Abstract
- PMID:
- 27898068
- DOI:
- 10.1038/tp.2016.234
Wednesday
Preliminary indications of the effect of a brief yoga intervention on markers of inflammation and DNA methylation in chronically stressed women
Tuesday
Lee Biosolutions Surprises Again with New Board Members
http://www.prweb.com/releases/2015/08/prweb12903762.htm
Lee Biosolutions is a healthcare biotech company that manufactures finished proteins for research and clinical diagnostic and life science market. Today we are proud to announce the promotion of Matthew Lee as President and Chief Operating Officer.
We are a global healthcare biotech company that specializes in process development and bulk manufacturing of finished human and animal enzymes and related proteins for research and clinical diagnostic tests. Our products are used for such pathologies as cardiac disease, cancer, diabetes, urine analysis, coagulation, obesity, inflammatory, neurological, autoimmune diseases and immunological disorders. Our expertise includes process optimization and scale-up, bioanalytical development, validation and purification of biologicals. We are known for our ability to take a bench top pilot process and scale up to commercialization that is efficient and cost effective for our clients.
Lee Biosolutions is a healthcare biotech company that manufactures finished proteins for research and clinical diagnostic and life science market. Today we are proud to announce the promotion of Matthew Lee as President and Chief Operating Officer.
Burton Lee, Chief Executive Officer of Lee Biosolutions stated, "Matt’s leadership skills and business acuity has helped us maintain double digit growth and increased profitability allowing us to expand our operations. His dedication to our team, vendors and customers has made this management move as the most logical choice in order to maximize our potential for growth.”
Matthew Lee holds a B.S. in Marketing Management from Missouri State University and joined Lee Biosolutions in 2012 as Logistics Manager. He was promoted to Vice-President of Business Operations in 2014 for his ability to improve operational efficiencies in the business. He is currently on the Board of Directors and not only continue running the day to day operations but will assist the CEO in applying creative solutions to strategic challenges.
About Lee Biosolutions, Inc.
We are a global healthcare biotech company that specializes in process development and bulk manufacturing of finished human and animal enzymes and related proteins for research and clinical diagnostic tests. Our products are used for such pathologies as cardiac disease, cancer, diabetes, urine analysis, coagulation, obesity, inflammatory, neurological, autoimmune diseases and immunological disorders. Our expertise includes process optimization and scale-up, bioanalytical development, validation and purification of biologicals. We are known for our ability to take a bench top pilot process and scale up to commercialization that is efficient and cost effective for our clients.
Monday
Ferritin protects kidneys against damage by controlling iron
A protein, FERRITIN, protects kidneys against a damaging after-effect of injury, heart failure or hardened arteries by controlling levels of iron, according to a study published today by researchers at the University of Alabama at Birmingham in the Journal of Clinical Investigation.
The research team was able to genetically engineer a mouse model that clarified the role of ferritin in iron homeostasis, setting the stage for a new line of research into future treatments that may be able to prevent acute kidney damage caused by iron.
The study results revolve around iron, the most common chemical element on Earth and a core player in the biochemical processes of animals that evolved in its presence. The human body uses iron because its atomic structure can readily accept or donate negatively charged atomic components called electrons, shifting back and forth as needed. Cells, and in particular the powerhouses within cells called mitochondria, pass around electrons and harness charge to drive life processes and make cellular energy with the help of iron.
Unfortunately, that same, useful atomic flexibility means that iron free in the body will react with almost anything it encounters, disrupting charge balances and creating highly reactive free radicals that tear apart delicate structures like DNA, a mechanism by which trauma and many diseases kill tissue.
Thus, iron is almost always bound to transporter and chaperone proteins. When the body suffers a crushing injury, however, iron-containing heme proteins like myoglobin spill out of crushed tissue into the bloodstream, get caught in the blood-filtering nephrons in the kidney and die, releasing their iron. When less oxygen reaches kidney tubules from a failing heart, the lack disables the heme proteins in the kidney cells, causing them to spill the iron they contain and damage tissues.
The current study results confirm a protein called ferritin is among the most important of proteins charged with mopping up free iron. Beyond showing its ability to prevent iron-related cellular damage, UAB researchers and lead co-authors Abolfazl Zarjou, M.D., Ph.D., and Subhashini Bolisetty, Ph.D., say their study is the first to reveal the role of the kidney in the regulation of iron metabolism, a function until now linked to the liver and the intestines.
"Ferritin is a giant globe that sequesters 4,500 iron ions in safe form, thus preventing acute kidney injury," said Zarjou, who is part of the American Board of Internal Medicine Research Pathway at UAB. "If this mechanism is confirmed, and if we can find ways to manipulate H-ferritin, this work would provide a platform for targeting iron sequestration as a new therapy against acute kidney damage."
The study's corresponding author, Anupam Agarwal, M.D., is interim senior vice president for Medicine and dean of the UAB School of Medicine; he directs the National Institutes of Health-funded UAB-University of California San Diego O'Brien Core Center for Acute Kidney Injury Research. Agarwal's team of researchers has spent years studying whether or not a protein called heme oxygenase-1 might represent the most important part of the system that protects the body from iron-driven free radical production. This protein defense degrades heme to release iron, but it also sends signals to turn up ferritin production. The current study found that this enzyme has no protective value if ferritin is removed from the system, and it may be ferritin - not heme oxygenase-1 - that is the key mediator of protection from iron.
Ferritin's importance
The ferritin shell is made of 24 subunits of heavy and light protein chains, heavy just meaning that one chain is usually large in the pairs in which such chains typically occur. The ferritin heavy chain converts the more unstable form of iron (Fe2+ or the ferrous) to a more stable (Fe3+ or the ferric) form that can be the safely sequestered and deposited within the ferritin shell.
The research team had hypothesized that deletion of ferritin heavy chain in proximal tubules, the workhouse area of nephrons, would result in an increased amount of the free, unstable form of the iron (Fe2+) to exacerbate injury. In addition, any form of kidney injury would ultimately lead to increased cell death and liberation of iron from the intracellular space of necrotic cells in a vicious circle.
"This study represents a leap in the field because we showed that you can knock out ferritin just in the proximal part of the nephron in a living mouse, and when we did so, that it made a huge difference in terms of kidney damage," said Bolisetty, a post-doctoral scholar in Agarwal's laboratory. "Past attempts to universally remove ferritin caused the mice to die, and so the role of this protein has remained elusive."
Shift to kidneys
In recent years, researchers have revealed that system-wide iron metabolism is watched over by certain organs, with most focus to date on the liver and the intestines. The small intestine is the major absorptive organ (where iron enters the body from the diet), and the liver is the main regulator of the processes by which cells turn food into energy (e.g. metabolism) via hormones. Diseases associated with chronic iron overload, including certain types of anemia, and the related deposition of iron, occur in the liver in such clinical disorders.
The kidneys regulate the amount of water and electrolytes in the blood, maintaining the right pH balance for human cells to work and function. A normal kidney contains about a million nephrons, tubes that filter the blood to remove waste products from cellular life, but also to recapture blood sugar (glucose), amino acids and other metabolites and route them back into the blood for re-use. For this reason, the nephrons are closely linked by signaling pathways to those mitochondria in all cells that produce energy. Because of their close ties to metabolism, the cells lining the kidney tubules have lots of mitochondria inside them, so lots of iron-containing heme proteins are concentrated there.
Given its anatomy and intricate function, the proximal tubule segment of the nephron is predictably the most susceptible to various forms of injury. Multiple molecular mechanisms have been proposed that aggravate kidney damage, but free radical-induced kidney injury is recognized as among the most important. Despite the recognition of iron as a culprit in acute kidney injury, little was known going into the current study about the nephron's ability to cope with increased iron levels and protect it from injury.
Study Results
The team genetically engineered mice using a molecular technique that cut DNA coding for ferritin out only in cells with markers present in kidney nephrons. Doing so system-wide is fatal, because ferritin has been shown to have many crucial roles in many cell types. Shutting down the role of the protein only in kidney tubules enabled the team to pinpoint its role there, and in a live mouse for the first time.
Both normal mice and those with ferritin production removed in their kidney nephrons were treated with the chemotherapy agent, Cisplatin. The drug is known to create free radicals that kill tumor cells, but also to make heme groups in mitochondria spill iron into the cells, triggering free radical production that damages the kidneys. Compared to control mice that still had ferritin in their kidney tubules, the ferritin knockout mice saw a 40 percent worsening of kidney function after three days of Cisplatin treatment.
Levels of both of heme oxygenase-1 and ferritin are known to rise in response to the injury caused by Cisplatin, but the current study found that heme oxygenase-1, despite having some protective qualities, could not protect kidney nephrons from oxidative damage when ferritin was absent.
Source: UAB School of Medicine
The research team was able to genetically engineer a mouse model that clarified the role of ferritin in iron homeostasis, setting the stage for a new line of research into future treatments that may be able to prevent acute kidney damage caused by iron.
The study results revolve around iron, the most common chemical element on Earth and a core player in the biochemical processes of animals that evolved in its presence. The human body uses iron because its atomic structure can readily accept or donate negatively charged atomic components called electrons, shifting back and forth as needed. Cells, and in particular the powerhouses within cells called mitochondria, pass around electrons and harness charge to drive life processes and make cellular energy with the help of iron.
Unfortunately, that same, useful atomic flexibility means that iron free in the body will react with almost anything it encounters, disrupting charge balances and creating highly reactive free radicals that tear apart delicate structures like DNA, a mechanism by which trauma and many diseases kill tissue.
Thus, iron is almost always bound to transporter and chaperone proteins. When the body suffers a crushing injury, however, iron-containing heme proteins like myoglobin spill out of crushed tissue into the bloodstream, get caught in the blood-filtering nephrons in the kidney and die, releasing their iron. When less oxygen reaches kidney tubules from a failing heart, the lack disables the heme proteins in the kidney cells, causing them to spill the iron they contain and damage tissues.
The current study results confirm a protein called ferritin is among the most important of proteins charged with mopping up free iron. Beyond showing its ability to prevent iron-related cellular damage, UAB researchers and lead co-authors Abolfazl Zarjou, M.D., Ph.D., and Subhashini Bolisetty, Ph.D., say their study is the first to reveal the role of the kidney in the regulation of iron metabolism, a function until now linked to the liver and the intestines.
"Ferritin is a giant globe that sequesters 4,500 iron ions in safe form, thus preventing acute kidney injury," said Zarjou, who is part of the American Board of Internal Medicine Research Pathway at UAB. "If this mechanism is confirmed, and if we can find ways to manipulate H-ferritin, this work would provide a platform for targeting iron sequestration as a new therapy against acute kidney damage."
The study's corresponding author, Anupam Agarwal, M.D., is interim senior vice president for Medicine and dean of the UAB School of Medicine; he directs the National Institutes of Health-funded UAB-University of California San Diego O'Brien Core Center for Acute Kidney Injury Research. Agarwal's team of researchers has spent years studying whether or not a protein called heme oxygenase-1 might represent the most important part of the system that protects the body from iron-driven free radical production. This protein defense degrades heme to release iron, but it also sends signals to turn up ferritin production. The current study found that this enzyme has no protective value if ferritin is removed from the system, and it may be ferritin - not heme oxygenase-1 - that is the key mediator of protection from iron.
Ferritin's importance
The ferritin shell is made of 24 subunits of heavy and light protein chains, heavy just meaning that one chain is usually large in the pairs in which such chains typically occur. The ferritin heavy chain converts the more unstable form of iron (Fe2+ or the ferrous) to a more stable (Fe3+ or the ferric) form that can be the safely sequestered and deposited within the ferritin shell.
The research team had hypothesized that deletion of ferritin heavy chain in proximal tubules, the workhouse area of nephrons, would result in an increased amount of the free, unstable form of the iron (Fe2+) to exacerbate injury. In addition, any form of kidney injury would ultimately lead to increased cell death and liberation of iron from the intracellular space of necrotic cells in a vicious circle.
"This study represents a leap in the field because we showed that you can knock out ferritin just in the proximal part of the nephron in a living mouse, and when we did so, that it made a huge difference in terms of kidney damage," said Bolisetty, a post-doctoral scholar in Agarwal's laboratory. "Past attempts to universally remove ferritin caused the mice to die, and so the role of this protein has remained elusive."
Shift to kidneys
In recent years, researchers have revealed that system-wide iron metabolism is watched over by certain organs, with most focus to date on the liver and the intestines. The small intestine is the major absorptive organ (where iron enters the body from the diet), and the liver is the main regulator of the processes by which cells turn food into energy (e.g. metabolism) via hormones. Diseases associated with chronic iron overload, including certain types of anemia, and the related deposition of iron, occur in the liver in such clinical disorders.
The kidneys regulate the amount of water and electrolytes in the blood, maintaining the right pH balance for human cells to work and function. A normal kidney contains about a million nephrons, tubes that filter the blood to remove waste products from cellular life, but also to recapture blood sugar (glucose), amino acids and other metabolites and route them back into the blood for re-use. For this reason, the nephrons are closely linked by signaling pathways to those mitochondria in all cells that produce energy. Because of their close ties to metabolism, the cells lining the kidney tubules have lots of mitochondria inside them, so lots of iron-containing heme proteins are concentrated there.
Given its anatomy and intricate function, the proximal tubule segment of the nephron is predictably the most susceptible to various forms of injury. Multiple molecular mechanisms have been proposed that aggravate kidney damage, but free radical-induced kidney injury is recognized as among the most important. Despite the recognition of iron as a culprit in acute kidney injury, little was known going into the current study about the nephron's ability to cope with increased iron levels and protect it from injury.
Study Results
The team genetically engineered mice using a molecular technique that cut DNA coding for ferritin out only in cells with markers present in kidney nephrons. Doing so system-wide is fatal, because ferritin has been shown to have many crucial roles in many cell types. Shutting down the role of the protein only in kidney tubules enabled the team to pinpoint its role there, and in a live mouse for the first time.
Both normal mice and those with ferritin production removed in their kidney nephrons were treated with the chemotherapy agent, Cisplatin. The drug is known to create free radicals that kill tumor cells, but also to make heme groups in mitochondria spill iron into the cells, triggering free radical production that damages the kidneys. Compared to control mice that still had ferritin in their kidney tubules, the ferritin knockout mice saw a 40 percent worsening of kidney function after three days of Cisplatin treatment.
Levels of both of heme oxygenase-1 and ferritin are known to rise in response to the injury caused by Cisplatin, but the current study found that heme oxygenase-1, despite having some protective qualities, could not protect kidney nephrons from oxidative damage when ferritin was absent.
Source: UAB School of Medicine
Thursday
Breastfeeding can reduce risk of childhood obesity
Lowers body mass index for offspring of diabetic pregnancies
AURORA, Colo. (Feb. 8, 2012) – Children of diabetic pregnancies have a greater risk of childhood obesity, but new research from the Colorado School of Public Health shows breastfeeding can reduce this threat.
Epidemiologist Tessa Crume, Ph.D., MSPH, and fellow researchers tracked 94 children of diabetic pregnancies and 399 of non-diabetic pregnancies from birth to age 13. They evaluated the influence of breastfeeding on the growth of body mass index (BMI), an indicator of childhood obesity.
"There are critical perinatal periods for defining obesity risk, pregnancy and early infant life," Crume said. "We looked at children exposed to over-nutrition in utero due to a diabetic pregnancy to determine if early life nutrition could alter their risk of childhood obesity."
Children of diabetic pregnancies who were breast-fed had a slower BMI growth as they grew older than those who nursed less than six months. A similar pattern emerged for children of non-diabetic pregnancies.
According to Crume, researchers know that children exposed to diabetes or obesity during gestation are at higher risk for childhood obesity and metabolic diseases. Now they know there is a second critical opportunity to normalize BMI growth by encouraging mothers to breast-feed for at least six months, the time recommended by the Academy of Pediatrics.
"Breast-feeding support represents an important clinical and public health strategy to reduce the risk of childhood obesity," said Crume. She hopes the research will further encourage mothers to breast-feed, especially those who experienced a diabetic pregnancy.
"We can work with pediatricians, obstetricians and the public health community to give these women targeted support immediately following birth," she said.
The research, "The impact of neonatal breast-feeding on growth trajectories of youth exposed and unexposed to diabetes in utero: the EPOCH Study," appears in the latest edition of the International Journal of Obesity. It was conducted as a partnership between the Colorado School of Public Health and Kaiser Permanente of Colorado
AURORA, Colo. (Feb. 8, 2012) – Children of diabetic pregnancies have a greater risk of childhood obesity, but new research from the Colorado School of Public Health shows breastfeeding can reduce this threat.
Epidemiologist Tessa Crume, Ph.D., MSPH, and fellow researchers tracked 94 children of diabetic pregnancies and 399 of non-diabetic pregnancies from birth to age 13. They evaluated the influence of breastfeeding on the growth of body mass index (BMI), an indicator of childhood obesity.
"There are critical perinatal periods for defining obesity risk, pregnancy and early infant life," Crume said. "We looked at children exposed to over-nutrition in utero due to a diabetic pregnancy to determine if early life nutrition could alter their risk of childhood obesity."
Children of diabetic pregnancies who were breast-fed had a slower BMI growth as they grew older than those who nursed less than six months. A similar pattern emerged for children of non-diabetic pregnancies.
According to Crume, researchers know that children exposed to diabetes or obesity during gestation are at higher risk for childhood obesity and metabolic diseases. Now they know there is a second critical opportunity to normalize BMI growth by encouraging mothers to breast-feed for at least six months, the time recommended by the Academy of Pediatrics.
"Breast-feeding support represents an important clinical and public health strategy to reduce the risk of childhood obesity," said Crume. She hopes the research will further encourage mothers to breast-feed, especially those who experienced a diabetic pregnancy.
"We can work with pediatricians, obstetricians and the public health community to give these women targeted support immediately following birth," she said.
The research, "The impact of neonatal breast-feeding on growth trajectories of youth exposed and unexposed to diabetes in utero: the EPOCH Study," appears in the latest edition of the International Journal of Obesity. It was conducted as a partnership between the Colorado School of Public Health and Kaiser Permanente of Colorado
Monday
A gradient of childhood self-control predicts health, wealth, and public safety
Policy-makers are considering large-scale programs aimed at self-control to improve citizens’ health and wealth and reduce crime. Experimental and economic studies suggest such programs could reap benefits. Yet, is self-control important for the health, wealth, and public safety of the population? Following a cohort of 1,000 children from birth to the age of 32 y, we show that childhood self-control predicts physical health, substance dependence, personal finances, and criminal offending outcomes, following a gradient of self-control. Effects of children's self-control could be disentangled from their intelligence and social class as well as from mistakes they made as adolescents. In another cohort of 500 sibling-pairs, the sibling with lower self-control had poorer outcomes, despite shared family background. Interventions addressing self-control might reduce a panoply of societal costs, save taxpayers money, and promote prosperity.
Thursday
Evaluation of the Overweight/Obese Child
Evaluation of the Overweight/Obese Child – Practical Tips for the Primary Health Care Provider: Recommendations from the Childhood Obesity Task Force of the European Association for the Study of Obesity
Summary
The prevalence of obesity among children and adolescents is on the rise. The majority of overweight or obese children are treated by primary health care providers including paediatricians, family practitioners, dieticians, nurses, and school health services – and not by specialists. The majority of obese children have no underlying medical disorder causing their obesity yet a significant proportion might suffer from obesity-related co-morbidities. This text is aimed at providing simple and practical tools for the identification and management of children with or at risk of overweight and obesity in the primary care setting. The tips and tools provided are based on data from the recent body of work that has been published in this field, official statements of several scientific societies along with expert opinion provided by the members of the Childhood Obesity Task Force (COTF) of the European Association for the Study of Obesity (EASO). We have attempted to use an evidence-based approach while allowing flexibility for the practicing clinician in domains where evidence is currently lacking and ensuring that treating the obese child involves the entire family as well.
Jennifer L. Bakera, Nathalie J. Farpour-Lambertb, Paulina Nowickac, Angelo Pietrobellid, Ram Weisse
a Institute of Preventive Medicine, Centre for Health and Society, Copenhagen, Denmark
b Obesity Care Program, Pediatric Cardiology Unit, Department of Child and Adolescent, University Hospital of Geneva, Switzerland
c Childhood Obesity Unit, University Hospital, Malmö, Sweden
d Pediatric Unit, Verona University Medical School, Italy
e Department of Human Metabolism and Nutrition, Hebrew University School of Medicine, Jerusalem, Israel
Summary
The prevalence of obesity among children and adolescents is on the rise. The majority of overweight or obese children are treated by primary health care providers including paediatricians, family practitioners, dieticians, nurses, and school health services – and not by specialists. The majority of obese children have no underlying medical disorder causing their obesity yet a significant proportion might suffer from obesity-related co-morbidities. This text is aimed at providing simple and practical tools for the identification and management of children with or at risk of overweight and obesity in the primary care setting. The tips and tools provided are based on data from the recent body of work that has been published in this field, official statements of several scientific societies along with expert opinion provided by the members of the Childhood Obesity Task Force (COTF) of the European Association for the Study of Obesity (EASO). We have attempted to use an evidence-based approach while allowing flexibility for the practicing clinician in domains where evidence is currently lacking and ensuring that treating the obese child involves the entire family as well.
Jennifer L. Bakera, Nathalie J. Farpour-Lambertb, Paulina Nowickac, Angelo Pietrobellid, Ram Weisse
a Institute of Preventive Medicine, Centre for Health and Society, Copenhagen, Denmark
b Obesity Care Program, Pediatric Cardiology Unit, Department of Child and Adolescent, University Hospital of Geneva, Switzerland
c Childhood Obesity Unit, University Hospital, Malmö, Sweden
d Pediatric Unit, Verona University Medical School, Italy
e Department of Human Metabolism and Nutrition, Hebrew University School of Medicine, Jerusalem, Israel
Monday
Germ Cell Tumors Biomarker Guidlines
hCG and LDH concentrations above the normal range can occur with any germ cell tumor histology
June 11, 2010 (Chicago, Illinois) — The American Society of Clinical Oncology (ASCO) has issued a guideline on the use of serum tumor markers in the diagnosis, treatment, and management of germ cell tumors in men, which include, most commonly, testicular cancer.
The germ cell tumors clinical practice guideline was announced at a press conference here at the organization's 2010 Annual Meeting.
This is the newest guideline on the use of biomarkers for specific cancers from ASCO — with more to come as part of an "expanded series" of guidelines on biomarkers.
The initial 2 guidelines on biomarkers were on breast (2007) and gastrointestinal cancers (2006).
Why has ASCO chosen germ cell tumors, which are rare — with fewer than 9000 cases annually in the United States — for their third tumor marker guideline?
According to the panel of authors of the guideline, which was published online June 7 in the Journal of Clinical Oncology, it is "because of the large volume of publications and the long history of using serum concentrations of human chorionic gonadotropin (hCG), alpha-fetoprotein (AFP), and lactate dehydrogenase (LDH) to guide management decisions for patients with GCT."
In short, there is clinical value in using biomarkers to help manage patients with germ cell tumors, the authors explain
At the press conference, the new guideline's lead author, Timothy D. Gilligan, MD, from the Cleveland Clinic in Ohio, said that these 3 biomarkers for germ cell tumors "play a critical role in the management of these tumors."
He also hinted that some tumor markers might not be as clinically useful as the germ cell tumor markers.
Medical tests that measure tumor biomarkers are not as rigorously examined by the US Food and Drug Administration (FDA) as drugs are, he explained.
"The FDA doesn't require that marker products improve outcome. The products are only required to measure what they claim to measure," he told reporters at the press conference.
He called for "better evidence about whether tumor markers for other cancers help provide better care for patients." Specifically, he called for proof that the tumor-marker products "improve medical outcomes or quality of life."
The stakes can be high when patients undergo biomarker tests, Dr. Gilligan noted.
"Medical tests are dangerous," he said. "They can lead to a waterfall of further tests and unnecessary treatment."
Dr. Gilligan cited the use of prostate-specific antigen (PSA) as a screening test for prostate cancer as an example of a problematic biomarker that has produced overdiagnosis and overtreatment of disease. The introduction of the PSA screening test in the mid-1980s led to an estimated 1 million cases of overdiagnosis of prostate cancer by 2009, as reported by Medscape Oncology.
Dr. Gilligan called for improved tests to detect cancer. "We need better tests to detect treatable cancers earlier so that treatment will be more effective."
The future of tumor biomarkers promises to be busy, suggested Dr. Gilligan. "This is a big area of research. There are a lot of new products coming out along these lines," he said.
What's New in Germ Cell Tumor Markers
The expert panel convened by ASCO, which included Dr. Gilligan, conducted a systematic review of medical research literature, in partnership with Cancer Care Ontario, to develop the new recommendations on germ cell tumors and related serum tumor markers.
Germ cell tumors might be rare but they are also among the most curable cancers, with more than 90% of men cured, according to Dr. Gilligan. Germ cell tumors most commonly start in sperm-producing cells in the testicles. Testicular cancers are typically detected when the patient notices a swelling or irregularity in the shower or when dressing, Dr. Gilligan explained.
"Testicular cancer is curable in most cases, but proper management is key because the stakes are high, both for survival and quality of life," said Dr. Gilligan in a press statement.
AFP, hCG, and LDH should not be used to screen for germ cell tumors, to help decide whether orchiectomy is needed, or to make treatment decisions for patients with cancer of unknown origin, notes the guideline.
This news about the latter practice — using germ cell tumor markers to choose a chemotherapy regimen for patients with a cancer of unknown primary — is worth highlighting, noted Dr. Gilligan "This has been the practice, but the literature does not support use of tumor markers for this," he said.
The other most notable new recommendation, said Dr. Gilligan, is about serum tumor markers: they should not be used as part of "surveillance for stage I seminomas."
The diagnosis of germ cell tumors in men is divided into 2 different types — seminoma and nonseminoma, said Dr. Gilligan.
Generally, seminomas are relatively slow-growing; nonseminomas tend to grow and spread more quickly and are treated differently.
Seminoma cells do not produce AFP. As a result, concentrations above the normal range of AFP can occur in patients with nonseminomas but not in those with pure seminoma. In contrast, hCG and LDH concentrations above the normal range can occur with any germ cell tumor histology, write the authors of the new guideline.
A rise in these markers generally indicates disease relapse in patients who have been treated, said Dr. Gilligan.
However, as noted above, Dr. Gilligan and his colleagues recommend against using these markers as part of surveillance in stage I seminomas.
Dr. Gilligan has disclosed no relevant financial relationships.
J Clin Oncol. Published online June 7, 2010. Abstract
June 11, 2010 (Chicago, Illinois) — The American Society of Clinical Oncology (ASCO) has issued a guideline on the use of serum tumor markers in the diagnosis, treatment, and management of germ cell tumors in men, which include, most commonly, testicular cancer.
The germ cell tumors clinical practice guideline was announced at a press conference here at the organization's 2010 Annual Meeting.
This is the newest guideline on the use of biomarkers for specific cancers from ASCO — with more to come as part of an "expanded series" of guidelines on biomarkers.
The initial 2 guidelines on biomarkers were on breast (2007) and gastrointestinal cancers (2006).
Why has ASCO chosen germ cell tumors, which are rare — with fewer than 9000 cases annually in the United States — for their third tumor marker guideline?
According to the panel of authors of the guideline, which was published online June 7 in the Journal of Clinical Oncology, it is "because of the large volume of publications and the long history of using serum concentrations of human chorionic gonadotropin (hCG), alpha-fetoprotein (AFP), and lactate dehydrogenase (LDH) to guide management decisions for patients with GCT."
In short, there is clinical value in using biomarkers to help manage patients with germ cell tumors, the authors explain
At the press conference, the new guideline's lead author, Timothy D. Gilligan, MD, from the Cleveland Clinic in Ohio, said that these 3 biomarkers for germ cell tumors "play a critical role in the management of these tumors."
He also hinted that some tumor markers might not be as clinically useful as the germ cell tumor markers.
Medical tests that measure tumor biomarkers are not as rigorously examined by the US Food and Drug Administration (FDA) as drugs are, he explained.
"The FDA doesn't require that marker products improve outcome. The products are only required to measure what they claim to measure," he told reporters at the press conference.
He called for "better evidence about whether tumor markers for other cancers help provide better care for patients." Specifically, he called for proof that the tumor-marker products "improve medical outcomes or quality of life."
The stakes can be high when patients undergo biomarker tests, Dr. Gilligan noted.
"Medical tests are dangerous," he said. "They can lead to a waterfall of further tests and unnecessary treatment."
Dr. Gilligan cited the use of prostate-specific antigen (PSA) as a screening test for prostate cancer as an example of a problematic biomarker that has produced overdiagnosis and overtreatment of disease. The introduction of the PSA screening test in the mid-1980s led to an estimated 1 million cases of overdiagnosis of prostate cancer by 2009, as reported by Medscape Oncology.
Dr. Gilligan called for improved tests to detect cancer. "We need better tests to detect treatable cancers earlier so that treatment will be more effective."
The future of tumor biomarkers promises to be busy, suggested Dr. Gilligan. "This is a big area of research. There are a lot of new products coming out along these lines," he said.
What's New in Germ Cell Tumor Markers
The expert panel convened by ASCO, which included Dr. Gilligan, conducted a systematic review of medical research literature, in partnership with Cancer Care Ontario, to develop the new recommendations on germ cell tumors and related serum tumor markers.
Germ cell tumors might be rare but they are also among the most curable cancers, with more than 90% of men cured, according to Dr. Gilligan. Germ cell tumors most commonly start in sperm-producing cells in the testicles. Testicular cancers are typically detected when the patient notices a swelling or irregularity in the shower or when dressing, Dr. Gilligan explained.
"Testicular cancer is curable in most cases, but proper management is key because the stakes are high, both for survival and quality of life," said Dr. Gilligan in a press statement.
AFP, hCG, and LDH should not be used to screen for germ cell tumors, to help decide whether orchiectomy is needed, or to make treatment decisions for patients with cancer of unknown origin, notes the guideline.
This news about the latter practice — using germ cell tumor markers to choose a chemotherapy regimen for patients with a cancer of unknown primary — is worth highlighting, noted Dr. Gilligan "This has been the practice, but the literature does not support use of tumor markers for this," he said.
The other most notable new recommendation, said Dr. Gilligan, is about serum tumor markers: they should not be used as part of "surveillance for stage I seminomas."
The diagnosis of germ cell tumors in men is divided into 2 different types — seminoma and nonseminoma, said Dr. Gilligan.
Generally, seminomas are relatively slow-growing; nonseminomas tend to grow and spread more quickly and are treated differently.
Seminoma cells do not produce AFP. As a result, concentrations above the normal range of AFP can occur in patients with nonseminomas but not in those with pure seminoma. In contrast, hCG and LDH concentrations above the normal range can occur with any germ cell tumor histology, write the authors of the new guideline.
A rise in these markers generally indicates disease relapse in patients who have been treated, said Dr. Gilligan.
However, as noted above, Dr. Gilligan and his colleagues recommend against using these markers as part of surveillance in stage I seminomas.
Dr. Gilligan has disclosed no relevant financial relationships.
J Clin Oncol. Published online June 7, 2010. Abstract
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