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Molecular battle in cancer cells offers clues for treatment

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Scientists around the world have been hot on the trail of a genetic mutation closely associated with some brain cancers and leukemia since the mutation’s discovery in 2008. The hunt is now yielding fruit. In the Jan. 18, 2011 issue of Cancer Cell, researchers reveal how the mutation contributes to cancer development and suggest potential ways to counter its effects.  About 75 percent of people with low-grade brain tumors and 20 percent of people with acute myeloid leukemia have a mutated version of a gene known as IDH. IDH helps cells metabolize, or eat, food. «We now know that IDH represents the most frequently mutated metabolic gene in human cancer. And that changes the landscape of cancer research in metabolism quite a lot,» said Yue Xiong, PhD, William R. Kenan Jr. professor of biochemistry and biophysics at the UNC Lineberger Comprehensive Cancer Center. Xiong and collaborators at UNC, the University of California San Diego, and the Shanghai Medical College of Fudan University in China discovered that the IDH mutation sets off a battle inside cells between two metabolites, small molecules produced by metabolic enzymes. On the good side—the side that leads to normal cell growth—is a molecule called ?-KG. On the bad side—the side that leads to cancer—is a molecule called 2-HG. The researchers discovered that cells with the IDH mutation produce less ?-KG and more 2-HG than normal cells. 2-HG then outcompetes ?-KG, disabling a whole family of enzymes that depend on ?-KG to do their jobs in the cell. Normal cell functions break down, contributing to the development of cancer. Two of the affected enzymes are also involved in controlling gene expression, so if 2-HG wins the battle, it can also activate other genes that lead to cancer growth.  Bolstering ?-KG to help fight 2-HG could offer a new treatment option for patients with the mutation. «?-KG is a natural product of the body. So we know we can survive it, we know it’s not toxic. That gives us a window of opportunity,» said Xiong. «In terms of future therapeutic interventions for IDH-mutated tumors, there are two directions we could go,» Xiong said. «One is developing a drug that inhibits the ability of the mutant enzyme from producing 2-HG. Another is to somehow provide ?-KG back to the patients with mutated IDH to battle 2-HG.»  Such therapies would help only those cancer patients with IDH mutations. «We no longer believe there will be a single silver bullet, a drug to treat and cure all types of cancers,» Xiong said. «Instead, we are looking into the therapeutic treatment of individual types of cancer. Therefore, a specific agent that is targeting a very specific event such as tumor with mutated IDH now becomes much more valuable.»  In 2010, more than 13,000 people died from brain and other nervous system cancers, and more than 20,000 died from leukemia. A drug that helps even a portion of patients with these cancers can still affect a lot of people, said Xiong.
http://www.eurekalert.org/pub_releases/2011-01/uonc-mb

En: Biología molecular, Noticias #

MIT scientists discover cancer-fighting role for cells. Blood-vessel cells can combat aggressive tumors, helping to prevent them from spreading through the body, new study finds

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MIT (Masschusetts Institute of Technology) scientists have discovered that cells lining the blood vessels secrete molecules that suppress tumor growth and keep cancer cells from invading other tissues, a finding that could lead to a new way to treat cancer. Elazer Edelman, professor in the MIT-Harvard Division of Health Sciences and Technology (HST), says that implanting such cells adjacent to a patient’s tumor could shrink a tumor or prevent it from growing back or spreading further after surgery or chemotherapy. He has already tested such an implant in mice, and MIT has licensed the technology to Pervasis Therapeutics, Inc., which plans to test it in humans.  Edelman describes the work, which appears in the Jan. 19 issue of the journal Science Translational Medicine, as a «paradigm shift» that could fundamentally change how cancer is understood and treated. «This is a cancer therapy that could be used alone or with chemotherapy radiation or surgery, but without adding any devastating side effects,» he says. Cells that line the blood vessels, known as endothelial cells, were once thought to serve primarily as structural gates, regulating delivery of blood to and from tissues. However, they are now known to be much more active. In the 1980s, scientists discovered that endothelial cells control the constriction and dilation of blood vessels, and in the early 1990s, Edelman and his postdoctoral advisor, Morris Karnovsky, and others, discovered an even more important role for endothelial cells: They regulate blood clotting, tissue repair, inflammation and scarring, by releasing molecules such as cytokines (small proteins that carry messages between cells) and large sugar-protein complexes. Many vascular diseases, notably atherosclerosis, originate with endothelial cells. For example, when a blood vessel is injured by cholesterol, inappropriately high blood sugar, or even physical stimuli, endothelial cells may overreact and provoke uncontrolled inflammation, which can further damage the surrounding tissue. Edelman and graduate student Joseph Franses hypothesized that endothelial cells might also play a role in controlling cancer behavior, because blood vessels are so closely entwined with tumors. It was already known that other types of cells within tumors, known collectively as the tumor stromal microenvironment, influence cancer cell growth and metastasis, but little was known about how endothelial cells might be similarly involved. In the new study, Edelman, Franses and former MIT postdoctoral fellows Aaron Baker and Vipul Chitalia showed that secretions from endothelial cells inhibit the growth and invasiveness of tumor cells, both in cells grown in the lab and in mice. Endothelial cells secrete hundreds of biochemicals, many of which may be involved in this process, but the researchers identified two that are particularly important: a large sugar-protein complex called perlecan, and a cytokine called interleukin-6. When endothelial cells secrete large amounts of perlecan but little IL-6 they are effective at suppressing cancer cell invasion, whereas they are ineffective in the opposite proportions.
The researchers theorize that there is a constant struggle between cancer cells and endothelial cells, and most of the time, the endothelial cells triumph. «All of us, every day, are exposed to factors that cause cancer, but relatively few of us exhibit disease,» says Edelman. «We believe that the body’s control mechanism wins out the bulk of the time, but when the balance of power is reversed cancer dominates.» The struggle also depends on a third player, the endothelial cells’ extracellular matrix — structural proteins that pave blood vessels and on which the endothelial cells reside. Endothelial cells only function properly when their extracellular matrix is stable and of the correct biochemical composition. Under normal conditions, if a cell becomes cancerous, the endothelial cell may then keep it in check. However, the cancer cell fights back by trying to destroy the extracellular matrix or change the endothelial cell directly, both of which hinder the endothelial cell’s efforts to control the cancer. «There is this three-way balance that needs to be achieved,» says Edelman. The more aggressive a cancer cell, the more likely it is to overcome the endothelial cells and extracellular matrix, allowing it to spread to other tissues. Several years ago, Edelman began using endothelial cells, grown within a scaffold made of denatured, compressed collagen (a protein that makes up much of human connective tissue), as an implantable device. The «matrix-embedded endothelial cells» served as a convenient unit that could be produced in bulk, tested for quality control, retained intact for months and implanted immediately when needed. This way, the healthiest cells could be selected to secrete all of the chemicals normally released by endothelial cells and placed in multiple locations in the body to control disease.  In clinical trials these implants were placed around blood vessels after vascular surgery and controlled local clotting and infection better than devices without cells. Significantly, because the endothelial cells were associated with a matrix mimicking their natural state, even cells from other people could be implanted without being rejected by the patients’ immune systems. No major side effects were seen in the clinical trials,  «Blood vessels and endothelial cells are the perfect regulatory units and our synthetic device recapitulated these control units perfectly,» says Franses. Blood vessels penetrate to the deepest recesses of tumors, and in doing so carry the powerful regulatory endothelial cells as close to cancer cells as possible. The extracellular matrix backbone of the vessels can keep the endothelial cells healthy and the healthy endothelial cells control nearby cancer cells. «This is what we mimicked with our devices,» he says. «In a sense it is like putting a cellular policeman on the corner of every tumor neighborhood.» In one mouse experiment reported in the new paper, endothelial cell implants significantly slowed tumor growth and prevented gross destructive change in tumor structure. Another experiment showed that cancer cells that had been grown in the secretions of endothelial cells were less able than standard cancer cells to metastasize and colonize the lungs of mice.  The new findings could also explain why drugs that suppress angiogenesis — growth of new blood vessels — have shown only transient and moderate benefit for cancer patients thus far. «You starve the tumor of its blood supply, but you also damage tumor blood vessel endothelial cells, so when the tumor comes back, there’s nothing to keep it in check. The vessels feed the tumor but their endothelial cells control the cancer cells within. Giving the endothelial cells without the blood vessels provides the best of both worlds and perhaps one day could provide new means of cancer therapy,» says Edelman.
http://www.eurekalert.org/pub_releases/2011-01/miot-msd011911.php

En: Noticias #

Cancer scientists discover genetic diversity in leukemic propagating cells

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Cancer scientists led by Dr. John Dick at the Ontario Cancer Institute (OCI) and collaborators at St Jude Children’s Research Hospital (Memphis) have found that defective genes and the individual leukemia cells that carry them are organized in a more complex way than previously thought. The findings, published today in Nature (DOI:10.1038/nature09733), challenge the conventional scientific view that cancer progresses as a linear series of genetic events and that all the cells in a tumour share the same genetic abnormalities and the same growth properties. «Our results show this is not the case and open the way to discover how genetic abnormalities transform normal cells into leukemic cells and the steps that have to happen to make the leukemic cells increasingly abnormal and aggressive, how leukemic cells at different steps of genetic evolution (or progression) respond to therapy, or contribute to relapse,» says Dr. Dick, Senior Scientist at OCI’s Campbell Family Institute for Cancer Research, the research arm of Princess Margaret Hospital, and the McEwen Centre for Regenerative Medicine at University Health Network. Dr. Dick is also a Professor in the Department of Molecular Genetics, University of Toronto, and Director of the Cancer Stem Cell Program at the Ontario Institute for Cancer Research.  The research team found that the leukemia cells taken from patients with acute lymphoblastic leukemia (ALL) are actually composed of multiple families of genetically distinct leukemia cells. They looked at how these families developed and retraced the ALL «family tree» back to its origins. They discovered that the so-called black sheep – the cells that propagate the disease and potentially survive therapy – persist through generations, and even branch off and evolve to form genetically distinct cancer families. Some of these genetic families dominate, making it appear that the leukemia cells only have one set of genetic abnormalities while other families are very rare, explaining why they had never been seen before.  The study results provide data linking genetic events in ALL taken from patients when first diagnosed to their future clinical survival. In the lab, the researchers reproduced human ALL in mice transplanted with patient leukemia samples. Sometimes the dominant genetic family would grow in the mice while in other mice the rarer families would grow.  «By looking at the genetic signatures of the leukemia cells in the different mice we were able to figure out their genetic ancestry and the evolutionary trajectory that that particular leukemia took. We found that if a particular gene family was mutated, the tumours were aggressive when grown in the mice. The patients with the corresponding tumours had poorer survival showing that the human-mouse transplant system could be very useful in predicting patient outcome.» This insight into genetic diversity has positive implications for cancer treatment, says Dr. Dick. «Understanding the complexity of cellular relationships and the existence of distinct genetic families of leukemia cells will shed light on why some cells of the cancer are not killed by the therapy and eventually regrow resulting in disease relapse, and help accelerate the development of tailored therapies to wipe out all the unwanted branches in the genetic tree.» Research collaborator Dr. Charles Mullighan, a hematologist at St. Jude Children’s Research Hospital, adds: «Overall, the study proved that many leukemias comprise multiple subpopulations with different genetic alterations, and that these genetic alterations may evolve over time. The main clinical implication is that we now need to extend this work to identify genetic changes at low levels at diagnosis that confer a high risk of treatment failure and relapse and find ways of targeting them.» The current research builds from earlier findings published in 2007 when the Dick team developed a method to convert normal human blood cells into «human» leukemia stem cells. The converted cells, when transplanted into special mice that permit the growth of human cells, can replicate the entire disease process from the very moment it begins.  In 1994, Dr. Dick identified the first cancer stem cell in leukemia, following on the original discovery in 1961 of the blood stem cell by renowned OCI scientists, Drs. Ernest McCulloch and James Till — a discovery that formed the basis of all current stem cell research. Dr. Dick, who holds the Canada Research Chair in Stem Cell Biology, has published other findings showing that colon cancer arises from stem cells specific to the tumour.
http://www.eurekalert.org/pub_releases/2011-01/uhn-csd011711.php

En: Noticias #

Photodynamic therapy against cancer. Photodynamic ablation of lymphatic vessels and intralymphatic cancer cells prevents metastasis

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Tumor cells have several routes that enable them to move from the primary tumor to distant tissues, a process called metastasis. It is metastasis of the primary tumor that kills most cancer patients. One of the least studied routes of metastasis is the lymphatic system. Many tumors produce factors that promote the formation of new lymphatic vessels (lymphangiogenesis). The newly formed lymphatic vessels enable tumor cells to travel from the primary tumor to the regional lymph nodes from whence they can spread throughout the body. Current treatment practice is to surgically remove the primary tumor as well as the metastatic lymph nodes, but tumor cells in metastatic transit inside the lymphatic vessels had not been given much attention.  In a new study, Dr Tuomas Tammela and colleagues at the University of Helsinki, Finland, investigated whether eradicating tumor-associated lymphatic vessels and the tumor cells they contain using photodynamic therapy (PDT) with a light-activated cytotoxic drug could reduce or eliminate tumor metastasis. They selected the mouse ear as their model system because it is easy to image both the lymphatic vessels and the in-transit tumor cells.  The researchers implanted mouse melanoma cells or human lung tumor cells into the mouse ear tip and waited two weeks for the primary tumors to become established and to induce lymphangiogenesis. Using deep-tissue microscopy, they observed that the newly formed lymphatic vessels contained in-transit tumor cells as well as small tumor nodules. Using pathology sections taken from a patient with recurrent melanoma, they confirmed that the tumor-associated lymphatic vessels of cancer patients contain in-transit tumor cells and tumor nodules. However, could PDT eliminate both tumor-associated lymphatic vessels and the tumor cells inside them? The researchers injected verteporfin in a liposomal preparation intradermally into the mouse ear and showed that this cytotoxic dye accumulated specifically in the lymphatic vessels. When they illuminated the mouse ear with infrared laser light, the lymphatic vessels started to shrink and fragment, and became leaky. Also, the researchers found that the mice receiving PDT and surgery had a much lower relapse rate than those that underwent surgery alone.  Using a pig model, the researchers also showed that PDT can target lymphatic vessels deep within the body and, thus, PDT could be useful eradicating tumor-associated lymphatic vessels deep within the tissues of human cancer patients.  «These findings are new and exciting, because the cells in metastatic transit in tumor-draining lymphatic vessels have not been given much attention previously», Dr. Tammela says.  «We do not expect PDT to replace current surgical techniques, which comprise removal of the primary tumor and metastatic lymph nodes. However, PDT could easily be combined with existing surgical techniques to destroy the lymphatic vessels draining from the tumor, as well as the tumor cell aggregates residing within them.» PDT using verteporfin is currently used clinically to destroy overgrown blood vessels in the retina of patients with macular degeneration. As both the drug and the PDT concept are already in use in patients, they are more likely to receive regulatory approval for targeting tumor-associated lymphatic vessels in cancer patients undergoing surgery than drugs still in earlier phases of development, Tammela states.
http://www.eurekalert.org/pub_releases/2011-02/uoh-pta020911.php

En: Noticias #

Sweeping view of prostate cancer genome yields deep insights. Using whole genome sequencing and multiple tumor samples, researchers uncover genes tied to prostate cancer growth

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For the first time, researchers have laid bare the full genetic blueprint of multiple prostate tumors, uncovering alterations that have never before been detected and offering a deep view of the genetic missteps that underlie the disease. The study, made possible by key advances in whole genome sequencing and analysis, points to several new prostate cancer genes and a critical category of genomic changes as important drivers of prostate cancer growth. The work was led by researchers from the Broad Institute, Dana-Farber Cancer Institute and Weill Cornell Medical College and appears in the February 10th issue of the journal Nature. Unlike other sequencing methods that target specific sections of the genome, whole genome sequencing enables researchers to look across the entire DNA landscape of a tumor, making it possible to discern global changes and patterns. Senior authors Levi Garraway and Mark Rubin and their colleagues used this strategy to view the complete genomes of seven prostate tumors and compare them to normal tissue samples to find regions of abnormality.  «Whole genome sequencing gives us fascinating new insights into a category of alterations that may be especially important in prostate cancer,» said Garraway, a senior associate member of the Broad Institute and a medical oncologist and assistant professor at the Dana–Farber and Harvard Medical School.  Prostate cancer is the second most lethal cancer in American men, responsible for more than 30,000 deaths and more than 200,000 new cases each year. A major goal of prostate cancer research is to identify potential drug targets as well as genetic characteristics within tumors that could distinguish indolent and aggressive forms of the disease, and ultimately improve diagnostics and treatment. Rubin, the Homer T. Hirst Professor of Oncology in Pathology and vice chair for experimental pathology at Weill Cornell Medical College, compares the Nature study to looking not just for spelling errors in the genome, but also for whole paragraphs or sections of genomic text that have been rearranged. «One of the big surprises is the fact that prostate cancer doesn’t have a large number of misspellings, but instead has a large, significant number of rearrangements,» said Rubin. «We would never have guessed that there were so many genomic alterations of this type before now because we didn’t have the right tools to look for them.» These alterations are known as genomic rearrangements — a kind of shuffling that occurs when a piece of DNA from one part of the genome breaks off and reattaches itself in another location. These rearrangements can create new genes (called «fusion genes»), allow a gene to operate unchecked, or prevent a gene from even working at all. Such changes can set a cell on a path toward cancer. By looking for genes affected by these rearrangements in multiple prostate cancer samples, the researchers unearthed new genes tied to the disease and found new mechanisms that may be driving cancer as a whole.  «This first whole genome view shows us tantalizing evidence for several new prostate cancer genes that likely would have remained undiscovered had we not been taking a genome-wide approach,» said Garraway.  Several tumors contained rearrangements disrupting the gene that codes for the protein CADM2, part of a family of proteins that prevent tumors from forming (known as «tumor suppressors»). Three samples also contained mutations involving members of the heat shock protein family, molecules that play an important, protective role and keep proteins from losing their proper shape. Anti-cancer drugs that inhibit these proteins are currently in clinical trials, but it is not yet clear whether prostate cancers will be vulnerable to such drugs. Other recurring genomic rearrangements involve the genes PTEN and MAGI2. PTEN is a well-known tumor suppressor gene and MAGI2 appears to be its helpmate; mutations to one or both genes may set cells on the path toward becoming cancerous. Drugs that inhibit the pathway these genes influence are also being developed, raising the possibility that the drugs could be applied to prostate cancer.  In addition to uncovering new and suspected genes, whole genome sequencing has also given Garraway, Rubin and their colleagues insights into how genomic rearrangements arise in the first place. With a catalog of rearrangements in hand, the researchers looked for where breaks and reattachments tended to occur, and found that these events are not distributed randomly across the genome. Rather, in some tumors these events tend to take place in areas of the genome that are inactive or silent, while in other tumors they occur in regions that are highly active. This pattern suggests that mistakes made by cells while turning genes on and off might give rise to DNA rearrangements and therefore play a formative role in cancer’s development. The researchers’ findings may also provide a key starting point for the development of new diagnostic tools for prostate cancer. Currently, when patients are diagnosed with prostate cancer, it is almost impossible for doctors to determine if the disease will advance quickly and therefore require aggressive treatment, or whether the tumors will remain slow-growing, necessitating a wait-and-see approach. «This study could enhance our ability to develop new, diagnostic markers for prostate cancer,» said Rubin. «We can also imagine eventually developing more personalized diagnostic tools for patients with recurrent tumors, to essentially follow the tumors’ progression by testing for new genomic alterations.»  Although the researchers’ findings need to be studied further and extended to larger numbers of tumor samples, this initial analysis has opened up many new avenues of investigation, underscoring the power of applying whole genome sequencing to cancer.  «Many of these features were invisible before,» said Garraway. «Now, we’re realizing that by sequencing whole genomes in prostate cancer, there’s a lot more to see. These discoveries are teaching us a great deal about prostate cancer biology that we simply hadn’t appreciated previously.»
http://www.eurekalert.org/pub_releases/2011-02/biom-svo020711.php

En: Noticias #

Algunos tumores de mama no requieren extirpación de nódulos linfáticos

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Las mujeres con cáncer de mama en estadio inicial no necesitarían someterse a una cirugía para remover los nódulos linfáticos cancerosos ubicados debajo de la axila, informaron investigadores estadounidenses. El hallazgo les evitaría a muchas mujeres el dolor y los años de efectos colaterales relacionados con este procedimiento.
Ciertas pacientes con cáncer de mama a las que solo se les extrae el nódulo linfático centinela -el más cercano al tumor- sobrevivieron el mismo tiempo que las mujeres sometidas a cirugías más exhaustivas para extirpar los nódulos linfáticos de la axila, una operación denominada disección del nódulo linfático auxiliar, ALND (axillary lymph node dissection).
Para el estudio, publicado en la Journal of the American Medical Association (JAMA), el equipo de Armando Giuliano, del Centro de Salud Saint John en California, analizó los dos procedimientos en mujeres con cáncer de mama invasivo a las que se les extirparon los tumores y se sometieron a radiación y quimioterapia.
Las tasas generales de supervivencia después de cinco años fueron casi las mismas en ambos grupos. La extirpación de nódulos linfáticos cancerosos en esas mujeres no sería necesaria porque la radiación y la quimioterapia atacan al cáncer en los nódulos linfáticos antes de que tengan tiempo de expandirse, explicó el equipo.
Los investigadores indicaron que extirpar los nódulos linfáticos de la axila implica un riesgo indiscutible y frecuentemente inaceptable de complicaciones, incluidas la infección y la inflamación crónica y dolorosa del brazo.
Los resultados, al combinarse con los de otros estudios, son lo suficientemente fuertes como para cambiar la forma en que son tratadas algunas mujeres con cáncer de mama.
«La implementación de este cambio de práctica mejoraría los resultados clínicos en miles de mujeres cada año al reducir las complicaciones asociadas con la ALND y mejorar la calidad de vida sin disminución en la supervivencia», escribió el equipo.
El cáncer de mama es la segunda causa de muerte por tumores entre las mujeres estadounidenses después del cáncer pulmonar. Causa la muerte de 500 000 personas y es diagnosticado en cerca de 1,3 millones en todo el mundo cada año.
Chicago, febrero 9/2011 (Reuters)

En: Noticias #

Innecesario y costoso el análisis de amígdalas extirpadas

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Un estudio de la Universidad de Michigan (UM) concluyó que extirpar las amígdalas a los niños y enviarlas a un estudio patológico para determinar problemas médicos es una práctica innecesaria y costosa.
Los resultados de la investigación, que se publican en la revista Otolaryngology-Head and Neck Surgery, destacan que cada año se gasta en Estados Unidos cerca de 35 millones de dólares en exámenes adicionales de amígdalas extirpadas.
Miles de niños se someten a esa cirugía para aliviar infecciones recurrentes y problemas obstructivos durante el sueño, y después hay un procedimiento de análisis de amígdalas extirpadas que rara vez conduce a descubrir alguna enfermedad escondida, dijo Marc C. Thorne. El profesor de Otorrinolaringología de la Escuela de Medicina de la UM, y autor principal del estudio, consideró este caso como «un asunto de economía y valores sociales, donde está en juego la forma de hacer un uso racional del dinero que se tiene en el país para el cuidado de la salud».
Los patólogos examinan los especímenes de amigdalotomía de dos maneras: una observación visual y un examen bajo microscopio. El examen con el microscopio cuesta casi tres veces más que la inspección visual.
El 42% de las muestras recibe una inspección ocular, el 38% se estudia bajo microscopio y el 20% se descarta sin observación alguna, según una encuesta hecha en el 2001 entre miembros de la Academia Estadounidense de Otorrinolaringología.
Para determinar la eficacia de cada práctica Thorne y sus colegas revisaron los datos de 5235 amigdalotomías llevadas a cabo en la UM entre 1996 y el 2008. En 4186 casos no se identificó una sola instancia de otra enfermedad adicional, pero el costo colectivo de esos exámenes fue de 150 000 dólares.
Si bien es más adecuado para la identificación de enfermedades el examen visual bajo microscopio, en el caso de las amígdalas ha encontrado muy pocos problemas adicionales. «La incidencia de otras enfermedades es tan baja que se necesitaría gastar más de 750 000 dólares por cada caso de linfoma que se encuentra», dijo.
De 1066 exámenes bajo microscopio se encontraron solo 18 casos de enfermedad, de los cuales se sospechaba antes de la cirugía por otros antecedentes. «Nadie sugiere que carezca de importancia el descubrimiento de cánceres ocultos u otras enfermedades, pero descuidamos otras cosas», agregó.
El investigador consideró que parte del problema se debe a la desconexión entre el servicio y el pago. Indicó que para un padre con seguro médico quizá no haya un costo adicional si la amígdala extirpada de su hijo se examina bajo microscopio, pero como sociedad tenemos que balancear estos deseos individuales con la carga que representan para todo el sistema.
Afirmó que si la decisión de continuar estos análisis se basa en que no importa el costo de detectar a tiempo un linfoma en un niño, entonces, más que exámenes visuales se requieren otros de mayor precisión. «De lo contrario seguimos gastando mucho dinero aunque sabemos que es poco probable que de esa forma detectemos algo», subrayó Thorne, quien, no obstante, estimó que el análisis rutinario de las amígdalas extirpadas tiene el beneficio no clínico para la instrucción de los patólogos. Chicago, febrero 8/2011 (Notimex)

En: Noticias #

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