancer patients who have major depression are not currently receiving treatment for depression, and that a new integrated treatment program is strikingly more effective at reducing depression and improving quality of life than current care.
quarta-feira, 18 de junho de 2014
Nanoshell shields foreign enzymes used to starve cancer cells from immune system
June 17, 2014
A nanoshell to protect foreign enzymes used to starve cancer cells as part of chemotherapy has been developed by nanoengineers. Enzymes are naturally smart machines that are responsible for many complex functions and chemical reactions in biology. However, despite their huge potential, their use in medicine has been limited by the immune system, which is designed to attack foreign intruders.
The shell’s pores are too small for the enzyme to escape but big enough for diffusion of amino acids that feed cancer cells in and out of the particle. The enzymes remain trapped inside where they deplete any amino acids that enter.
A nanoshell to protect foreign enzymes was used to starve cancer cells as part of chemotherapy.
Enzymes are naturally smart machines that are responsible for many complex functions and chemical reactions in biology. However, despite their huge potential, their use in medicine has been limited by the immune system, which is designed to attack foreign intruders. For example, doctors have long relied on an enzyme called asparaginase to starve cancer cells as a patient undergoes chemotherapy. But because asparaginase is derived from a nonhuman organism, E. Coli, it is quickly neutralized by the patient's immune system and sometimes produces an allergic reaction. In animal studies with asparaginase, and other therapeutic enzymes, the study found that their porous hollow nanoshell effectively shielded enzymes from the immune system, giving them time to work.
Asparaginase works by reacting with amino acids that are an essential nutrient for cancer cells. The reaction depletes the amino acid, depriving the abnormal cells from the nutrients they need to proliferate.
It’s is a pure engineering solution to a medical problem.
The nanoshell acts like a filter in the bloodstream. The enzymes are loaded into the nanoparticle very efficiently through pores on its surface and later encapsulated with a shell of nanoporous silica. The shell's pores are too small for the enzyme to escape but big enough for diffusion of amino acids that feed cancer cells in and out of the particle. The enzymes remain trapped inside where they deplete any amino acids that enter.
This is a platform technology that may find applications in many different fields. The starting point was solving a problem for cancer therapeutics.
domingo, 1 de junho de 2014
One step closer to a breath test for lung cancer
May 31, 2014
University of Colorado Cancer Center
A test of organic compounds in exhaled breath can not only distinguish patients with lung cancer from patients with chronic obstructive pulmonary disease (COPD), but can also define the stage of any cancer present, new research shows. The device requires blowing up a balloon, which is then attached to an extremely sensitive gold nanoparticle sensor. The particles in the sensor trap and then help to analyze volatile organic compounds in the exhaled breath.
Results of a University of Colorado Cancer Center study presented at the 50th Annual Meeting of the American Society for Clinical Oncology (ASCO) show that a test of organic compounds in exhaled breath can not only distinguish patients with lung cancer from patients with chronic obstructive pulmonary disease (COPD), but can also define the stage of any cancer present.
"This could totally revolutionize lung cancer screening and diagnosis. The perspective here is the development of a non-traumatic, easy, cheap approach to early detection and differentiation of lung cancer," says Fred R. Hirsch, MD, PhD, investigator at the CU Cancer Center and professor of medical oncology at the University of Colorado School of Medicine.
The device requires blowing up a balloon, which is then attached to an extremely sensitive gold nanoparticle sensor. The particles in the sensor trap and then help to analyze volatile organic compounds in the exhaled breath. (A USB device has recently been developed, which can be plugged into a computer for rapid analysis).
"The metabolism of lung cancer patients is different than the metabolism of healthy people," Hirsch says, and it is these differences in metabolism that can define the signatures of healthy breath, COPD or lung cancer.
Hirsch points out the need for new lung cancer screening and diagnosis tools in the context of recent lung cancer screening guidelines by the U.S. Preventative Task Force showing that screening via low-dose computed tomography can reduce disease mortality by 20 percent. However, along with more sensitive screening comes a much higher incidence of false positives, primarily in the form of non-cancerous lung nodules.
"You detect many, many nodules in those screenings and unfortunately, around 90 percent of them are benign. So you need to find out how to better distinguish malignant from benign modules. The goal of this tool is to use breath biomarkers to distinguish malignant from benign screen-detected nodules," Hirsch says.
The developing device represents a collaboration between the University of Colorado Cancer Center and researchers from the Nobel-Prize-winning institution Technion University in Haifa, Israel.
The device's potential uses go beyond diagnosis.
"In addition to using levels of volatile organic compounds to diagnose lung cancer, we could eventually measure the change in patients' levels of VOCs across time with the intent of, for example, monitoring how well a patient responds to specific treatments," Hirsch says.
A breath now and a breath after treatment could define whether a patient should stay with a drug regimen or explore other options. In fact, a study with this goal was recently initiated at the University of Colorado Cancer Center.
Additionally, Hirsch points out that next generations of the device could potentially help doctors quickly, simply, and inexpensively define patients' lung cancer subtypes, allowing doctors to pair molecularly targeted therapies with subtypes early in the treatment process.
"If it works, you can imagine standing in the grocery store and having high risk people blow into a balloon or a USB device, and the profile of the organic compounds in their breath would tell you if they are at risk for developing or having lung cancer, which then could lead to further, focused tests," Hirsch says.
Story Source:
The above story is based on materials provided by University of Colorado Cancer Center. The original article was written by Garth Sundem. Note: Materials may be edited for content and length.
terça-feira, 27 de maio de 2014
An area's level of poverty or wealth may affect the distribution of cancer types
A new analysis has found that certain cancers are more concentrated in areas with high poverty, while other cancers arise more often in wealthy regions. Also, areas with higher poverty had lower cancer incidence and higher mortality than areas with lower poverty. Published early online in Cancer, a peer-reviewed journal of the American Cancer Society, the study's findings demonstrate the importance of including measures of socioeconomic status in national cancer surveillance efforts.
Overall, socioeconomic status is not related to cancer risk -- cancer strikes the rich and poor alike. However, socioeconomic status does seem to influence the type of cancer a person may develop. To look closely at the issue, Francis Boscoe, PhD, of the New York State Cancer Registry and his colleagues compared people living in areas with the highest poverty with those living in areas with the lowest poverty. The investigators assigned nearly three million tumors diagnosed between 2005 and 2009 from 16 states plus Los Angeles (an area covering 42 percent of the US population) into one of four groupings based on the poverty rate of the residential census tract at time of diagnosis.
For all cancer types combined, there was a negligible association between cancer incidence and poverty; however, 32 of 39 cancer types showed a significant association with poverty (14 positively associated and 18 negatively associated). Certain cancers -- Kaposi sarcoma and cancers of the larynx, cervix, penis, and liver -- were more likely in the poorest neighborhoods, while other cancers -- melanoma, thyroid, other non-epithelial skin, and testis -- were more likely in the wealthiest neighborhoods. "At first glance, the effects seem to cancel one another out. But the cancers more associated with poverty have lower incidence and higher mortality, and those associated with wealth have higher incidence and lower mortality," explained Dr. Boscoe. "When it comes to cancer, the poor are more likely to die of the disease while the affluent are more likely to die with the disease."
Dr. Boscoe noted that recent gains in technology have made it much easier to link patient addresses with neighborhood characteristics, therefore making it possible to incorporate socioeconomic status into cancer surveillance. "Our hope is that our paper will illustrate the value and necessity of doing this routinely in the future," he said.
Story Source:
The above story is based on materials provided by Wiley. Note: Materials may be edited for content and length.
Journal Reference:
- Francis P. Boscoe, Christopher J. Johnson, Recinda L. Sherman, David G. Stinchcomb, Ge Lin, Kevin A. Henry. The relationship between area poverty rate and site-specific cancer incidence in the United States. Cancer, 2014; DOI: 10.1002/cncr.28632
Refugees struggling to access cancer treatment, experts warn
May 25 / 2014
The Lancet
There is a high demand for costly cancer treatment among refugees from the recent conflicts in Iraq and Syria, with host countries struggling to find the money and the medicine to treat their new patients, new research concludes. The findings have prompted calls from the United Nations High Commissioner for Refugees (UNHCR) Chief Medical Expert, for innovative financing schemes to improve access to affordable high-quality cancer care for refugees.
A study published in The Lancet Oncology journal reveals a high demand for costly cancer treatment among refugees from the recent conflicts in Iraq and Syria, with host countries struggling to find the money and the medicine to treat their new patients. The findings have prompted calls from lead author Dr Paul Spiegel, the United Nations High Commissioner for Refugees (UNHCR) Chief Medical Expert, for innovative financing schemes to improve access to affordable high-quality cancer care for refugees.
In the first study of its kind, Spiegel and colleagues examined data from funding applications made to the UNHCR Exceptional Care Committee (ECC) from refugees in Jordan and Syria whose cancer treatment costs were likely to exceed US$2000 a year.
The findings show that cancer is an important public health problem in refugee settings and highlight the huge challenges and immense costs that national health systems and humanitarian organizations face when overwhelmed by massive influxes of refugees.
For example, in Jordan the ECC assessed 1989 applications for treatment between 2010 and 2012, of which roughly a quarter (511) were for cancer -- breast cancer and colorectal cancer being the most common. Around half (48%) of these cases were approved and funded. The main reasons for denied funding were a poor prognosis (43% of cases in 2011 and 31% in 2012) or that the treatment was too costly (25% in 2011). The average amount requested from the ECC for cancer treatment was US$11 540 in 2011 and US$5151 in 2012; however, the amounts approved were substantially lower -- US$4626 in 2011 and US$3501 in 2012.
"The countries in the Middle East have welcomed millions of refugees, first from Iraq and then Syria. This massive influx has strained health systems at all levels. Despite help from international organizations and donors to expand health facilities and pay for additional personnel and drugs, it has been insufficient. The burden has fallen disproportionately on the host countries to absorb the costs. For example, the Jordanian Ministry of Health footed an estimated $53 million bill for medical care for refugees in the first four months of 2013," says Dr Spiegel.
The authors call for improved cancer prevention and treatment in refugee settings through the use of innovative financing schemes, better primary care including screening for common cancers (eg, colonoscopies and mammograms), and the development of electronic web-based cancer registries to prevent interruption of treatment.
According to Dr Spiegel, "Until now, the response to humanitarian crises have been primarily based on experiences from refugee camps in sub-Saharan Africa where infectious diseases and malnutrition have been the priority. In the 21st century, refugee situations are substantially longer and increasingly occur in middle-income countries where the levels of chronic diseases, including cancer, are higher. Cancer diagnosis and care in humanitarian emergencies typifies a growing trend towards more costly chronic disease care, something that seems to have been overlooked, but is of increasing importance because the number of refugees is growing."
Story Source:
The above story is based on materials provided by The Lancet. Note: Materials may be edited for content and length.
Journal Reference:
- Paul Spiegel, Adam Khalifa, Farrah J Mateen. Cancer in refugees in Jordan and Syria between 2009 and 2012: challenges and the way forward in humanitarian emergencies. The Lancet Oncology, 2014; 15 (7): e290 DOI: 10.1016/S1470-2045(14)70067-1
How signals trigger cancer cells to spread
This electron micrograph shows a cancer cell (upper darker area) that has formed three invadopodia that are penetrating the adjacent extracellular matrix (lower lighter area).
Researchers at Albert Einstein College of Medicine of Yeshiva University have discovered a signaling pathway in cancer cells that controls their ability to invade nearby tissues in a finely orchestrated manner. The findings offer insights into the early molecular events involved in metastasis, the deadly spread of cancer cells from primary tumor to other parts of the body. The study was published today in the online edition of Nature Cell Biology.
To migrate from a primary tumor, a cancer cell must first break through surrounding connective tissue known as the extracellular matrix (ECM). The cancer cell does so by forming short-lived invadopodia--foot-like protrusions these cells use to invade. Invadopodia release enzymes that degrade the ECM, while other protrusions pull the cancer cell along, much like a locomotive pulls a train. The invading cancer cell relies on the cycle of invadopodium formation/disappearance to successfully travel from the tumor and enter nearby blood vessels to be carried to distant parts of the body.
"We've known for some time that invadopodia are driven by protein filaments called actin," said study leader Louis Hodgson, Ph.D., assistant professor of anatomy and structural biology at Einstein. "But exactly what was regulating the actin in invadopodia was not clear."
Previous studies had suggested that a protein called Rac1 played a role in cancer-cell invasion. When Rac1 levels are elevated, cancer cells display more invasive characteristics. But this suspected Rac1 activity in invadopodia had never been directly observed, only indirectly inferred.
To surmount this hurdle, Dr. Hodgson and his colleagues in the Gruss Lipper Biophotonics Center at Einstein devised a new fluorescent protein biosensor that, combined with live-cell imaging, revealed exactly when and where Rac1 is activated inside cancer cells.
Using this biosensor in highly invasive breast cancer cells taken from rodents and humans, the Einstein team discovered that when an individual invadopodium forms and is actively degrading the ECM, its Rac1 levels are low; on the other hand, elevated Rac1 levels coincide with the invadopodium's disappearance. "So high levels of Rac1 induce the disappearance of ECM-degrading invadopodia, while low levels allow them to stay -- which is the complete opposite of what Rac1 was thought to be doing in invadopodia," said Dr. Hodgson.
To confirm this observation, the researchers used siRNAs (molecules that silence gene expression) to turn off the RAC1 gene, which synthesizes Rac1 protein. When the gene was silenced, ECM degradation increased. Conversely, when Rac1 activity was enhanced -- using light to activate a form of the Rac1 protein -- the invadopodia disappeared.
In subsequent experiments, the Einstein team deciphered other parts of the Rac1 signaling cascade during invasion and showed that this signaling mechanism is regulated differently in normal breast epithelial cells.
"Rac1 levels in invadopodia of invasive tumor cells appear to surge and ebb at precisely timed intervals in order to maximize the cells' invasive capabilities," said Dr. Hodgson.
Most of the 580,000 U.S. cancer deaths each year are caused by complications from the spread of cancer to distant tissues and organs, rather than from the primary tumor itself. So throwing a monkey wrench into the inner workings of invasive tumor cells -- perhaps with a drug that prevents them from locally activating or inhibiting Rac1 -- could be extremely useful.
"Rac1 inhibitors have been developed," Dr. Hodgson said, "but it wouldn't be safe to use them indiscriminately. Rac1 is an important molecule in healthy cells, including immune cells. So we'd need to find a way to shut off this signaling pathway specifically in cancer cells."
Story Source:
The above story is based on materials provided by Albert Einstein College of Medicine of Yeshiva University. Note: Materials may be edited for content and length.
Journal Reference:
- Yasmin Moshfegh, Jose Javier Bravo-Cordero, Veronika Miskolci, John Condeelis, Louis Hodgson. A Trio–Rac1–Pak1 signalling axis drives invadopodia disassembly. Nature Cell Biology, 2014; DOI: 10.1038/ncb2972
Fighting cancer with dietary changes
May 26 / 2014
Thomas Jefferson University
Calorie restriction during treatment for breast cancer changes cellular programming in a way that lowers the chance of metastases in mice. Breast cancer patients are often treated with hormonal therapy to block tumor growth, and steroids to counteract the side effects of chemotherapy. However, both treatments can cause a patient to have altered metabolism which can lead to weight gain. In fact, women gain an average of 10 pounds in their first year of treatment. Recent studies have shown that too much weight makes standard treatments for breast cancer less effective, and those who gain weight during treatment have worse cancer outcomes.
Calorie restriction, a kind of dieting in which food intake is decreased by a certain percentage, has been touted as way to help people live longer. New research suggests that there may be other benefits, including improving outcomes for women in breast cancer. According to a study published May 26th in Breast Cancer Research and Treatment, the triple negative subtype of breast cancer -- one of the most aggressive forms -- is less likely to spread, or metastasize, to new sites in the body when mice were fed a restricted diet.
"The diet turned on a epigenetic program that protected mice from metastatic disease," says senior author Nicole Simone, M.D., an associate professor in the department of Radiation Oncology at Thomas Jefferson University. Indeed, when mouse models of triple negative cancer were fed 30 percent less than what they ate when given free access to food, the cancer cells decreased their production of microRNAs 17 and 20 (miR 17/20). Researchers have found that this group of miRs is often increased in triple negative cancers that metastasize.
Breast cancer patients are often treated with hormonal therapy to block tumor growth, and steroids to counteract the side effects of chemotherapy. However, both treatments can cause a patient to have altered metabolism which can lead to weight gain. In fact, women gain an average of 10 pounds in their first year of treatment. Recent studies have shown that too much weight makes standard treatments for breast cancer less effective, and those who gain weight during treatment have worse cancer outcomes. "That's why it's important to look at metabolism when treating women with cancer," says Dr. Simone.
In earlier studies, Dr. Simone and colleagues had shown that calorie restriction boosted the tumor-killing effects of radiation therapy. This study aimed to examine which molecular pathways were involved in this cooperative effect.
The investigators noticed that microRNAs -- a type of RNA that regulates other genes in the cell -- specifically miR 17 and 20, decreased the most when mice were treated with both radiation and calorie restriction. This decrease in turn increased the production of proteins involved in maintaining the extracellular matrix. "Calorie restriction promotes epigenetic changes in the breast tissue that keep the extracellular matrix strong," says Dr. Simone. "A strong matrix creates a sort of cage around the tumor, making it more difficult for cancer cells to escape and spread to new sites in the body."
Understanding the link to miR 17 also gives researchers a molecular target for diagnosing cancers that are more likely to metastasize and, potentially, for developing a new drug to treat the cancers. In theory, a drug that decreased miR 17 could have the same effect on the extracellular matrix as calorie restriction. However, targeting a single molecular pathway, such as the miR17 is unlikely to be as effective as calorie restriction, says Dr. Simone. Triple negative breast cancers tend to be quite different genetically from patient to patient. If calorie restriction is as effective in women as it is in animal models, then it would likely change the expression patterns of a large set of genes, hitting multiple targets at once without toxicity.
In order to test that this hypothesis is true in humans, Dr. Simone is currently enrolling patients in the CaReFOR (Calorie Restriction for Oncology Research) trial. As the first trial like it in the country, women undergoing radiation therapy for breast cancer receive nutritional counseling and are guided through their weight loss plan as they undergo their treatment for breast cancer.
Story Source:
The above story is based on materials provided by Thomas Jefferson University. Note: Materials may be edited for content and length.
Journal Reference:
- Lianjin Jin, Meng Lim, Shuping Zhao, Yuri Sano, Brittany A. Simone, Jason E. Savage, Eric Wickstrom, Kevin Camphausen, Richard G. Pestell, Nicole L. Simone. The metastatic potential of triple-negative breast cancer is decreased via caloric restriction-mediated reduction of the miR-17~92 cluster. Breast Cancer Research and Treatment, 2014; DOI: 10.1007/s10549-014-2978-7
sábado, 24 de maio de 2014
Cancer avatars for personalized medicine help researchers find genomic signatures of cancers
Researchers at University of California, San Diego School of Medicine and Moores Cancer Center have used computer simulations of cancer cells -- cancer avatars -- to identify drugs most likely to kill cancer cells isolated from patients' brain tumors.
The findings, published in May 21 online issue of the Journal of Translational Medicine, may help researchers stratify cancer patients for clinical trials according to their cancers' genomic signatures and predicted sensitivities to different cancer drugs.
Such an approach would allow scientists to selectively test cancer drugs on those who would be most likely to respond to them, while simultaneously reducing patients' exposures to toxic drugs that would likely be ineffective.
"Genomics tells us that cancers are a lot like snowflakes. No two cancers are alike so it does not make sense to give all patients the same drugs. This is the idea behind personalizing therapies for cancer," said lead author Sandeep Pingle, MD, PhD, a project scientist in the laboratory of Santosh Kesari, MD, PhD, chief of the division of Neuro-Oncology, professor in the department of neurosciences, director of Neuro-Oncology at UC San Diego Moores Cancer Center and the study's senior author.
"With the virtual cell model, we can take into account all the complexity of cellular processes to predict which drugs will be the most effective against a particular tumor based on its genomic profile," Pingle said. "This is a first step toward personalized medicine."
Researchers developed a virtual cell that represents the internal workings of a normal, healthy cell, depicting them as a complex collection of signaling pathways and metabolic networks. The virtual healthy cell can be made cancerous. Indeed, it can be turned into any kind of cancer cell by distorting specific points and pathways in the system. These cellular distortions represent a person's so-called cancer avatar. Once the avatar is generated, a computer model predicts which drugs, based upon their known functions, are most likely to kill a real cancer cell.
For the study, researchers generated cancer avatars for cells obtained from patients with glioblastoma, a highly aggressive cancer of the brain's glial cells. The condition has a five-year survival rate of about 10 percent. The computer generated predictions were then "truth-checked" against standard, cultured cells in drug-sensitivity experiments.
"The advantage of computational modeling is the ability to incorporate the wealth of genomic and proteomic information on cancer cells and to screen drugs and combinations of drugs much faster and cost effectively," said Kesari. "Our ultimate goal is to take this technology to the clinic to identify the best drugs for treating each individual cancer patient."
Story Source:
The above story is based on materials provided by University of California, San Diego Health Sciences. Note: Materials may be edited for content and length.
Journal Reference:
- Sandeep C Pingle, Zeba Sultana, Sandra Pastorino, Pengfei Jiang, Rajesh Mukthavaram, Ying Chao, Ila Bharati, Natsuko Nomura, Milan Makale, Taher Abbasi, Shweta Kapoor, Ansu Kumar, Shahabuddin Usmani, Ashish Agrawal, Shireen Vali, Santosh Kesari. In silico modeling predicts drug sensitivity of patient-derived cancer cells. Journal of Translational Medicine, 2014; 12 (1): 128 DOI: 10.1186/1479-5876-12-128
sexta-feira, 23 de maio de 2014
Going beyond the surface: New tech could take light-based cancer treatment deep inside the body
May 15 / 2014
University at Buffalo
Photodynamic therapy (PDT) is an effective treatment for easily accessible tumors such as oral and skin cancer. But the procedure, which uses lasers to activate special drugs called photosensitizing agents, isn't adept at fighting cancer deep inside the body. Thankfully, that's changing due to new technology that could bring PDT into areas of the body which were previously inaccessible. The new tech involves using near-infrared beams of light that, upon penetrating deep into the body, are converted into visible light that activates the drug and destroys the tumor.
The laser irradiated area (the white square) shows live cancer cells (green) as well as dead cancer cells (red) as a result of the irradiation.
Photodynamic therapy (PDT) is an effective treatment for easily accessible tumors such as oral and skin cancer.
But the procedure, which uses lasers to activate special drugs called photosensitizing agents, isn't adept at fighting cancer deep inside the body. Thankfully, that's changing due to new technology that could bring PDT into areas of the body which were previously inaccessible.
Described May 11 in the journal Nature Photonics, the approach involves using near-infrared beams of light that, upon penetrating deep into the body, are converted into visible light that activates the drug and destroys the tumor.
"We expect this will vastly expand the applications for an effective cancer phototherapy that's already in use," said co-author Tymish Ohulchanskyy, PhD, University at Buffalo research associate professor and deputy director for photomedicine at the university's Institute for Lasers, Photonics and Biophotonics (ILPB).
Doctors have used PDT to treat cancer for decades. Cancer cells absorb the drug, which is delivered to the tumor via the bloodstream or locally. Visible light is then applied to the site, which causes the drug to react with oxygen and create a burst of free radicals that kill the tumor.
Unfortunately, visible light does not penetrate tissue well. Conversely, near-infrared light penetrates tissue well but doesn't activate the drugs efficiently.
To solve this problem, some researchers are developing drugs that absorb near-infrared light. This method is limited, however, because stable and efficient near-infrared absorbing photosenzitizers are notoriously difficult to synthesize.
The UB-led team took a different approach, which uses the tumor's natural environment to tune the light into the necessary wavelengths.
For example, the near-infrared laser beam interacts with the natural protein collagen, which is found in connective tissues. The interaction changes the near-infrared light to visible light, a process known as second harmonic generation. Likewise, natural proteins and lipids within the cells interact with near-infrared laser light and change it to visible light through another process called four-wave mixing.
Thus, visible light can be generated in tumors deep inside the body, and it can be absorbed by the drug. This activates the drug, which then destroys the tumor.
The procedure has numerous advantages, said the study's leader, Paras Prasad, PhD, SUNY Distinguished Professor in chemistry, physics, electrical engineering, and medicine at UB, and the ILPB's executive director.
"There are no long-term side effects for PDT, it's less invasive than surgery, and we can very precisely target cancer cells," he said. "With our approach, PDT is enriched to provide another tool that doctors can use to alleviate the pain of millions of people suffering from cancer."
UB has applied for a patent to protect the team's discovery, and the university's Office of Science, Technology Transfer and Economic Outreach (UB STOR) is discussing potential license agreements with companies interested in commercializing it.
Story Source:
The above story is based on materials provided by University at Buffalo. The original article was written by Cory Nealon. Note: Materials may be edited for content and length.
Journal Reference:
- A. V. Kachynski, A. Pliss, A. N. Kuzmin, T. Y. Ohulchanskyy, A. Baev, J. Qu, P. N. Prasad. Photodynamic therapy by in situ nonlinear photon conversion. Nature Photonics, 2014; DOI: 10.1038/nphoton.2014.90
Key mechanism in metabolic pathway that fuels cancers identified
May 22 / 2014
UT Southwestern Medical Center
A significant step in cracking the code of an atypical metabolic pathway that allows certain cancerous tumors to thrive has been cracked, providing a possible roadmap for defeating such cancers. "With this finding, we have learned there are particular enzymes that work together to enable the reverse pathway to function, much like the tiny gears that turn in opposite directions to power a mechanical clock," commented the lead author.
Ralph DeBerardinis, M.D., Ph.D.
In a breakthrough discovery at the Children's Medical Center Research Institute at UT Southwestern (CRI), a research team led by Ralph DeBerardinis, M.D., Ph.D., has taken a significant step in cracking the code of an atypical metabolic pathway that allows certain cancerous tumors to thrive, providing a possible roadmap for defeating such cancers.
Published in Cell Reports, andfollowing up on Dr. DeBerardinis' landmark finding in 2011, this most recent discovery identifies the triggering mechanism that plays a key role in causing a series of energy-generating chemical reactions known as the Krebs cycle to run in reverse.
"With this finding, we have learned there are particular enzymes that work together to enable the reverse pathway to function, much like the tiny gears that turn in opposite directions to power a mechanical clock," said Dr. DeBerardinis, director of CRI's Genetic and Metabolic Disease Program and associate professor in the Department of Pediatrics and the Eugene McDermott Center for Human Growth and Development at UT Southwestern Medical Center.
The identification of the mechanism could provide a future target for drugs that would attack tumors relying upon the reverse pathway for sustenance and growth. Tumors of this type, often found in the brain, lungs and kidneys, tend to be difficult for oncologists to treat because cells using the atypical pathway seem to resist existing treatments like chemotherapy.
"Prior to this discovery, we didn't have enough information about how to tap into the reverse metabolic pathway without disrupting the pathways that were operating in the typical, forward manner," said Dr. DeBerardinis, senior author of the study. "We now believe there is a specific enzyme critical to the reverse pathway that can be deleted without impairing normal function. If we can eliminate that enzyme, we may be able to starve tumors of their supply of building blocks for growth."
Story Source:
The above story is based on materials provided by UT Southwestern Medical Center. Note: Materials may be edited for content and length.
Journal Reference:
- Andrew R. Mullen, Zeping Hu, Xiaolei Shi, Lei Jiang, Lindsey K. Boroughs, Zoltan Kovacs, Richard Boriack, Dinesh Rakheja, Lucas B. Sullivan, W. Marston Linehan, Navdeep S. Chandel, Ralph J. DeBerardinis. Oxidation of Alpha-Ketoglutarate Is Required for Reductive Carboxylation in Cancer Cells with Mitochondrial Defects. Cell Reports, 2014; DOI: 10.1016/j.celrep.2014.04.037