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    Displaying items by tag: cancer

    stem-cells-molecule-gentaurDiscovered a new molecule - the first of its kind that allows multiplication of stem cells from umbilical cord. This discovery is very important as these cells are used for transplantation for the treatment of blood diseases such as leukemia, lymphoma and myeloma.
     
    The blood from the umbilical cord of the infant is considered an excellent source of hematopoietic stem cells that could be used for transplants.
     
    These stem cells are less likely to cause an adverse reaction by the immunity in the recipient thereof to whom they are transplanted.
     
    Furthermore, unlike the adult stem cells from bone marrow, it is not necessary, and the donor recipient has to have immunological compatibility for successful transplantation.
     
    Such type of treatment, however, can not always lead to successful healing in adults, since the number of the collected stem cells from umbilical cord blood is small and insufficient. Scientists believe that by using the new molecule will be possible multiplication of stem cells to a sufficient quantity for the conduct of successful treatment.
     
    Molecule is called the UM171 and was discovered by researchers from the Institute of Cancer Research and immunological and the University of Montreal, Canada.
     
    Doctrine argue that UM171 has the potential to increase the number of blood units, ready for transplant to 10 times.

    Published in News

    360w-molecular-marker-could-predict-tumor-progression--mouse-dr4-stem-cell-differentiation-neural-stem-cells-rat-models-gene-targeting-rosa26The U.S. Food and Drug Administration-approved drugs, gefitinib (Iressa) and erlotinib (Tarceva), are prescribed for lung and pancreatic cancer patients but only a few who have mutations in the EGFR gene usually benefit with a prolonged reduction of tumor size. The two drugs block the gene's ramped-up protein production, but patients' response to the drug varies widely -- from no survival benefit to several years. The average is several months.
    "Clinicians have had no reliable method for distinguishing patients who are not likely to respond to EGFR inhibitors and those who will respond very well," says David Sidransky, M.D., professor of otolaryngology, oncology, pathology, urology, and genetics at Johns Hopkins. Looking at the precise level of protein production from the EGFR gene alone in specific patients was not proven to be a good indicator of patients' response to EGFR-blocking drugs, but the presence or absence of Mig 6 might be, he adds.
    In a preliminary study, described July 31 in the online journal, PLoS ONE, the Johns Hopkins scientists found the genetic marker in a series of experiments that began with laboratory-derived lung and head and neck cancer cell lines resistant to EGFR-inhibitor drugs. In the cell lines, the team found very high levels of protein production from the Mig 6 gene -- up to three times the level in sensitive cell lines. Mig 6 is one of the molecules that controls the activity of the EGFR protein.
    "In the first set of experiments, we found that higher levels of Mig 6 occur often in cells that don't respond to EGFR inhibitors," says Sidransky. "Most tumors are known to have high Mig 6 levels and are not expected to respond to EGFR inhibitors."
    Next, the research team studied Mig 6 levels in a variety of tumors that were directly engrafted into mice, a research model known as a xenograft, and treated with an EGFR inhibitor. These new models contain a more complete sampling of the tumor that includes "stromal" cells, which surround and interact with the cancer cells. "These tumors are implanted along with their own microenvironment, into the mice, and we believe this model may be more predictive of what happens in human patients," says Sidransky.
    In the xenografts of tumors without EGFR mutations, as Mig 6 levels increased, so did the resistance to EGFR inhibitors, suggesting a correlation between high Mig 6 and lack of response to the drugs. To confirm the correlation, the scientists tested tissue samples of 65 lung cancer patients treated with EGFR inhibitors to compare their Mig 6 levels with outcomes.
    Of 18 patients with low Mig 6 levels, five of them survived more than a year without progression of their cancer; four survived more than two years progression-free. Among 16 patients with higher Mig 6 levels, two survived more than one year and none survived, progression-free, beyond two years.
    "The beauty of this finding is that it's simple. We're looking for tumors with low levels of Mig 6 to predict clinical benefit, and there aren't many of them," says Sidransky.
    Sidransky's team expects to license the Mig 6 marker to a biotechnology or pharmaceutical company and conduct further tests in larger groups of patients.

    Published in News
    Wednesday, 04 December 2013 11:16

    6 Simple ways to decrease your risk of cancer

    Pharma would make tens of thousands of dollars off of your cancer diagnosis. They wouldn’t really solve your prolem, but would merely prolong your illness so you can continue to spend your savings (and beyond) on their toxic cancer drugs. What the medical industry doesn’t seem to want to discuss (in addition to a cure) is how to prevent cancer. The fact is: cancer can be prevented.
    Untitled1

    Cancer rates have climbed significantly over the past 100 years and that’s due, in part, to our diets and lifestyle choices. Fortunately, we can take this knowledge and take big steps towards cancer prevention. Best of all, we can start now.
    In addition to eating these cancer-fighting foods, here are 6 simple ways to prevent cancer:

    1. Do Exercises - As Dr. Mercola reports, exercise can reduce your risk of cancer and improve cancer treatment outcomes. Go outside and walk in the sun, do some strength training, and improve balance and flexibility with yoga. Exercising outside can be especially beneficial.

    2. Remove Processed Foods - Processed carbohydrates and sugars are cancer fuel. They feed cancer cells and essentially help them grow. Eliminating these foods ensures you don’t have a cancer-friendly environment waiting for the cancerous cells to arrive. At the very least, avoid all processed sugars and foods, instead getting any sugar from natural fruits.

    3. Increase Vitamin D - While you are outside exercising in the sunshine, you’ll already be ahead of the game, creating natural vitamin D for immune function and immediately reducing your cancer risk. Don’t underestimate the connection between vitamin D and cancer reduced cancer risk.

    4. Minimize Radiation Exposure - You can minimize your risk of radiation exposure simply by using your phone less. Use speakerphone when you can to avoid holding the cell phone to your head. Never sleep with your phone next to you on your pillow. (Don’t laugh, you would be surprised at how many people do this). Also, reduce your exposure to medical scans including x-rays and CT scans.

    5. Optimize Essential Fat Consumption - The modern western diet is laden with omega-6 fats and deficient in omega-3s. Normalize your ratio of omega 3 and omega 6 fats by reducing your consumption of omega-6 by limiting the use of processed vegetable oils.

    6. Sleep Plenty and Decrease Stress - Cancer thrives in bodies that are imbalanced or otherwise unhealthy. A stress-free and well-rested person is naturally a healthier person. Make sure you are getting plenty of sleep and doing everything you can do eliminate what has been called the mother of all disease – stress.

    Published in News
    Thursday, 04 July 2013 10:31

    Stem-cell transplants may purge HIV

    Daniel-KuritzkeTwo men with HIV may have been cured after they received stem-cell transplants to treat the blood cancer lymphoma, their doctors announced today at the International AIDS Society Conference in Kuala Lumpur.

    One of the men received stem-cell transplants to replace his blood-cell-producing bone marrow about three years ago, and the other five years ago. Their regimens were similar to one used on Timothy Ray Brown, the 'Berlin patient' who has been living HIV-free for six years and is the only adult to have been declared cured of HIV. Last July, doctors announced that the two men — the ‘Boston patients’ — appeared to be living without detectable levels of HIV in their blood, but they were still taking antiretroviral medications at that time.

    Timothy Henrich, an HIV specialist at Brigham and Women’s Hospital in Boston, Massachusetts, who helped to treat the men, says that they have now stopped their antiretroviral treatments with no ill effects. One has been off medication for 15 weeks and the other for seven. Neither has any trace of HIV DNA or RNA in his blood, Henrich says.

    If the men stay healthy, they would be the third and fourth patients ever to be cured of HIV, after Brown and a baby in Mississippi who received antiretroviral therapy soon after birth.

    But Henrich and Daniel Kuritzkes, a colleague at Brigham who also worked with the men, caution that it is still too early know whether or not the Boston patients have been cured. For that, doctors will need to follow the men closely for at least a year, because the virus may be hiding out in 'reservoirs' — parts of the men’s bodies, such as their brain or gut, that can harbour the virus for decades.

    “We’re being very careful not to say that these patients are cured,” Kuritzkes says. “But the findings to date are very encouraging.”

    HIV researcher Steven Deeks of the University of California, San Francisco, says that doctors might need to wait at least two years before declaring that a cure has been achieved. “Any evidence that we might be able to cure HIV infection remains a major advance,” Deeks says. But, he adds, “there have been cases of patients who took many weeks off therapy before the virus took off”.

    Exciting news

    Still, researchers and doctors are excited about the news, especially because the Boston patients’ treatment differed from the Berlin patient’s regimen in one key way. Brown was given stem cells that were predisposed to resist HIV infection, because the donor happened to have a mutated version of a key protein — CCR5 — that is needed for HIV to infect cells. So Brown’s transplant was akin to gene therapy with HIV-resistant cells.

    But the Boston patients received stem cells without the protective mutation. The transplanted cells must therefore have been protected from infection by the antiretroviral drugs taken during cancer treatment. Their doctors think that an immune response called graft-versus-host disease — a post-transplant reaction in which donated cells kill off a patient’s own cells — may have then wiped out the patients’ HIV reservoirs, potentially curing the men.

    Transplant specialist Christine Durand of Johns Hopkins University School of Medicine in Baltimore, Maryland, says that the case of the Boston patients may show that current antiretroviral drugs are powerful enough, on their own, to protect the transplanted cells. “If cure has been achieved in the Boston patients, then it was the antiretroviral therapy, not gene therapy, that protected the donor cells,” she says.

    The finding is very important for people with HIV who also need blood-cell transplants, but the treatment is unlikely to be used more generally because the risks from transplants are high. Durand says that Johns Hopkins is now revising its transplant procedures to keep people with both cancer and HIV on antiretroviral drugs during the transplant regimen.

    Separately, the International Maternal Pediatric Adolescent AIDS Clinical Trials (IMPAACT) Group, based in Silver Spring, Maryland, is trying to replicate the Berlin patient’s cure by giving CCR5-mutated HIV-resistant blood from umbilical cords to children and adults with HIV and cancer. 

    Everyone with HIV could benefit from this work, researchers say, because it could yield valuable information about how to eliminate the HIV reservoir.

    “We are still a long way off from a viable cure option for most patients,” Durand says. “But every step counts, and these cases can teach us important lessons.”

     

    Published in News

    Researchers from the Hebrew University of Jerusalem and the Weizmann Institute of Science have developed a technique to cause apoptosis, or programmed cell death, that could lead to new approaches to treating cancer. 

    Apoptosis is an essential defense mechanism against the spread of abnormal cells such as cancer. It is a complex process that occurs through networks of proteins that interact with each other. Cancer cells usually avoid this process due to mutations in the genes that encode the relevant proteins. The result is that the cancer cells survive and take over while healthy cells die.

    The research, by graduate student Chen Hener-Katz at the Hebrew University, involved collaboration between Prof. Assaf Friedler of the Hebrew University's Institute of Chemistry and Prof. Atan Gross of the Weizmann Institute's Department of Biological Regulation. It was published in the Journal of Biological Chemistry under the title ''Molecular Basis of the Interaction between Proapoptotic Truncated BID (tBID) Protein and Mitochondrial Carrier Homologue 2 (MTCH2) Protein.''

    The study examined the interaction between two important proteins involved in cell death: mitochondrial carrier homologue 2 (MTCH2), which was discovered in the lab of Prof. Gross, and truncated BID (tBID), which are both involved in the apoptotic process. The researchers found the regions in the two proteins that are responsible for binding to each other, a critical step in initiating apoptosis. Following their discovery, the researchers developed short synthetic protein fragments, or peptides, that mimicked the areas on the proteins that bind to each other, and by doing so inhibited this binding. In lab experiments conducted on cell cultures, this resulted in the death of cancer cells of human origin.

    ''These protein segments could be the basis of future anti-cancer therapies in cases where the mechanism of natural cell death is not working properly,'' said Prof. Friedler. ''We have just begun to uncover the hidden potential in the interaction between these proteins. This is an important potential target for the development of anticancer drugs that will stimulate apoptosis by interfering with its regulation. ''

    Prof. Friedler is the head of the school of chemistry at the Hebrew University. His major research interests are using peptides to study protein-protein interactions in health and disease, and developing peptides as drug leads that modulate these interactions, specifically in relation to HIV and cancer. Prof. Friedler won the prestigious starting grant from the ERC (European Research Council) as well as the outstanding young scientist prize by the Israeli Chemical Society. His research was supported by a grant from the Israel Ministry of Health and by a starting grant from the European Research Council. 

    Published in News
    Thursday, 16 May 2013 14:42

    CA-19-9 ELISA kit

    Name

    CA-19-9 ELISA kit

    Category Name Cancer ELISA kits
    Test 96
    Method ELISA method: Enzyme Linked Immunosorbent Assay
    Principle ELISA principle- Peroxidase conjugated
    Detection Range 0-240U/mL
    Sample 50µl serum
    Specificity 97%
    Sensitivity 5U/mL
    Total Time ~140 min
    Shelf Life 12-14 months

     

    CA-19-9 (Gastrointestinal Cancer Antigen) ELISA Kit which is an enzyme-linked immunosorbent assay for the quantitative measurement of Gastrointensinal Cancer Antigen (CA-19-9) concentration in human serum. An elevated serum CA19-9 suggests the need for further clinical management. The CA-19-9 ELISA kit, like many ELISA KITS, is for diagnostic laboratory use only.

    As in other Cancer ELISA Kits, the CA-19-9 ELISA kit is a solid phase two-site immunoassay. The CA-19-9 ELISA kit is intended to be used as a monitoring and screening test, and is useful for patients in clinical remission, as post-operative serum CA-19-9 values which fail to return to normal, strongly suggest the presence of residual tumor. Tumor recurrence is often accompanied by a rise of serum levels before progressive disease is clinically evident. The sensitivity of the CA-19-9 ELISA kit is 5 U/ml and the specificity is 97%.

    Notable features of Cancer ELISA Kits:

    ▪ User-friendly directions and explanation of test procedures
    ▪ Simple and safe reagent preparation
    ▪ Clear instructions on specimen collection
    ▪ Comprehensive package of required materials
    ▪ Explicit quality control and storage guidelines
    ▪ Reliable and easy-to-read test results

    Product inserts for most Cancer ELISA kits follow a similar method. See the CA-19-9 ELISA Kit product insert for details on preparation, procedures, quality control, and test result interpretation.

    Gentaur also provides other ELISA Kits

    For more information download PDF file 

    Order Button1

    Published in Top Products

    cellsThe biggest breakthrough in understanding the genetics of cancer before. So Iyls Ross, professor of cancer genetics at the Institute of Cancer Research in London, described the results of an international effort of more than 1,000 scientists, presented in late Wednesday.

    Their study - the largest ever study of "faults" of DNA that promote the development of cancer - revealed a series of genetic markers with which can identify people most likely to develop these conditions. In this case for three of the most encountered its forms - prostate, breast and ovarian.

    According to London's "Guardian" doctors have said that they can in five years with a simple saliva test based markers make for each risk profile and create a foundation for individual monitoring. For people with an increased risk of developing cancer would go more often reviewing and possibly developing cancer will be detected at an early stage, when there is a much greater chance of prolonging life.

    Test based on genetic markers can identify men who are 50% likely to become ill from prostate cancer. This would not only allow the UK have called for a national program. screening of men, it will stop the practice because of inaccurate blood tests a quarter of people with this diagnosis are treated, there was no need.

    To identify genetic markers for prostate cancer, the researchers compared the DNA data of 25,000 patients with the disease with the same number of healthy men. So were discovered 23 new "defect" in the DNA, increasing the risk of disease, 16 were identified as "culprits" to reach the most aggressive form. In practice, few men wear markers for prostate cancer, but 1% of them have DNA "defects" that increase the risk of developing it 5 times.

    The same procedure has found 49 new DNA "defect" associated with the risk of developing breast cancer.

    The third part of the project included the 130 institutes worldwide to compare DNA profiles of women with ovarian cancer with this healthy. This established eight new sections of DNA associated with increased risk of disease.

    Professor Iyls believe that a simple test in the GP's office soon enough every patient to have a personal account of the risk of these diseases. Physicians can improve performance by adding factors of lifestyle specific person - the risk of breast cancer, for example, alcohol increases and decreases from birth and breastfeeding.

    The big problem started after that - experts disagree on what age should these tests, complement it with ultrasound, magnetic rezonas and biopsies and what kind therapy to apply.

    The result of the research was published in Nature Genetics and several other scientific journals.

    Published in News

    clinical trails dna rna monoclonal antibody targattMedicine for the treatment of cancer based on a virus destroying tumor cells for the first time successfully passed clinical trials in advanced stage, said U.S. pharmaceutical manufacturer Amgen.

    A statement from the company product has achieved the main objective of the Phase III clinical trial in patients with advanced melanoma - the most aggressive type of skin cancer. The results showed that 16% of patients who received treatment had a significant tumor poured lasting six months or more, compared with only 2% of the control group.

    A spokesman for the company declined to say whether the company will apply for registration to the FDA on the basis of this study.

    It contains the virus Talimogene laherparepvec, genetically modified in a way that causes him to multiply only in rapidly growing cells. The product is injected directly into the tumor, after which the virus enters the cancer cells and causes them to synthesize large amounts of granulocyte-monocyte colony stimulating factor - the hormone that stimulates the maturation of immune cells. When cancerous cells die, they release new amounts of virus and acquired therein colony stimulating factor, which boost the immune system.

    The study was conducted in 400 patients, two thirds of whom received injections every two weeks. The rest of the participants received injections only granulocyte-monocyte colony stimulating factor. According to Dr. Anthony Ribas, melanoma specialist at the University of Los Angeles, the study results are positive, but it is uncertain whether sufficient authorization for use.

    Published in News

    monoclonal antibodyResearchers have discovered a unique monoclonal antibody that can effectively reach inside a cancer cell, a key goal for these important anticancer agents, since most proteins that cause cancer or are associated with cancer are buried inside cancer cells. Scientists from Memorial Sloan-Kettering Cancer Center and Eureka Therapeutics have collaborated to create the new human monoclonal antibody, which targets a protein associated with many types of cancer and is of great interest to cancer researchers.

    Unlike other human therapeutic monoclonal antibodies, which can target only proteins that remain on the outside of cancer cells, the new monoclonal antibody, called ESK1, targets a protein that resides on the inside of the cell. ESK1 is directed at a protein called WT1, which is overexpressed in a range of leukemias and other cancers including myeloma and breast, ovarian, and colorectal cancers. WT1 is a high priority target for cancer drugs because it is an oncogenic protein, meaning that it supports the formation of cancer. In addition, it is found in few healthy cells, so there are less likely to be side effects from drugs that target it. "This is a new approach for attacking WT1, an important cancer target, with an antibody therapy. This is something that was previously not possible," said David A. Scheinberg, MD, PhD, Chair of the Sloan-Kettering Institute's Molecular Pharmacology and Chemistry Program and an inventor of the antibody. "There has not been a way to make small molecule drugs that can inhibit WT1 function. Our research shows that you can use a monoclonal antibody to recognize a cancer-associated protein inside a cell, and it will destroy the cell." 

    The first studies of the antibody are showing promise in preclinical research as a treatment for leukemia as reported March 13, 2013, in Science Translational Medicine. "ESK1 represents a paradigm change for the field of human monoclonal antibody therapeutics," said Cheng Liu, PhD, President and Chief Executive Officer of Eureka Therapeutics. "This research suggests that human antibody therapy is no longer limited to targeting proteins present outside cancer cells, but can now target proteins within the cancer cell itself."

    ESK1 was engineered to mimic the functions of a T cell receptor, a key component of the immune system. T cells have a receptor system that is designed to recognize proteins that are inside the cell. As proteins inside the cell get broken down as part of regular cellular processes, molecules known as HLA molecules carry fragments of those proteins -- known as peptides -- to the surface. When T cells recognize certain peptides as abnormal, the T cell kills the diseased cell. In the current study, the investigators showed that ESK1 alone was able to recognize WT1 peptides and kill cancer cells in the test tube and also in mouse models for two different types of human leukemia. "We were surprised that the antibody worked so well on its own," said Dr. Scheinberg, senior author of the paper. "We had originally expected that we might need to use the antibody as a carrier to deliver a drug or a radioactive therapy to kill the cancer cells, but this was not necessary."

    Additional studies must be done in the laboratory before ESK1 is ready to be tested in patients. But the monoclonal antibody was engineered to be fully human, which should speed the time it takes to move the drug into the clinic. Researchers expect that the first clinical trials, for leukemia, could begin in about a year.

    The antibody was developed under a collaborative effort between Memorial Sloan-Kettering and Eureka, which have jointly filed for patent protection. This work was supported by grants from the Leukemia and Lymphoma Society, the National Cancer Institute, the Sloan-Kettering Institute's Experimental Therapeutics Center and Technology Development Fund, the Commonwealth Foundation for Cancer Research, the Tudor and Glades Foundations, the Merker Fund, the Lymphoma Foundation, and the Mesothelioma Applied Research Foundation.

    http://www.sciencedaily.com

    Published in News

    cancer-antibodies-gentaur-1Un bebé de dos años que nació con el VIH ha sanado con terapia antirretroviral precoz

    Ayer, investigadores de amfAR, (Fundación para la investigación del sida en Estados Unidos) hicieron público en el marco de la 2013 Conference on Retroviruses and Opportunistic Infections, el primer caso documentado de curación de sida en un bebé nacido con VIH. Esta sanación, que fue posible con terapia precoz de antirretrovirales según los médicos, señala la necesidad de investigar más sobre el efecto de estos tratamientos en recién nacidos.

    Deborah Persaud, doctora de la Johns Hopkins University de Estados Unidos, describió ayer, tres de marzo de 2013, el primer caso documentado de un bebé curado del sida. Su anuncio fue realizado en la 2013 Conference on Retroviruses and Opportunistic Infections (CROI) de Atlanta (EEUU). 


    Persaud, investigadora de amfAR (The Foundation for AIDS Research) , detalló el caso de un bebé de dos años de edad de Mississippi diagnosticado con VIH al nacer, y que enseguida fue sometido a terapia antirretroviral. 

    A los 18 meses, el bebé dejó de tomar los antirretrovirales y su seguimiento médico se interrumpió. Cuando los médicos volvieron a verlo a los 23 meses, a pesar de que había dejado de su terapia durante cinco meses, constataron que el bebé tenía una carga viral indetectable. Una batería de pruebas altamente sensibles posteriores confirmó la ausencia del VIH. 

    La confirmación de la curación fue posible gracias a una donación que amfAR concedió a la doctora Persaud y a la doctora Katherine Luzuriaga, de la Universidad de Massachusetts, en septiembre de 2012. 

    La donación permitió que las médicos establecieran un colaboratorio de investigación para explorar y documentar posibles casos pediátricos de curación del VIH. En este colaboratorio participan además los doctores e investigadores Stephen Spector y Richman Doug, de la Universidad de California, San Diego; el Dr. Frank Maldarelli, del Instituto Nacional del Cáncer, y el Dr. Tae-Wook Chun, del Instituto Nacional de Alergias y Enfermedades Infecciosas.

     

    Diversas formas de tratamiento del VIH

    "El pediatra del bebé de Mississippi conocía nuestro trabajo y comunicó el caso a nuestro equipo, tan pronto como se enteró," explica Rowena Johnston, vicepresidenta de amfAR. "Gracias a que este colaboratorio ya estaba en marcha, los investigadores pudieron movilizarse inmediatamente y realizar las pruebas necesarias para determinar si realmente se trataba de un caso de curación del SIDA infantil”. 

    Según Persaud, pruebas exhaustivas han confirmado sin lugar a dudas que la madre y el bebé eran VIH positivo cuando este nació, y que en la actualidad no quedan signos de infección por VIH en el bebé, según los análisis realizados con los medios más sensibles disponibles. 

    El único caso documentado de cura del VIH hasta la fecha había sido el de Timothy Brown, el llamado "paciente de Berlín." En 2006, mientras era tratado por el VIH, al Sr. Brown le diagnosticaron leucemia. 

    Su médico trató entonces su leucemia con un trasplante de células madre de una persona nacida con una mutación genética que causa la inmunidad a la infección por VIH. Después del trasplante, el Sr. Brown pudo abandonar el tratamiento para el VIH sin recaídas. 

    Este nuevo caso apunta a la posibilidad de que diferentes poblaciones de personas con VIH podrían ser curadas de esta enfermedad de diferentes maneras. Mientras que el caso del señor Brown fue el resultado de una serie de complejos y costoso procedimientos de alto riesgo, este nuevo caso parece haber sido el resultado directo de una terapia antirretroviral relativamente barata. 

    "Teniendo en cuenta que esta sanación parece haberse logrado solo con terapia antirretroviral, es imperativo que aprendamos más acerca del sistema inmunológico de los recién nacidos y en qué se diferencia este del sistema inmunológico de los adultos; así como sobre los factores que han hecho posible que el bebé se haya curado”, explica Johnston. 

    El caso de Mississippi también pone de relieve la importancia de la identificación del VIH en mujeres embarazadas y de ampliar el acceso a tratamientos para prevenir la transmisión materno-infantil de la enfermedad. Asimismo, revela la necesidad de tratar de inmediato con antirretrovirales a los bebés que nacen seropositivos. 

    Acerca de amfAR

    amfAR, la Fundación para la Investigación del SIDA, es una de las principales organizaciones sin fines de lucro del mundo dedicada al apoyo de la investigación del SIDA, prevención del VIH, educación, tratamiento y su incidencia en las políticas públicas. Desde 1985, amfAR ha invertido más de 366 millones de dólares (unos 280 millones de euros) en sus programas y ha otorgado becas a más de 2.000 equipos de investigación de todo el mundo.

     

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