Daiichi Sankyo Europe GmbH today announced the enrolment of the first patient into the PREvention oF thromboembolic events - European Registry in Atrial Fibrillation (PREFER in AF). Taking a comprehensive approach to the patient registry, PREFER in AF will gather data on the full spectrum of AF patients including those with valvular and non valvular forms of the condition. The registry will also track the impact of new anticoagulant therapies on stroke prevention, in addition to collating insights into patients' satisfaction with their entire AF management, the impact of AF and its management on patient quality of life, and the overall health economic burden of AF across Europe.
In 2010, the World Heart Federation highlighted the need for new multi-national registries to help fill knowledge gaps around AF management and outcomes. Enrolling 5,000 patients from across seven European countries, PREFER in AF will tackle this need by generating robust data on patient attitudes and management approaches, across a broad spectrum of different AF severities. As the AF treatment paradigm continues to change rapidly, these data will also help to establish whether current treatment developments are translating into optimally-balanced anticoagulation in practice, to give patients the best chance of a normal life.
Endorsing the urgent need for this study, Professor José Luis Zamorano, co-Chair of the PREFER in AF Steering Committee and Professor of Cardiology at the University Clinic San Carlos, Madrid, Spain, said, "The potential impact of AF to Europeans is staggering, with numbers affected estimated to rise over the coming years. PREFER in AF is a timely patient registry, which will give us highly valuable insights into the current management of AF patients and the health economic impact of the condition, whilst informing us about how to move forward with patient treatment."
Collecting data from Austria, France, Germany, Italy, Spain, Switzerland and UK, the size of the PREFER in AF registry will generate nationally representative data on stroke prevention management approaches, patient satisfaction scores regarding anticoagulant treatment and management, and quality of life markers. Additionally, health economic data on drug treatment, disease and treatment complications including hospitalisation will be collected to estimate the true cost of AF for the European healthcare systems.
Professor José Luis Zamorano further comments on the registry: "This essential patient registry is important as it is focused on patients' quality of life and treatment satisfaction, which are key factors when considering optimal patient care. AF is a condition associated with high morbidity and mortality and when patients are satisfied with their treatment, they stay on treatment."
AF is a leading cause of hospitalisation amongst all cardiac diseases and is the most frequent cardiac arrhythmia in clinical practice, with approximately one to two per cent of the general population being affected. AF is also a major cause of stroke and strokes associated with AF are more severe and have a poorer prognosis than non-AF related strokes.
Daiichi Sankyo, a global leader in cardiovascular medicine, is the sponsor of this registry study. Reinhard Bauer, CEO of Daiichi Sankyo Europe GmbH, comments on the start of the study today: "Daiichi Sankyo is proud to support such a valuable pan-European patient registry and we are very excited that the first patient has enrolled in this important observational study. This registry is an example of our on-going commitment to cardio-vascular medicine striving to further improve the treatment of AF patients and to better understand the real impact of AF on patients, physicians and the health care system."
16 January 2012
Thousands of seniors lack access to lifesaving organs, despite survival benefit
Thousands more American senior citizens with kidney disease are good candidates for transplants and could get them if physicians would get past outdated medical biases and put them on transplant waiting lists, according to a new study by Johns Hopkins researchers. The Hopkins investigators estimate that between 1999 and 2006, roughly 9,000 adults over 65 would have been "excellent" transplant candidates and approximately 40,000 more older adults would have been "good" candidates for new kidneys. None, however, were given the chance.
"Doctors routinely believe and tell older people they are not good candidates for kidney transplant, but many of them are if they are carefully selected and if factors that really predict outcomes are fully accounted for," says transplant surgeon Dorry L. Segev, M.D., Ph.D., an associate professor of surgery at the Johns Hopkins University School of Medicine and leader of the study being published in the January issue of the Journal of the American Geriatric Society. "Many older adults can enjoy excellent transplant outcomes in this day and age," he says, and should "be given consideration for this lifesaving treatment."
Those ages 65 and older make up over one-half of people with end-stage renal disease in the United States, and appropriately selected patients in this age group will live longer if they get new kidneys as opposed to remaining on dialysis, Segev says. The trouble is, he adds, that very few older adults are even put on transplant waiting lists. In 2007, only 10.4 percent of dialysis patients between the ages of 65 and 74 were on waiting lists, compared to 33.5 percent of 18- to 44-year-old dialysis patients and 21.9 percent of 45- to 64-year-old dialysis patients.
Segev cautions that some older kidney disease patients are indeed poor transplant prospects, because they have other age-related health problems. But he says his team's new findings, in addition to other recent research, show that new organs can greatly improve survival even in this age group.
Segev and his team constructed a statistical model for predicting how well older adults would be expected to do after kidney transplantation by taking into account age, smoking, diabetes and 16 other health-related variables. Using those data to define an "excellent" candidate, the information was then applied to every person 65 and older on dialysis during the seven-year study period. The researchers also determined whether these candidates were already on the waiting list.
"We have this regressive attitude toward transplantation in older adults," Segev says, "one based on historical poor outcomes in older patients, which no longer hold up. Anyone who can benefit from kidney transplantation should at least be given a chance. They should at least be put on the list."
Segev says he knows there is a shortage of kidneys and some will question whether scarce organs would be put to better use in younger patients. But Segev's study predicts that more than 10 percent of older patients would get kidneys from living relatives or friends, which would have little impact on the nationwide shortage of deceased donor kidneys. But finding a living donor first requires referral for transplantation.
"By not referring older adults for transplant, we're not just denying them a chance at a kidney from a deceased donor, but we're potentially denying them a kidney from a live donor," he adds.
According to research by Segev and his team published last year in the Journal of the American Medical Association, live kidney donation is very safe for both donor and recipient, and more older adults are donating their kidneys to relatives. Other research done by Segev has shown that older kidney transplant recipients do well with kidneys from older donors, organs that are otherwise be rejected for use in younger patients.
*Source: Johns Hopkins Medicine
"Doctors routinely believe and tell older people they are not good candidates for kidney transplant, but many of them are if they are carefully selected and if factors that really predict outcomes are fully accounted for," says transplant surgeon Dorry L. Segev, M.D., Ph.D., an associate professor of surgery at the Johns Hopkins University School of Medicine and leader of the study being published in the January issue of the Journal of the American Geriatric Society. "Many older adults can enjoy excellent transplant outcomes in this day and age," he says, and should "be given consideration for this lifesaving treatment."
Those ages 65 and older make up over one-half of people with end-stage renal disease in the United States, and appropriately selected patients in this age group will live longer if they get new kidneys as opposed to remaining on dialysis, Segev says. The trouble is, he adds, that very few older adults are even put on transplant waiting lists. In 2007, only 10.4 percent of dialysis patients between the ages of 65 and 74 were on waiting lists, compared to 33.5 percent of 18- to 44-year-old dialysis patients and 21.9 percent of 45- to 64-year-old dialysis patients.
Segev cautions that some older kidney disease patients are indeed poor transplant prospects, because they have other age-related health problems. But he says his team's new findings, in addition to other recent research, show that new organs can greatly improve survival even in this age group.
Segev and his team constructed a statistical model for predicting how well older adults would be expected to do after kidney transplantation by taking into account age, smoking, diabetes and 16 other health-related variables. Using those data to define an "excellent" candidate, the information was then applied to every person 65 and older on dialysis during the seven-year study period. The researchers also determined whether these candidates were already on the waiting list.
"We have this regressive attitude toward transplantation in older adults," Segev says, "one based on historical poor outcomes in older patients, which no longer hold up. Anyone who can benefit from kidney transplantation should at least be given a chance. They should at least be put on the list."
Segev says he knows there is a shortage of kidneys and some will question whether scarce organs would be put to better use in younger patients. But Segev's study predicts that more than 10 percent of older patients would get kidneys from living relatives or friends, which would have little impact on the nationwide shortage of deceased donor kidneys. But finding a living donor first requires referral for transplantation.
"By not referring older adults for transplant, we're not just denying them a chance at a kidney from a deceased donor, but we're potentially denying them a kidney from a live donor," he adds.
According to research by Segev and his team published last year in the Journal of the American Medical Association, live kidney donation is very safe for both donor and recipient, and more older adults are donating their kidneys to relatives. Other research done by Segev has shown that older kidney transplant recipients do well with kidneys from older donors, organs that are otherwise be rejected for use in younger patients.
*Source: Johns Hopkins Medicine
Una modelo de tallas grandes se convierte en la imagen de una conocida firma de lencería
Lucy Moore, que saltó a la fama hace algo más de un año como modelo de tallas grandes de lencería, acaba de ganar un concurso que le ha convertido en la nueva imagen de la firma de moda íntima Ann Summer's, tras barrer a más de 4.000 aspirantes con silueta filiforme, desprovista de curvas, según informa The Sun.
Esta británica de 20 años, que estudia la carrera de Derecho en la Universidad de Westminster, siempre ha defendido la estética de las mujeres reales y dice que pese a utilizar una talla 46, a sus prominentes curvas y sus kilos de más, puede lucir con gran sensualidad los diseños de ropa íntima.
Esta británica de 20 años, que estudia la carrera de Derecho en la Universidad de Westminster, siempre ha defendido la estética de las mujeres reales y dice que pese a utilizar una talla 46, a sus prominentes curvas y sus kilos de más, puede lucir con gran sensualidad los diseños de ropa íntima.
Researchers find new, noninvasive way to identify lymph node metastasis
Using two cell surface markers found to be highly expressed in breast cancer lymph node metastases, researchers at Moffitt Cancer Center, working with colleagues at other institutions, have developed targeted, fluorescent molecular imaging probes that can non-invasively detect breast cancer lymph node metastases. The new procedure could spare breast cancer patients invasive and unreliable sentinel lymph node (SLN) biopsies and surgery-associated negative side effects. Their study was published in a recent issue of Clinical Cancer Research (18:1), a publication of the American Association for Cancer Research.
"The majority of breast cancer patients, up to 74 percent, who undergo SLN biopsy are found to be negative for axillary nodal, or ALN, metastases," said corresponding author David L. Morse, Ph.D., an associate member at Moffitt whose research areas include experimental therapeutics and diagnostic imaging. "Determining the presence or absence of ALN metastasis is critical to breast cancer staging and prognosis. Because of the unreliability of the SLN biopsy and its potential for adverse effects, a noninvasive, more accurate method to assess lymph node involvement is needed."
The authors note that the postoperative complications to the SLN biopsy can include lymphedema, seroma formation, sensory nerve injury and limitations in patient range of motion. In addition, biopsies fail to identify disease in axillary lymph nodes in five to 10 percent of patients.
In developing targeted molecular probes to identify breast cancer in axillary lymph nodes, the research team from Moffitt, the University of Arizona and University of Florida used two surface cell markers -- CAIX and CAXII. CAIX is a cell surface marker known to be "highly and broadly expressed in breast cancer lymph node metastases" and absent in normal tissues.
CAIX and CAXII are both integral plasma membrane proteins with large extracellular components that are accessible for binding of targeted imaging probes, explained Morse. In addition, several studies have shown that CAIX expression is associated with negative prognosis and resistance to chemo and radiation therapy for breast cancer. CAXII is a protein expressed in over 75 percent of axillary lymph node metastases.
The researchers subsequently developed their targeting agents by using monoclonal antibodies specific for binding CAIX and CAXII, both of which are known to promote tumor growth.
According to the researchers, a number of noninvasive optical imaging procedures for SLN evaluation have been investigated, but the approaches have lacked the ability to target tumor metastasis biomarkers.
"These methods provide only anatomic maps and do not detect tumor cells present in lymph nodes," explained Morse. "Using mouse models of breast cancer metastasis and a novel, monoclonal anti-body-based molecular imaging agents, we developed a targeted, noninvasive method to detect ALN metastasis using fluorescence imaging."
In addition to the imaging study with mice, the researchers also reported that the combination of CAIX and CAXII covered 100 percent of patient-donated samples used in their tissue microarray (TMA) study.
"The imaging probes detected tumor cells in ALNs with high sensitivity," explained Morse. "Either CAIX or CAXII were expressed in 100 percent of the breast cancer lymph node metasatsis samples we surveyed in this study. These imaging probes have potential for providing a noninvasive way to stage breast cancer in the clinic without unneeded and costly surgery."
*Source: Moffitt Cancer Center
"The majority of breast cancer patients, up to 74 percent, who undergo SLN biopsy are found to be negative for axillary nodal, or ALN, metastases," said corresponding author David L. Morse, Ph.D., an associate member at Moffitt whose research areas include experimental therapeutics and diagnostic imaging. "Determining the presence or absence of ALN metastasis is critical to breast cancer staging and prognosis. Because of the unreliability of the SLN biopsy and its potential for adverse effects, a noninvasive, more accurate method to assess lymph node involvement is needed."
The authors note that the postoperative complications to the SLN biopsy can include lymphedema, seroma formation, sensory nerve injury and limitations in patient range of motion. In addition, biopsies fail to identify disease in axillary lymph nodes in five to 10 percent of patients.
In developing targeted molecular probes to identify breast cancer in axillary lymph nodes, the research team from Moffitt, the University of Arizona and University of Florida used two surface cell markers -- CAIX and CAXII. CAIX is a cell surface marker known to be "highly and broadly expressed in breast cancer lymph node metastases" and absent in normal tissues.
CAIX and CAXII are both integral plasma membrane proteins with large extracellular components that are accessible for binding of targeted imaging probes, explained Morse. In addition, several studies have shown that CAIX expression is associated with negative prognosis and resistance to chemo and radiation therapy for breast cancer. CAXII is a protein expressed in over 75 percent of axillary lymph node metastases.
The researchers subsequently developed their targeting agents by using monoclonal antibodies specific for binding CAIX and CAXII, both of which are known to promote tumor growth.
According to the researchers, a number of noninvasive optical imaging procedures for SLN evaluation have been investigated, but the approaches have lacked the ability to target tumor metastasis biomarkers.
"These methods provide only anatomic maps and do not detect tumor cells present in lymph nodes," explained Morse. "Using mouse models of breast cancer metastasis and a novel, monoclonal anti-body-based molecular imaging agents, we developed a targeted, noninvasive method to detect ALN metastasis using fluorescence imaging."
In addition to the imaging study with mice, the researchers also reported that the combination of CAIX and CAXII covered 100 percent of patient-donated samples used in their tissue microarray (TMA) study.
"The imaging probes detected tumor cells in ALNs with high sensitivity," explained Morse. "Either CAIX or CAXII were expressed in 100 percent of the breast cancer lymph node metasatsis samples we surveyed in this study. These imaging probes have potential for providing a noninvasive way to stage breast cancer in the clinic without unneeded and costly surgery."
*Source: Moffitt Cancer Center
La anorexia en la tercera edad
Ha perdido cuatro kilos en apenas un mes. A sus 75 años no quiere comer porque «no tiene ganas», y apenas sale de casa. Sufre lo que los expertos denominan «anorexia senil». Según Alberto López Rocha, presidente de la Sociedad Española de Médicos de Residencias (Semer) «provoca una disminución del apetito que en la mayoría de los casos se debe a causas sociales, fisiológicas o psicológicas». Y esta última es importante, pues «en la actualidad todavía hay un millón y medio de mayores de 65 años que viven solos y que tienen que enfrentarse a barreras arquitectónicas». Y eso no sólo quita las ganas de comer, sino que, además, les hace desconfiados. «No se fían de las personas que ponen a su disposición para ayudarles, por ejemplo, a hacer la compra, y como ellos no pueden bajar a por ella, terminan consumiendo «monoalimentos». Otro factor psicológico es la depresión y los estados de tristeza en los que se ven inmersos y que de forma indirecta repercuten en su alimentación.
No obstante, no hay que confundir este trastorno con la denominada hiporexia, que, tal y como aclara Fernando Gómez-Busto, miembro del grupo de nutrición de la Sociedad Española de Geriatría y Gerontología «es poco apetito». No es como la anorexia de envejecimiento, que se caracteriza por una disminución gradual de la ingesta en respuesta cambios corporales, a las menores necesidades energéticas, y a la menor actividad física». Entre los 20 y los 80 años, esta disminución se calcula, entre 600 Kcal/ día (mujeres) y 1.300 Kcal/ día (hombres) especialmente entre los 60 y 70 años y después de los 80. En cuanto al balance nutricional del paciente se produce «una disminución de la ingesta de proteínas y lípidos. Entre los micronutrientes, disminuye principalmente la ingesta de vitaminas A y D, calcio, folatos y magnesio», matiza Gómez-Busto.
Otro factor es la impactación fecal. «El 50 por ciento de los mayores sufre estreñimiento, lo que hace que tengas aún menos ganas de comer», señala el presidente de la Semer. La pérdida de peso también puede ser consecuencia de una mala dentición, alteraciones del gusto, infecciones o prótesis, así como de la demencia o enfermedades neurodegenerativas.RiesgoCuando el anciano deja de comer, el peligro principal es la desnutrición, que se asocia a pérdida de masa muscular y «mayor riesgo de caídas, menor capacidad inmunológica y mayor aumento de fragilidad».
Según los expertos, este problema está presente en entre el 1 y el 8 por ciento de los mayores que viven en sus domicilios. «Entre los ancianos hospitalizados y los ingresados en centros geriátricos, que tienen mayores problemas de enfermedad y dependencia, estas cifras son bastante más elevadas», dice el miembro de la Sociedad Española de Geriatría y Gerontología. Algo que corrobora López Rocha, pues, a su juicio «el 37 por ciento de los españoles mayores de 70 años que está hospitalizado muestra síntomas de desnutrición producida por dicha anorexia».
Para hacer frente al trastorno hay que acudir al médico de cabecera para que descarte otras patologías como, una enfermedad tumoral. En casa, hacer los platos más atractivos, ya que muchas veces el problema es que al no poder masticar, ingieren purés, cuyo aspecto no despierta las ganas de comer. Otra clave es tener cuidado con las siestas y, en lugar de que duerman nada más comer, es preferible que den un paseo.
**Publicado en "LA RAZON"
No obstante, no hay que confundir este trastorno con la denominada hiporexia, que, tal y como aclara Fernando Gómez-Busto, miembro del grupo de nutrición de la Sociedad Española de Geriatría y Gerontología «es poco apetito». No es como la anorexia de envejecimiento, que se caracteriza por una disminución gradual de la ingesta en respuesta cambios corporales, a las menores necesidades energéticas, y a la menor actividad física». Entre los 20 y los 80 años, esta disminución se calcula, entre 600 Kcal/ día (mujeres) y 1.300 Kcal/ día (hombres) especialmente entre los 60 y 70 años y después de los 80. En cuanto al balance nutricional del paciente se produce «una disminución de la ingesta de proteínas y lípidos. Entre los micronutrientes, disminuye principalmente la ingesta de vitaminas A y D, calcio, folatos y magnesio», matiza Gómez-Busto.
Otro factor es la impactación fecal. «El 50 por ciento de los mayores sufre estreñimiento, lo que hace que tengas aún menos ganas de comer», señala el presidente de la Semer. La pérdida de peso también puede ser consecuencia de una mala dentición, alteraciones del gusto, infecciones o prótesis, así como de la demencia o enfermedades neurodegenerativas.RiesgoCuando el anciano deja de comer, el peligro principal es la desnutrición, que se asocia a pérdida de masa muscular y «mayor riesgo de caídas, menor capacidad inmunológica y mayor aumento de fragilidad».
Según los expertos, este problema está presente en entre el 1 y el 8 por ciento de los mayores que viven en sus domicilios. «Entre los ancianos hospitalizados y los ingresados en centros geriátricos, que tienen mayores problemas de enfermedad y dependencia, estas cifras son bastante más elevadas», dice el miembro de la Sociedad Española de Geriatría y Gerontología. Algo que corrobora López Rocha, pues, a su juicio «el 37 por ciento de los españoles mayores de 70 años que está hospitalizado muestra síntomas de desnutrición producida por dicha anorexia».
Para hacer frente al trastorno hay que acudir al médico de cabecera para que descarte otras patologías como, una enfermedad tumoral. En casa, hacer los platos más atractivos, ya que muchas veces el problema es que al no poder masticar, ingieren purés, cuyo aspecto no despierta las ganas de comer. Otra clave es tener cuidado con las siestas y, en lugar de que duerman nada más comer, es preferible que den un paseo.
**Publicado en "LA RAZON"
New 'smart' nanotherapeutics can deliver drugs directly to the pancreas
A research collaboration between the Wyss Institute for Biologically Inspired Engineering at Harvard University and Children's Hospital Boston has developed "smart" injectable nanotherapeutics that can be programmed to selectively deliver drugs to the cells of the pancreas. Although this nanotechnology will need significant additional testing and development before being ready for clinical use, it could potentially improve treatment for Type I diabetes by increasing therapeutic efficacy and reducing side effects. The approach was found to increase drug efficacy by 200-fold in in vitro studies based on the ability of these nanomaterials to both protect the drug from degradation and concentrate it at key target sites, such as regions of the pancreas that contain the insulin-producing cells. The dramatic increase in efficacy also means that much smaller amounts of drugs would be needed for treatment, opening the possibility of significantly reduced toxic side effects, as well as lower treatment costs.
The research was led by Wyss Institute Founding Director Donald Ingber M.D., Ph.D. and Kaustabh Ghosh, Ph.D., a former postdoctoral fellow at Children's Hospital Boston. Their findings appear in the current issue of Nano Letters. Ingber is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School and Children's Hospital Boston, and Professor of Bioengineering at Harvard's School of Engineering and Applied Sciences. Ghosh is now an Assistant Professor of Bioengineering at the University of California, Riverside. Wyss Institute Postdoctoral Fellows, Umai Kanapathipillai and Netanel Korin, also contributed to the work, as did Jason McCarthy, Assistant Professor in Radiology at Harvard Medical School and an Assistant in Chemistry at Massachusetts General Hospital.
Type I diabetes, which often strikes children and young adults, is a debilitating disease in which the body's immune system progressively destroys the cells in the pancreas that produce insulin. According to the Juvenile Diabetes Research Foundation, as many as 3 million Americans have the disease and some 30,000 new cases are diagnosed every year. The risk of developing Type I diabetes, which can lead to serious health complications such as kidney failure and blindness, can be predicted with 90 percent accuracy. But therapeutic intervention for people identified as high risk has been limited because many systemic treatments are barred from clinical use due to the severe side effects they produce when used at the high doses required to achieve a therapeutic response.
"The consequences of Type I diabetes are felt in both the people who live with the disease and in the terrible strain that treatment costs put on the economy," said Ingber. "In keeping with our vision at the Wyss Institute, we hope that the programmable nanotherapy we have developed here will have a major positive impact on people's lives in the future."
Using nanoparticles that can be programmed to deliver drug or stem cell therapies to specific disease sites is an excellent alternative to systemic treatments because improved responses can be obtained with significantly lower therapeutic doses and hence, fewer side effects. To date, such nanotherapeutics have been developed primarily to treat cancer, since they can home in on the tumor via its leaky blood vessels. The challenge has been to develop ways to selectively deliver drugs to treat other diseases in which the tissues of interest are not as easily targeted. The research team addressed this problem by using a unique homing peptide molecule to create "smart" nanoparticles that can seek out and bind to the capillary blood vessels in the islets of the pancreas that feed the insulin-producing cells most at risk during disease onset.
*Source: Wyss Institute for Biologically Inspired Engineering at Harvard
The research was led by Wyss Institute Founding Director Donald Ingber M.D., Ph.D. and Kaustabh Ghosh, Ph.D., a former postdoctoral fellow at Children's Hospital Boston. Their findings appear in the current issue of Nano Letters. Ingber is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School and Children's Hospital Boston, and Professor of Bioengineering at Harvard's School of Engineering and Applied Sciences. Ghosh is now an Assistant Professor of Bioengineering at the University of California, Riverside. Wyss Institute Postdoctoral Fellows, Umai Kanapathipillai and Netanel Korin, also contributed to the work, as did Jason McCarthy, Assistant Professor in Radiology at Harvard Medical School and an Assistant in Chemistry at Massachusetts General Hospital.
Type I diabetes, which often strikes children and young adults, is a debilitating disease in which the body's immune system progressively destroys the cells in the pancreas that produce insulin. According to the Juvenile Diabetes Research Foundation, as many as 3 million Americans have the disease and some 30,000 new cases are diagnosed every year. The risk of developing Type I diabetes, which can lead to serious health complications such as kidney failure and blindness, can be predicted with 90 percent accuracy. But therapeutic intervention for people identified as high risk has been limited because many systemic treatments are barred from clinical use due to the severe side effects they produce when used at the high doses required to achieve a therapeutic response.
"The consequences of Type I diabetes are felt in both the people who live with the disease and in the terrible strain that treatment costs put on the economy," said Ingber. "In keeping with our vision at the Wyss Institute, we hope that the programmable nanotherapy we have developed here will have a major positive impact on people's lives in the future."
Using nanoparticles that can be programmed to deliver drug or stem cell therapies to specific disease sites is an excellent alternative to systemic treatments because improved responses can be obtained with significantly lower therapeutic doses and hence, fewer side effects. To date, such nanotherapeutics have been developed primarily to treat cancer, since they can home in on the tumor via its leaky blood vessels. The challenge has been to develop ways to selectively deliver drugs to treat other diseases in which the tissues of interest are not as easily targeted. The research team addressed this problem by using a unique homing peptide molecule to create "smart" nanoparticles that can seek out and bind to the capillary blood vessels in the islets of the pancreas that feed the insulin-producing cells most at risk during disease onset.
*Source: Wyss Institute for Biologically Inspired Engineering at Harvard
Researchers find first major gene mutation associated with hereditary prostate cancer risk
After a 20-year quest to find a genetic driver for prostate cancer that strikes men at younger ages and runs in families, researchers have identified a rare, inherited mutation linked to a significantly higher risk of the disease. A report on the discovery, published in the January 12, 2012 issue of the New England Journal of Medicine, was led by investigators at the Johns Hopkins University School of Medicine and the University of Michigan Health System. The research team found that men who inherit this mutation have a 10 to 20 times higher risk of developing prostate cancer.
While accounting for only a small fraction of all prostate cancer cases, the discovery may provide important clues about how this common cancer develops and help to identify a subset ofmen who might benefit from additional or earlier screening. This year, an estimated 240,000 men in the United States will be diagnosed with prostate cancer.
"This is the first major genetic variant associated with inherited prostate cancer," says Kathleen A. Cooney, M.D., professor of internal medicine and urology at the U-M Medical School, one of the study's two senior authors.
"It's what we've been looking for over the past 20 years," adds William B. Isaacs, Ph.D., professor of urology and oncology at the Johns Hopkins University School of Medicine, the study's other senior author. "It's long been clear that prostate cancer can run in families, but pinpointing the underlying genetic basis has been challenging and previous studies have provided inconsistent results."
For this study, the researchers collaborated with John Carpten, Ph.D., at the Translational Genomics Research Institute (TGen) in Phoenix, Arizona, who used the latest technology to sequence the DNA of more than 200 genes in a human chromosome region known as 17q21-22.
Cooney, working with Ethan Lange, Ph.D., of the University of North Carolina on the U-M Prostate Cancer Genetics Project, was the first to identify 17q21-22 as a region of interest.
Researchers started with samples from the youngest patients with prostate cancer in 94 families who had participated in studies at U-M and Johns Hopkins. Each of those families had multiple cases of the disease among close relatives, such as between fathers and sons or among brothers.
Members of four different families were found to have the same mutation in the HOXB13 gene, which plays an important role in the development of the prostate during the fetal stage and its function later in life. The mutation was carried by all 18 men with prostate cancer in these four families.
The researchers collaborated with Jianfeng Xu, Ph.D., and Lilly Zheng, Ph.D., at Wake Forest University to look for the same HOXB13 gene mutation among 5,100 men who had been treated for prostate cancer at either Johns Hopkins or U-M. The mutation was found in 1.4 percent -- or 72 of the men. It turned out that those men were much more likely to have at least one first-degree relative, a father or brother, who also had been diagnosed. The researchers also looked for the mutation in a control group of 1,400 men without prostate cancer, and only one of those men carried the mutation. In addition, the researchers studied men who were specifically enrolled in studies of early-onset or familial prostate cancer.
"We found that the mutation was significantly more common in men with a family history and early diagnosis compared with men diagnosed later, after age 55, without a family history. The difference was 3.1 percent versus 0.62 percent, Cooney says.
"We had never seen anything like this before. It all came together to suggest that this single change may account for at least a portion of the hereditary form of the disease," says study co-author Patrick Walsh, M.D., professor of urology at Johns Hopkins, who is one of the pioneers in prostate cancer treatment. In the 1980s, Walsh was one of the first to publish a study showing that the risk of prostate cancer was higher among men with close relatives who also had the disease.
The researchers say with further study, it may be possible one day to have genetic test for inherited prostate cancer in much the same way that tests are available to look for BRCA1 and BRCA2 mutations that greatly increase a woman's chance of developing breast and/or ovarian cancer.
"We need to continue studying this variant and look at larger groups of men. Our next step will be to develop a mouse model with this mutation to see if it causes prostate cancer," says Isaacs. He adds, "Future DNA sequencing may also identify additional rare variants that contribute to prostate cancer risk in families."
This particular mutation was found in families of European descent, while two different mutations on the HOXB13 gene were identified in families of African descent. Since only seven of the 94 families studied were of African descent, more research will be required before the significance of those mutations is known. African-American men are more likely to be diagnosed with prostate cancer at younger ages and have a more aggressive form of the disease.
Cooney says patients with questions about prostate cancer screening, particularly if the disease runs in their families, are encouraged to speak with their doctor.
*Source: Johns Hopkins Medical Institutions
While accounting for only a small fraction of all prostate cancer cases, the discovery may provide important clues about how this common cancer develops and help to identify a subset ofmen who might benefit from additional or earlier screening. This year, an estimated 240,000 men in the United States will be diagnosed with prostate cancer.
"This is the first major genetic variant associated with inherited prostate cancer," says Kathleen A. Cooney, M.D., professor of internal medicine and urology at the U-M Medical School, one of the study's two senior authors.
"It's what we've been looking for over the past 20 years," adds William B. Isaacs, Ph.D., professor of urology and oncology at the Johns Hopkins University School of Medicine, the study's other senior author. "It's long been clear that prostate cancer can run in families, but pinpointing the underlying genetic basis has been challenging and previous studies have provided inconsistent results."
For this study, the researchers collaborated with John Carpten, Ph.D., at the Translational Genomics Research Institute (TGen) in Phoenix, Arizona, who used the latest technology to sequence the DNA of more than 200 genes in a human chromosome region known as 17q21-22.
Cooney, working with Ethan Lange, Ph.D., of the University of North Carolina on the U-M Prostate Cancer Genetics Project, was the first to identify 17q21-22 as a region of interest.
Researchers started with samples from the youngest patients with prostate cancer in 94 families who had participated in studies at U-M and Johns Hopkins. Each of those families had multiple cases of the disease among close relatives, such as between fathers and sons or among brothers.
Members of four different families were found to have the same mutation in the HOXB13 gene, which plays an important role in the development of the prostate during the fetal stage and its function later in life. The mutation was carried by all 18 men with prostate cancer in these four families.
The researchers collaborated with Jianfeng Xu, Ph.D., and Lilly Zheng, Ph.D., at Wake Forest University to look for the same HOXB13 gene mutation among 5,100 men who had been treated for prostate cancer at either Johns Hopkins or U-M. The mutation was found in 1.4 percent -- or 72 of the men. It turned out that those men were much more likely to have at least one first-degree relative, a father or brother, who also had been diagnosed. The researchers also looked for the mutation in a control group of 1,400 men without prostate cancer, and only one of those men carried the mutation. In addition, the researchers studied men who were specifically enrolled in studies of early-onset or familial prostate cancer.
"We found that the mutation was significantly more common in men with a family history and early diagnosis compared with men diagnosed later, after age 55, without a family history. The difference was 3.1 percent versus 0.62 percent, Cooney says.
"We had never seen anything like this before. It all came together to suggest that this single change may account for at least a portion of the hereditary form of the disease," says study co-author Patrick Walsh, M.D., professor of urology at Johns Hopkins, who is one of the pioneers in prostate cancer treatment. In the 1980s, Walsh was one of the first to publish a study showing that the risk of prostate cancer was higher among men with close relatives who also had the disease.
The researchers say with further study, it may be possible one day to have genetic test for inherited prostate cancer in much the same way that tests are available to look for BRCA1 and BRCA2 mutations that greatly increase a woman's chance of developing breast and/or ovarian cancer.
"We need to continue studying this variant and look at larger groups of men. Our next step will be to develop a mouse model with this mutation to see if it causes prostate cancer," says Isaacs. He adds, "Future DNA sequencing may also identify additional rare variants that contribute to prostate cancer risk in families."
This particular mutation was found in families of European descent, while two different mutations on the HOXB13 gene were identified in families of African descent. Since only seven of the 94 families studied were of African descent, more research will be required before the significance of those mutations is known. African-American men are more likely to be diagnosed with prostate cancer at younger ages and have a more aggressive form of the disease.
Cooney says patients with questions about prostate cancer screening, particularly if the disease runs in their families, are encouraged to speak with their doctor.
*Source: Johns Hopkins Medical Institutions
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