WASHINGTON, D.C. – 7/17/2014 - Several members of Congress are pushing a bill to better protect consumers – particularly the elderly, pregnant women children, and workers – from a known toxic hormone disruptor bisphenol-A, or BPA.
Introduced by long-time champion Sen. Ed Markey (D-Mass.), the Ban Poisonous Additives Act of 2014 would ban BPA from food and beverage containers. It would also grant waivers to manufacturers seeking safer replacements for BPA while requiring them to place specific warning labels on any packaging that still contains the toxic substance. The legislation would also mandate the U.S. Food and Drug Administration to review the safety of all materials deemed safe for use in food and beverage containers .
Reps. Lois Capps (D-Calif.) and Grace Meng (D-N.Y.) introduced a companion bill in the House.
“Science shows that BPA is present in the vast majority of Americans and is harmful to human health,” said Jason Rano, EWG’s director of government affairs. “It has been linked to cancer, obesity, diabetes, infertility, hormone disruption and early puberty in children. Congress is taking an important step on behalf of our most vulnerable populations to help reduce exposure to BPA.”
BPA, a synthetic estrogen, is in the epoxy linings that coat the inside of most canned foods and beverages and ultimately leaches into those products. Some companies have voluntarily taken BPA out of the linings of their containers, and in 2012 the FDA banned BPA in baby bottles and children's sippy cups.
“It was an important step when the FDA banned BPA in baby bottles and sippy cups, but BPA has no place in food packaging and must be replaced with alternatives that don’t pose a serious health threats to humans,” added Rano. “This legislation would help make that a reality while providing manufacturers with the additional time they need to find safer options.”
EWG recommends that consumers limit their intake of canned food and beverages and look for products labeled “BPA-free” or packed in glass jars or cardboard cartons, not metal cans.
Source: Environmental Working Group
Showing posts with label Cancer. Show all posts
Showing posts with label Cancer. Show all posts
Study: Obesity Primes the Colon for Cancer
(NIH) - 4/5/2014 - Obesity, rather than diet, causes changes in the colon that may lead to colorectal cancer, according to a study in mice by the National Institutes of Health. The finding bolsters the recommendation that calorie control and frequent exercise are not only key to a healthy lifestyle, but a strategy to lower the risk for colon cancer, the second leading cause of cancer-related death in the United States.
Paul Wade, Ph.D., and Thomas Eling, Ph.D., scientists at the National Institute of Environmental Health Sciences (NIEHS), part of NIH, led a collaborative team that made the discovery. The study appeared online April 1 in the journal Cell Metabolism.
A large body of scientific literature says people who are obese are predisposed to a number of cancers, particularly colorectal cancer, Eling said. To better understand the processes behind this link, he and his colleagues fed two groups of mice a diet in which 60 percent of the calories came from lard. The first group of mice contained a human version of a gene called NAG-1, which has been shown to protect against colon cancer in other rodent studies. The second group lacked the NAG-1 gene.
The NAG-1 mice did not gain weight after eating the high-fat diet, while mice that lacked the NAG-1 gene grew plump.
The researchers noticed another striking difference between the two groups of animals.
“The obese mice exhibited molecular signals in their gut that led to the progression of cancer, but the NAG-1 mice didn’t have those same indicators,” Eling said.
The researchers looked for molecular clues, by isolating cells from the colons of the mice and analyzing a group of proteins called histones. Histones package and organize DNA in a cell’s nucleus, and sometimes undergo a process known as acetylation, in which chemical tags bind to their surface. The pattern of acetylation varies depending on the chemical processes taking place in the cell.
Wade explained that the acetylation patterns for the obese mice and the thin NAG-1 mice were drastically different. Patterns from the obese mice resembled those from mice with colorectal cancer. The additional weight they carried also seemed to activate more genes that are associated with colorectal cancer progression, suggesting the obese mice are predisposed to colon cancer.
“Any preexisting colon lesions in these animals are more likely to evolve rapidly into malignant tumors,” Wade said. “The same thing may happen in humans.”
Wade and Eling want to find out exactly how obesity prompts the body to develop colorectal cancer. Wade said that the likely candidates for triggering tumor growth in the colon are fat cells, but there are many more possibilities. Finding these cellular switches may give rise to production of medications to keep people from getting colorectal cancer.
“Once we identify the signaling pathways and understand how the signal is transduced, we may be able to design ways to treat colorectal cancer in obese patients,” Wade said.
Source: National Institutes of Health
Paul Wade, Ph.D., and Thomas Eling, Ph.D., scientists at the National Institute of Environmental Health Sciences (NIEHS), part of NIH, led a collaborative team that made the discovery. The study appeared online April 1 in the journal Cell Metabolism.
A large body of scientific literature says people who are obese are predisposed to a number of cancers, particularly colorectal cancer, Eling said. To better understand the processes behind this link, he and his colleagues fed two groups of mice a diet in which 60 percent of the calories came from lard. The first group of mice contained a human version of a gene called NAG-1, which has been shown to protect against colon cancer in other rodent studies. The second group lacked the NAG-1 gene.
The NAG-1 mice did not gain weight after eating the high-fat diet, while mice that lacked the NAG-1 gene grew plump.
The researchers noticed another striking difference between the two groups of animals.
“The obese mice exhibited molecular signals in their gut that led to the progression of cancer, but the NAG-1 mice didn’t have those same indicators,” Eling said.
The researchers looked for molecular clues, by isolating cells from the colons of the mice and analyzing a group of proteins called histones. Histones package and organize DNA in a cell’s nucleus, and sometimes undergo a process known as acetylation, in which chemical tags bind to their surface. The pattern of acetylation varies depending on the chemical processes taking place in the cell.
Wade explained that the acetylation patterns for the obese mice and the thin NAG-1 mice were drastically different. Patterns from the obese mice resembled those from mice with colorectal cancer. The additional weight they carried also seemed to activate more genes that are associated with colorectal cancer progression, suggesting the obese mice are predisposed to colon cancer.
“Any preexisting colon lesions in these animals are more likely to evolve rapidly into malignant tumors,” Wade said. “The same thing may happen in humans.”
Wade and Eling want to find out exactly how obesity prompts the body to develop colorectal cancer. Wade said that the likely candidates for triggering tumor growth in the colon are fat cells, but there are many more possibilities. Finding these cellular switches may give rise to production of medications to keep people from getting colorectal cancer.
“Once we identify the signaling pathways and understand how the signal is transduced, we may be able to design ways to treat colorectal cancer in obese patients,” Wade said.
Source: National Institutes of Health
Cancer Study Reveals Potential Drug Targets
(NIH) - 1/31/2014 - Investigators with The Cancer Genome Atlas (TCGA) Research Network have identified new potential therapeutic targets for a major form of bladder cancer, including important genes and pathways that are disrupted in the disease. They also discovered that, at the molecular level, some subtypes of bladder cancer — also known as urothelial carcinoma — resemble subtypes of breast, head and neck and lung cancers, suggesting similar routes of development.
The researchers’ findings provide important insights into the mechanisms underlying bladder cancer, which is estimated to cause more than 15,000 deaths in the United States in 2014. TCGA is a collaboration jointly supported and managed by the National Cancer Institute (NCI) and the National Human Genome Research Institute (NHGRI), both parts of the National Institutes of Health.
“TCGA Research Network scientists continue to unravel the genomic intricacies of many common and often intractable cancers, and these findings are defining new research directions and accelerating the development of new cancer therapies,” NIH Director Francis Collins said.
In this study, published online Jan. 29, 2014 in Nature, investigators examined bladder cancer that invades the muscle of the bladder, the deadliest form of the disease. The current standard treatments for muscle-invasive bladder cancer include surgery and radiation combined with chemotherapy. There are no recognized second-line therapies — second choices for treatments when the initial therapy does not work — and no approved targeted agents for this type of bladder cancer. Approximately 72,000 new cases of bladder cancer will be diagnosed in the United States in 2014.
“This project has dramatically improved our understanding of the molecular basis of bladder cancers and their relationship to other cancer types,” said lead author John Weinstein, M.D., Ph.D., professor and chair of the Department of Bioinformatics and Computational Biology at The University of Texas M.D. Anderson Cancer Center in Houston. “In the long run, the potential molecular targets identified may help us to personalize therapy based on the characteristics of each patient’s tumor.”
“The real excitement about this project is that we now have a menu of treatment and research directions to pursue,” said Seth Lerner, M.D., professor and chair in urologic oncology at Baylor College of Medicine in Houston, and one of the senior authors of the paper. “The field is poised to use this information to make new advances toward therapies for a very-difficult-to-treat form of bladder cancer.”
The research team analyzed DNA, RNA and protein data generated from the study of 131 muscle-invasive bladder cancer from patients who had not yet been treated with chemotherapy. The scientists found recurrent mutations in 32 genes, including nine that were not previously known to be significantly mutated. They discovered mutations in the TP53 gene in nearly half of the tumor samples, and mutations and other aberrations in the RTK/RAS pathway (which is commonly affected in cancers) in 44 percent of tumors. TP53 makes the p53 tumor suppressor protein, which helps regulate cell division. RTK/RAS is involved in regulating cell growth and development.
The investigators also showed that genes that regulate chromatin — a combination of DNA and protein within a cell’s nucleus that determines how genes are expressed — were more frequently mutated in bladder cancer than in any other common cancer studied to date. These findings suggest the possibility of developing therapies to target alterations in chromatin remodeling.
Overall, the researchers identified potential drug targets in 69 percent of the tumors evaluated. They found frequent mutations in the ERBB2, or HER2, gene. The researchers also identified recurring mutations as well as fusions involving other genes such as FGFR3 and in the PI3-kinase/AKT/mTOR pathway, which help control cell division and growth and for which targeted drugs already exist.
Because the HER2 gene and its encoded protein, HER2 — which affects cell growth and development — are implicated in a significant portion of breast cancers, scientists would like to find out if new agents under development against breast cancer can also be effective in treating subsets of bladder cancer patients.
“We’ve organized our medical care around the affected organ system,” Dr. Lerner said. “We have thought of each of these cancers as having its own characteristics unique to the affected organ. Increasingly, we are finding that cancers cross those lines at the molecular level, where some individual cancers affecting different organs look very similar. As targeted drug agents go through preclinical and clinical development, we hope that rather than treating 10 percent of breast cancers or 5 percent of bladder cancers, it eventually will make sense to treat multiple cancer types where the target is expressed.” The same theme runs through TCGA’s Pan-Cancer project, which is aimed at identifying genomic similarities across cancer types, with the goal of gaining a more global understanding of cancer behavior and development.
“It is increasingly evident that there are genomic commonalities among cancers that we can take advantage of in the future,” NHGRI Director Eric Green said. “TCGA is providing us with a repertoire of possibilities for developing new cancer therapeutics.”
The scientists also uncovered a potential viral connection to bladder cancer. It is known that animal papilloma viruses can cause bladder cancer. In a small number of cases, DNA from viruses — notably, from HPV16, a form of the virus responsible for cervical cancer — was found in bladder tumors. This suggests that viral infection can contribute to bladder cancer development.
Tobacco is a major risk factor for bladder cancer; more than 70 percent of the cases analyzed in this study occurred in former or current smokers. However, the analysis did not identify major molecular differences between the tumors that developed in patients with or without a history of smoking.
“The definitive molecular portrait of bladder cancer by the TCGA Network has uncovered a promising array of potential therapeutic targets that provides a blueprint for investigations into the activity of existing and novel therapeutic agents in this cancer,” said Louis Staudt, M.D., Ph.D., director, NCI Center for Cancer Genomics.
The researchers’ findings provide important insights into the mechanisms underlying bladder cancer, which is estimated to cause more than 15,000 deaths in the United States in 2014. TCGA is a collaboration jointly supported and managed by the National Cancer Institute (NCI) and the National Human Genome Research Institute (NHGRI), both parts of the National Institutes of Health.
“TCGA Research Network scientists continue to unravel the genomic intricacies of many common and often intractable cancers, and these findings are defining new research directions and accelerating the development of new cancer therapies,” NIH Director Francis Collins said.
In this study, published online Jan. 29, 2014 in Nature, investigators examined bladder cancer that invades the muscle of the bladder, the deadliest form of the disease. The current standard treatments for muscle-invasive bladder cancer include surgery and radiation combined with chemotherapy. There are no recognized second-line therapies — second choices for treatments when the initial therapy does not work — and no approved targeted agents for this type of bladder cancer. Approximately 72,000 new cases of bladder cancer will be diagnosed in the United States in 2014.
“This project has dramatically improved our understanding of the molecular basis of bladder cancers and their relationship to other cancer types,” said lead author John Weinstein, M.D., Ph.D., professor and chair of the Department of Bioinformatics and Computational Biology at The University of Texas M.D. Anderson Cancer Center in Houston. “In the long run, the potential molecular targets identified may help us to personalize therapy based on the characteristics of each patient’s tumor.”
“The real excitement about this project is that we now have a menu of treatment and research directions to pursue,” said Seth Lerner, M.D., professor and chair in urologic oncology at Baylor College of Medicine in Houston, and one of the senior authors of the paper. “The field is poised to use this information to make new advances toward therapies for a very-difficult-to-treat form of bladder cancer.”
The research team analyzed DNA, RNA and protein data generated from the study of 131 muscle-invasive bladder cancer from patients who had not yet been treated with chemotherapy. The scientists found recurrent mutations in 32 genes, including nine that were not previously known to be significantly mutated. They discovered mutations in the TP53 gene in nearly half of the tumor samples, and mutations and other aberrations in the RTK/RAS pathway (which is commonly affected in cancers) in 44 percent of tumors. TP53 makes the p53 tumor suppressor protein, which helps regulate cell division. RTK/RAS is involved in regulating cell growth and development.
The investigators also showed that genes that regulate chromatin — a combination of DNA and protein within a cell’s nucleus that determines how genes are expressed — were more frequently mutated in bladder cancer than in any other common cancer studied to date. These findings suggest the possibility of developing therapies to target alterations in chromatin remodeling.
Overall, the researchers identified potential drug targets in 69 percent of the tumors evaluated. They found frequent mutations in the ERBB2, or HER2, gene. The researchers also identified recurring mutations as well as fusions involving other genes such as FGFR3 and in the PI3-kinase/AKT/mTOR pathway, which help control cell division and growth and for which targeted drugs already exist.
Because the HER2 gene and its encoded protein, HER2 — which affects cell growth and development — are implicated in a significant portion of breast cancers, scientists would like to find out if new agents under development against breast cancer can also be effective in treating subsets of bladder cancer patients.
“We’ve organized our medical care around the affected organ system,” Dr. Lerner said. “We have thought of each of these cancers as having its own characteristics unique to the affected organ. Increasingly, we are finding that cancers cross those lines at the molecular level, where some individual cancers affecting different organs look very similar. As targeted drug agents go through preclinical and clinical development, we hope that rather than treating 10 percent of breast cancers or 5 percent of bladder cancers, it eventually will make sense to treat multiple cancer types where the target is expressed.” The same theme runs through TCGA’s Pan-Cancer project, which is aimed at identifying genomic similarities across cancer types, with the goal of gaining a more global understanding of cancer behavior and development.
“It is increasingly evident that there are genomic commonalities among cancers that we can take advantage of in the future,” NHGRI Director Eric Green said. “TCGA is providing us with a repertoire of possibilities for developing new cancer therapeutics.”
The scientists also uncovered a potential viral connection to bladder cancer. It is known that animal papilloma viruses can cause bladder cancer. In a small number of cases, DNA from viruses — notably, from HPV16, a form of the virus responsible for cervical cancer — was found in bladder tumors. This suggests that viral infection can contribute to bladder cancer development.
Tobacco is a major risk factor for bladder cancer; more than 70 percent of the cases analyzed in this study occurred in former or current smokers. However, the analysis did not identify major molecular differences between the tumors that developed in patients with or without a history of smoking.
“The definitive molecular portrait of bladder cancer by the TCGA Network has uncovered a promising array of potential therapeutic targets that provides a blueprint for investigations into the activity of existing and novel therapeutic agents in this cancer,” said Louis Staudt, M.D., Ph.D., director, NCI Center for Cancer Genomics.
Reference
The Cancer Genome Atlas Research Network. Comprehensive molecular characterization of urothelial bladder carcinoma. Nature. Online January 29, 2014. DOI: 10.1038/nature12965.
Genetic link found between fetal growth, cancer
(NIH) - 4/16/2013 - Two researchers at the National Institutes of Health discovered a new genetic link between the rapid growth of healthy fetuses and the uncontrolled cell division in cancer. The findings shed light on normal development and on the genetic underpinnings of common cancers.
The work, conducted using mouse and human tissue, appears in a recent issue of the Proceedings of the National Academy of Sciences. The authors, Julian C. Lui, Ph.D., and Jeffrey Baron, M.D., work at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD).
“We’ve long known that some of the genes that promote rapid growth in prenatal and early postnatal life become reactivated in cancer cells,” Baron said. “Now we’ve identified a molecular switch that appears to turn on some of these genes, taking us a step forward in understanding normal body growth and the abnormal growth in some types of cancer.”
Before birth, a team of more than 200 growth-promoting genes is highly active, fueling the fetus’ explosive growth. After birth, these genes are gradually switched off, apparently to slow body growth as we age and approach adult size. In cancer cells, some of these genes can be switched back on.
One of the major growth-promoting genes is called IGF2. This gene is critical for normal prenatal body growth and is reactivated in many types of cancer, showing remarkably high activity in bladder and prostate cancer and some childhood cancers.
For years, scientists did not know what turned IGF2 on and off. Now, using a variety of techniques and tissue types, Drs. Lui and Baron found evidence that a protein known as E2F3 activates the IGF2 gene in normal development and in cancer — in particular, in bladder and metastatic prostate cancers.
More broadly, E2F3 appears to regulate not just IGF2, but also many other genes on the body-growth team. When E2F3 levels are high, these genes are active. When E2F3 takes a dive, so do these genes. The upshot is that E2F3 may function as one of the master switches that limit body growth. As such, it is of great interest as researchers seek to understand the complex genetic choreography responsible for normal growth and the diseases that result when it goes awry.
Source: National Institutes of Health
The work, conducted using mouse and human tissue, appears in a recent issue of the Proceedings of the National Academy of Sciences. The authors, Julian C. Lui, Ph.D., and Jeffrey Baron, M.D., work at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD).
“We’ve long known that some of the genes that promote rapid growth in prenatal and early postnatal life become reactivated in cancer cells,” Baron said. “Now we’ve identified a molecular switch that appears to turn on some of these genes, taking us a step forward in understanding normal body growth and the abnormal growth in some types of cancer.”
Before birth, a team of more than 200 growth-promoting genes is highly active, fueling the fetus’ explosive growth. After birth, these genes are gradually switched off, apparently to slow body growth as we age and approach adult size. In cancer cells, some of these genes can be switched back on.
One of the major growth-promoting genes is called IGF2. This gene is critical for normal prenatal body growth and is reactivated in many types of cancer, showing remarkably high activity in bladder and prostate cancer and some childhood cancers.
For years, scientists did not know what turned IGF2 on and off. Now, using a variety of techniques and tissue types, Drs. Lui and Baron found evidence that a protein known as E2F3 activates the IGF2 gene in normal development and in cancer — in particular, in bladder and metastatic prostate cancers.
More broadly, E2F3 appears to regulate not just IGF2, but also many other genes on the body-growth team. When E2F3 levels are high, these genes are active. When E2F3 takes a dive, so do these genes. The upshot is that E2F3 may function as one of the master switches that limit body growth. As such, it is of great interest as researchers seek to understand the complex genetic choreography responsible for normal growth and the diseases that result when it goes awry.
Source: National Institutes of Health
Study: Certain Leukemias Related to Treatment
(NIH) - 2/22/2013 0 - A new study describes the pattern of risk for one form of cancer, acute myeloid leukemia (AML), that has risen over the past three decades for adults who have previously been treated with chemotherapy for other forms of cancer, notably non-Hodgkin’s lymphoma.
The findings, from researchers at the National Cancer Institute (NCI), part of NIH, and colleagues, appeared online in Blood on Feb.14, 2013. Although these findings were based on small numbers of patients, they are intriguing in light of recent changes in treatment practices for these cancer patients.
The researchers noted that chemotherapy is often a very effective treatment for cancer, and the subsequent risk of leukemia is generally low for an individual patient. The authors indicated that the increased risk among NHL survivors could be due to prolonged survival in recent years for some lymphoma subtypes that are associated with multiple courses of chemotherapy.
Over the study time period, the researchers observed declining risk among patients treated for ovarian cancer, myeloma, and possibly lung cancer. The decreased risk among patients with ovarian cancer is consistent with a shift from use of an alkylating agent called melphalan to platinum-based chemotherapy in the early 1980s.
“It has long been known that some types of chemotherapy are associated with a high risk of developing subsequent leukemia, particularly when treatments include certain alkylating agents,” said lead author Lindsay Morton, Ph.D., in NCI’s Radiation Epidemiology Branch in the Division of Cancer Epidemiology and Genetics. “The goal of this study was to better understand how cancer patients’ risk of developing leukemia has changed over time.”
The authors also found evidence that the risk of treatment-related AML has increased since 2000 among patients treated for esophageal, prostate, and cervical cancer and since the 1990s among patients treated for cancers of the bones and joints and of the endometrium.
Morton and colleagues used data from NCI’s Surveillance Epidemiology and End Results (SEER) cancer registries to evaluate the risk of leukemia in more than 426,000 adults who had been diagnosed with cancer between 1975 and 2008 and who had received chemotherapy as part of their initial cancer treatment.
The findings, from researchers at the National Cancer Institute (NCI), part of NIH, and colleagues, appeared online in Blood on Feb.14, 2013. Although these findings were based on small numbers of patients, they are intriguing in light of recent changes in treatment practices for these cancer patients.
The researchers noted that chemotherapy is often a very effective treatment for cancer, and the subsequent risk of leukemia is generally low for an individual patient. The authors indicated that the increased risk among NHL survivors could be due to prolonged survival in recent years for some lymphoma subtypes that are associated with multiple courses of chemotherapy.
Over the study time period, the researchers observed declining risk among patients treated for ovarian cancer, myeloma, and possibly lung cancer. The decreased risk among patients with ovarian cancer is consistent with a shift from use of an alkylating agent called melphalan to platinum-based chemotherapy in the early 1980s.
“It has long been known that some types of chemotherapy are associated with a high risk of developing subsequent leukemia, particularly when treatments include certain alkylating agents,” said lead author Lindsay Morton, Ph.D., in NCI’s Radiation Epidemiology Branch in the Division of Cancer Epidemiology and Genetics. “The goal of this study was to better understand how cancer patients’ risk of developing leukemia has changed over time.”
The authors also found evidence that the risk of treatment-related AML has increased since 2000 among patients treated for esophageal, prostate, and cervical cancer and since the 1990s among patients treated for cancers of the bones and joints and of the endometrium.
Morton and colleagues used data from NCI’s Surveillance Epidemiology and End Results (SEER) cancer registries to evaluate the risk of leukemia in more than 426,000 adults who had been diagnosed with cancer between 1975 and 2008 and who had received chemotherapy as part of their initial cancer treatment.
Among these patients, the authors identified 801 people who subsequently developed AML. Because the data came from SEER cancer registries, information on specific drugs used to treat each individual patient was not available. A unique feature of the study was the ability to evaluate leukemia risks in a large number of patients treated with chemotherapy in the current treatment era (2001-2008).
The researchers say it is important to identify patient groups that have the highest risks of treatment-related leukemia, particularly for patients with cancers that have favorable survival potential, so that efforts to prevent a return of the disease can be implemented where possible. Future studies are needed to gather information on the risks associated with specific chemotherapy agents, which could not be obtained from this study.
“In addition, it will be interesting to evaluate the role of a patient’s genetic susceptibility to treatment-related leukemia,” added Morton. “If certain inherited traits predispose patients to a second malignancy as a result of treatment, clinicians could more accurately weigh the risk of leukemia against the established benefits of chemotherapy.”
“In addition, it will be interesting to evaluate the role of a patient’s genetic susceptibility to treatment-related leukemia,” added Morton. “If certain inherited traits predispose patients to a second malignancy as a result of treatment, clinicians could more accurately weigh the risk of leukemia against the established benefits of chemotherapy.”
Source: National Institutes of Health
Link identified between metabolism, breast cancer
(NIH) - 2/6/2013 - A protein associated with conditions of metabolic imbalance, such as diabetes and obesity, may play a role in the development of aggressive forms of breast cancer, according to new findings by researchers at the National Cancer Institute (NCI), part of the National Institutes of Health, and their colleagues. Metabolic imbalance is often caused by elevated carbohydrate intake, which can lead to over-activating a molecule called C-terminal binding protein (CtBP). This over-activation, in turn, can increase the risk of breast cancer. Results of their work appeared in Nature Communications, Feb. 5, 2013.
“Modifying diet and maintaining a healthy diet, combined with developing pharmacological ways of lessening CtBP activity, may one day lead to a way to break the link between cancer and obesity,” said Kevin Gardner, M.D., Ph.D., head of NCI’s Transcription Regulation Section, Genetics Branch.
It has been known, primarily through population based studies, that there is a strong link between obesity and cancer. But the mechanism behind this link has been uncertain. A previous study conceived and carried out in Gardner’s laboratory found that CtBP repressed expression of a gene associated with breast cancer (BRCA1) at an early age by sensing when the cell was in a high metabolic state that, in turn, led to processing large amounts of carbohydrates in the body.
This early study suggested that obesity and weight gain may contribute to breast cancer by decreasing the level of the BRCA1 tumor suppressor gene expression in response to high carbohydrate intake. This explains, in part, why women who have hereditary mutations of BRCA1 also experience an increased risk of breast cancer if they gain weight.
Gardner’s new study expands upon his past work. He analyzed prior gene expression studies to determine if gene pathways, repressed by CtBP, were diminished in breast cancer patients who suffered from more aggressive clinical outcomes. Gardner’s team began first with the human breast cancer cells in the laboratory. They measured the association of CtBP and the genes it bound to in order to regulate expression. The researchers combined this approach with genome sequencing to confirm how, and where, CtBP bound to genes associated with breast cancer. Next, they integrated analyses with gene expression studies in cells in which they observed decreased the levels of CtBP by RNA interference (a process that inhibits gene expression), or by decreasing carbohydrate feeding of the cells.
The scientists found that, under conditions where they decreased the levels of CtBP, DNA repair increased and the cells developed stability and growth control. They determined that gene pathways targeted by CtBP were also disrupted in more aggressive breast cancers. Moreover, patients with high levels of CtBP in their tumors had shortened survival. And they showed that a small molecular inhibitor previously shown to bind to CtBP was able to reverse the gene-repressive effects of CtBP in breast cancer cells even under conditions of high carbohydrate feeding.
“Our new work suggests that targeting CtBP may provide a way of treating breast cancer and possibly preventing breast cancer,” Gardner said. “Research should continue to focus on the link between obesity, CtBP and breast cancer. This will require more population-based studies and multi-disciplinary teams of scientist to investigate these links.”
This project was funded by NCI project number 1Z01BC010847-01.
Source: National Institutes of Health
“Modifying diet and maintaining a healthy diet, combined with developing pharmacological ways of lessening CtBP activity, may one day lead to a way to break the link between cancer and obesity,” said Kevin Gardner, M.D., Ph.D., head of NCI’s Transcription Regulation Section, Genetics Branch.
It has been known, primarily through population based studies, that there is a strong link between obesity and cancer. But the mechanism behind this link has been uncertain. A previous study conceived and carried out in Gardner’s laboratory found that CtBP repressed expression of a gene associated with breast cancer (BRCA1) at an early age by sensing when the cell was in a high metabolic state that, in turn, led to processing large amounts of carbohydrates in the body.
This early study suggested that obesity and weight gain may contribute to breast cancer by decreasing the level of the BRCA1 tumor suppressor gene expression in response to high carbohydrate intake. This explains, in part, why women who have hereditary mutations of BRCA1 also experience an increased risk of breast cancer if they gain weight.
Gardner’s new study expands upon his past work. He analyzed prior gene expression studies to determine if gene pathways, repressed by CtBP, were diminished in breast cancer patients who suffered from more aggressive clinical outcomes. Gardner’s team began first with the human breast cancer cells in the laboratory. They measured the association of CtBP and the genes it bound to in order to regulate expression. The researchers combined this approach with genome sequencing to confirm how, and where, CtBP bound to genes associated with breast cancer. Next, they integrated analyses with gene expression studies in cells in which they observed decreased the levels of CtBP by RNA interference (a process that inhibits gene expression), or by decreasing carbohydrate feeding of the cells.
The scientists found that, under conditions where they decreased the levels of CtBP, DNA repair increased and the cells developed stability and growth control. They determined that gene pathways targeted by CtBP were also disrupted in more aggressive breast cancers. Moreover, patients with high levels of CtBP in their tumors had shortened survival. And they showed that a small molecular inhibitor previously shown to bind to CtBP was able to reverse the gene-repressive effects of CtBP in breast cancer cells even under conditions of high carbohydrate feeding.
“Our new work suggests that targeting CtBP may provide a way of treating breast cancer and possibly preventing breast cancer,” Gardner said. “Research should continue to focus on the link between obesity, CtBP and breast cancer. This will require more population-based studies and multi-disciplinary teams of scientist to investigate these links.”
This project was funded by NCI project number 1Z01BC010847-01.
Source: National Institutes of Health
CT Scans Linked to Leukemia, Brain Cancer
(NIH) - 6/12/2012 - Children and young adults scanned multiple times by computed tomography (CT), a commonly used diagnostic tool, have a small increased risk of leukemia and brain tumors in the decade following their first scan. These findings are from a study of more than 175,000 children and young adults that was led by researchers at the National Cancer Institute (NCI), part of the National Institutes of Health, and at the Institute of Health and Society, Newcastle University, England.
The researchers emphasize that when a child suffers a major head injury or develops a life-threatening illness, the benefits of clinically appropriate CT scans should outweigh future cancer risks. The results of the study were published online in The Lancet on June 7.
"This cohort study provides the first direct evidence of a link between exposure to radiation from CT and cancer risk in children," said senior investigator Amy Berrington de González, Ph.D., Division of Cancer Epidemiology and Genetics, NCI. "Ours is the first population-based study to capture data on every CT scan to an individual during childhood or young adulthood and then measure the subsequent cancer risk."
Despite the elevation in cancer risk, these two malignancies are relatively rare and the actual number of additional cases caused by radiation exposure from CT scans is small. The most recent (2009) U.S. annual cancer incidence rates for children from birth through age 21 for leukemia and brain and other nervous system cancers are 4.3 per 100,000 and 2.9 per 100,000, respectively. The investigators estimate that for every 10,000 head CT scans performed on children 10 years of age or younger, one case of leukemia and one brain tumor would occur in the decade following the first CT beyond what would have been expected had no CT scans been performed.
CT scans deliver a dose of ionizing radiation to the body part being scanned and to nearby tissues. Even at relatively low doses, ionizing radiation can break the chemical bonds in DNA, causing damage to genes that may increase a person’s risk of developing cancer. Children typically face a higher risk of cancer from ionizing radiation exposure than do adults exposed to similar doses.
The investigators obtained CT examination records from radiology departments in hospitals across Britain and linked them to data on cancer diagnoses and deaths. The study included people who underwent CT scans at British National Health Service hospitals from birth to 22 years of age between 1985 and 2002. Information on cancer incidence and mortality from 1985 through 2008 was obtained from the National Health Service Central Registry, a national database of cancer registrations, deaths and emigrations.
Approximately sixty percent of the CT scans were of the head, with similar proportions in males and females. The investigators estimated cumulative doses from the CT scans received by each patient, and assessed the subsequent cancer risk for an average of 10 years after the first CT. The researchers found a clear relationship between the increase in cancer risk and increasing cumulative dose of radiation. A three-fold increase in the risk of brain tumors appeared following a cumulative absorbed dose to the head of 50 to 60 milligray (abbreviated mGy, which is a unit of estimated absorbed dose of ionizing radiation). Similarly, a three-fold increase in the risk of leukemia appeared after the same dose to bone marrow (the part of the body responsible for generating blood cells). The comparison group consisted of individuals who had cumulative doses of less than 5 mGy to the relevant regions of the body.
The absorbed dose from a CT scan depends on factors including age at exposure, sex, examination type, and year of scan. Broadly speaking, two or three CT scans of the head using current scanner settings would be required to yield a dose of 50 to 60 mGy to the brain. The same dose to bone marrow would be produced by five to 10 head CT scans, using current scanner settings for children under age 15.
In countries like the United States and Britain, the use of CT scans in children and adults has increased rapidly since their introduction 30 years ago. Due to efforts by medical societies, government regulators, and CT manufacturers, scans performed on young children in 2012 can have 50 percent lower radiation doses, compared to scans carried out in the 1980s and 1990s, say the investigators. However, the amount of radiation delivered during a single CT scan can still vary greatly and is often up to 10 times higher than that delivered in a conventional X-ray procedure.
The lead author of the study was Mark S. Pearce, Ph.D., Institute of Health and Society, Newcastle University. “CT can be highly beneficial for early diagnosis, for clinical decision-making, and for saving lives. However, greater efforts should be made to ensure clinical justification and to keep doses as low as reasonably achievable,” Pearce said.
The researchers emphasize that when a child suffers a major head injury or develops a life-threatening illness, the benefits of clinically appropriate CT scans should outweigh future cancer risks. The results of the study were published online in The Lancet on June 7.
"This cohort study provides the first direct evidence of a link between exposure to radiation from CT and cancer risk in children," said senior investigator Amy Berrington de González, Ph.D., Division of Cancer Epidemiology and Genetics, NCI. "Ours is the first population-based study to capture data on every CT scan to an individual during childhood or young adulthood and then measure the subsequent cancer risk."
Despite the elevation in cancer risk, these two malignancies are relatively rare and the actual number of additional cases caused by radiation exposure from CT scans is small. The most recent (2009) U.S. annual cancer incidence rates for children from birth through age 21 for leukemia and brain and other nervous system cancers are 4.3 per 100,000 and 2.9 per 100,000, respectively. The investigators estimate that for every 10,000 head CT scans performed on children 10 years of age or younger, one case of leukemia and one brain tumor would occur in the decade following the first CT beyond what would have been expected had no CT scans been performed.
CT scans deliver a dose of ionizing radiation to the body part being scanned and to nearby tissues. Even at relatively low doses, ionizing radiation can break the chemical bonds in DNA, causing damage to genes that may increase a person’s risk of developing cancer. Children typically face a higher risk of cancer from ionizing radiation exposure than do adults exposed to similar doses.
The investigators obtained CT examination records from radiology departments in hospitals across Britain and linked them to data on cancer diagnoses and deaths. The study included people who underwent CT scans at British National Health Service hospitals from birth to 22 years of age between 1985 and 2002. Information on cancer incidence and mortality from 1985 through 2008 was obtained from the National Health Service Central Registry, a national database of cancer registrations, deaths and emigrations.
Approximately sixty percent of the CT scans were of the head, with similar proportions in males and females. The investigators estimated cumulative doses from the CT scans received by each patient, and assessed the subsequent cancer risk for an average of 10 years after the first CT. The researchers found a clear relationship between the increase in cancer risk and increasing cumulative dose of radiation. A three-fold increase in the risk of brain tumors appeared following a cumulative absorbed dose to the head of 50 to 60 milligray (abbreviated mGy, which is a unit of estimated absorbed dose of ionizing radiation). Similarly, a three-fold increase in the risk of leukemia appeared after the same dose to bone marrow (the part of the body responsible for generating blood cells). The comparison group consisted of individuals who had cumulative doses of less than 5 mGy to the relevant regions of the body.
The absorbed dose from a CT scan depends on factors including age at exposure, sex, examination type, and year of scan. Broadly speaking, two or three CT scans of the head using current scanner settings would be required to yield a dose of 50 to 60 mGy to the brain. The same dose to bone marrow would be produced by five to 10 head CT scans, using current scanner settings for children under age 15.
In countries like the United States and Britain, the use of CT scans in children and adults has increased rapidly since their introduction 30 years ago. Due to efforts by medical societies, government regulators, and CT manufacturers, scans performed on young children in 2012 can have 50 percent lower radiation doses, compared to scans carried out in the 1980s and 1990s, say the investigators. However, the amount of radiation delivered during a single CT scan can still vary greatly and is often up to 10 times higher than that delivered in a conventional X-ray procedure.
The lead author of the study was Mark S. Pearce, Ph.D., Institute of Health and Society, Newcastle University. “CT can be highly beneficial for early diagnosis, for clinical decision-making, and for saving lives. However, greater efforts should be made to ensure clinical justification and to keep doses as low as reasonably achievable,” Pearce said.
NIH Study: Arsenic Turns Stem Cells Cancerous
(NIH) - 4/7/2011 - Researchers at the National Institutes of Health have discovered how exposure to arsenic can turn normal stem cells into cancer stem cells and spur tumor growth. Inorganic arsenic, which affects the drinking water of millions of people worldwide, has been previously shown to be a human carcinogen. A growing body of evidence suggests that cancer is a stem-cell based disease. Normal stem cells are essential to normal tissue regeneration, and to the stability of organisms and processes. But cancer stem cells are thought to be the driving force for the formation, growth, and spread of tumors.
Michael Waalkes, Ph.D., and his team at the National Toxicology Program Laboratory, National Institute of Environmental Health Sciences, part of NIH, had shown previously that normal cells become cancerous when they are treated with inorganic arsenic. This new study shows that when these cancer cells are placed near, but not in contact with normal stem cells, the normal stem cells very rapidly acquire the characteristics of cancer stem cells. It demonstrates that malignant cells are able to send molecular signals through a semi-permeable membrane, where cells can't normally pass, and turn the normal stem cells into cancer stem cells.
“This paper shows a different and unique way that cancers can expand by recruiting nearby normal stem cells and creating an overabundance of cancer stem cells,” Waalkes said. “The recruitment of normal stem cells into cancer stem cells could have broad implications for the carcinogenic process in general, including tumor growth and metastases.”
This reveals a potentially important aspect of arsenic carcinogenesis and may help explain observances by researchers working with arsenic that arsenic often causes multiple tumors of many types to form on the skin or inside the body. The paper is online in Environmental Health Perspectives.Waalkes' lab started working with stem cells about five years ago. The researchers used a prostate stem cell line, not embryonic stem cells.
“Using stem cells to answer questions about disease is an important new growing area of research. Stem cells help to explain a lot about carcinogenesis, and it is highly likely that stem cells are contributing factors to other chronic diseases,” Waalkes said.
Stem cells are unique in the body. They stay around for a long time and are capable of dividing and renewing themselves. “Most cancers take 30 or 40 years to develop,” said Linda Birnbaum, Ph.D., director of NIEHS and NTP. “It makes sense that stem cells may play a role in the developmental basis of adult disease. We know that exposures to toxicants during development and growth can lead to diseases later in life.”
Next, the laboratory team will look to see if this finding is unique to arsenic or if it is applicable to other organic and inorganic carcinogens.
Source: http://www.nih.gov/
Michael Waalkes, Ph.D., and his team at the National Toxicology Program Laboratory, National Institute of Environmental Health Sciences, part of NIH, had shown previously that normal cells become cancerous when they are treated with inorganic arsenic. This new study shows that when these cancer cells are placed near, but not in contact with normal stem cells, the normal stem cells very rapidly acquire the characteristics of cancer stem cells. It demonstrates that malignant cells are able to send molecular signals through a semi-permeable membrane, where cells can't normally pass, and turn the normal stem cells into cancer stem cells.
“This paper shows a different and unique way that cancers can expand by recruiting nearby normal stem cells and creating an overabundance of cancer stem cells,” Waalkes said. “The recruitment of normal stem cells into cancer stem cells could have broad implications for the carcinogenic process in general, including tumor growth and metastases.”
This reveals a potentially important aspect of arsenic carcinogenesis and may help explain observances by researchers working with arsenic that arsenic often causes multiple tumors of many types to form on the skin or inside the body. The paper is online in Environmental Health Perspectives.Waalkes' lab started working with stem cells about five years ago. The researchers used a prostate stem cell line, not embryonic stem cells.
“Using stem cells to answer questions about disease is an important new growing area of research. Stem cells help to explain a lot about carcinogenesis, and it is highly likely that stem cells are contributing factors to other chronic diseases,” Waalkes said.
Stem cells are unique in the body. They stay around for a long time and are capable of dividing and renewing themselves. “Most cancers take 30 or 40 years to develop,” said Linda Birnbaum, Ph.D., director of NIEHS and NTP. “It makes sense that stem cells may play a role in the developmental basis of adult disease. We know that exposures to toxicants during development and growth can lead to diseases later in life.”
Next, the laboratory team will look to see if this finding is unique to arsenic or if it is applicable to other organic and inorganic carcinogens.
Source: http://www.nih.gov/
Single DNA Mutation Linked to Proteus Syndrome
Finding Holds Promise in Cancer Fight-------------------------------------------------------------
By Steve Rensberry
srensberry@rensberrypublishing.com
(RPC) - 8/25/2011 - The National Institutes of Health issued a report this month announcing that scientists had pinpointed the mutation they believe is responsible for the very unusual Proteus Syndrome, a finding which they suggested may hold promise in understanding and treating cancer. For more information about Proteus Syndrome, see: FAQ.
Details of the study were first published this month in the New England Journal of Medicine here: A Mosaic Activating Mutation in AKT1 Associated with the Proteus Syndrome.
Proteus Syndrome is an extremely rare condition involving the uncontrolled, typically asymmetric overgrowth of various body tissues, bones and other parts. Identification involves noting the unequal distribution of affected areas, the appearance of the suspected syndrome among only one member in a family, and continued growth over time of the body areas experiencing accelerated growth.
"Proteus syndrome does not run in families, but faulty genes were believed to be responsible. Some experts proposed that the condition might be a genetic mosaicism. Mosaic disorders arise when a genetic mutation occurs spontaneously during embryonic development," the NIH report states.
A research team at the NIH’s National Human Genome Research Institute (NHGRI) used a technique called whole-exome sequencing to examine the cells of six affected individuals in order to determine if their hypothesis was correct. What they discovered was a gene that had already been implicated in cancer studies and related therapies.
"The analysis reveled a single-letter misspelling in the genome of affected cells," The NIA states. "The mutated gene, called AKT1, is a known ocogene—a gene that can promote the uncontrolled cell growth associated with cancer."
Further confirmation of the role played by a gene defect was found by testing 29 others, for who 26 showed the variation. No variations have been found beyond affected individuals.
Accelerated AKT protein activity had been observed in previous research into the cause of the syndrome.
The focus now is on developing a drug to inhibit the increase in AKT protein activity.
For further reading, see: Gene Variant in Proteus Syndrome Identified.
Widespread Water Contamination Causes Concern
Report says millions ingesting chromium-6, a known carcinogen
-----------------------------------By Steve Rensberry
rensberrypublishing.com
-----------------------------------
(RPC) - 12/26/2010 - The environmental and regulatory fallout from a recent report by the non-profit Environmental Working Group (EWG), showing widespread contamination of the toxic metal hexavalent chromium (chromium-6), continues to force the hand of government officials and others implicated in the.
According to the study, available here, toxic chromium-6 levels were found in the tap water of 31 out of 35 metropolitan areas across the United States, used by an estimated 26 million people. And this was only a sampling.
U.S. Environmental Protection Agency (EPA) Administrator Lisa Jackson met with a handful of senators on Dec. 22 to brief them on the agency's response.
Present were senators Richard Durbin (D-Ill.), Mark Kirk (D-Ill.), Debbie Stabenow (D-Michigan), Bob Casey (D-Penn.), Ben Nelson (Neb.), Bill Nelson (D-Fla.), Daniel Alaska (D-Ha.), Dianne Feinstein (D-Calif.), Jeff Bingaman (D-N.M.), and Jeff Merkley (D-Oregon).
So far, there appears to be little doubt that the EWG's latest report could well produce a firestorm of litigation and policy changes.
"The total number of Americans drinking tap water contaminated with this compound is likely far higher than is indicated by EWG's tests. At least 74 million people in nearly 7,000 communities drink tap water polluted with “total chromium,” which includes hexavalent and other forms of the metal, according to EWG’s 2009 analysis of water utility tests from 48,000 communities in 42 states (EWG 2009)," the report says.
Anderson said she herself is concerned about the presence of chromium-6 in drinking water, both as a mother and as head of the EPA, but that the EWG's report provided only a brief "snapshot" of the problem at one specific time. The agency intends to work both local and state officials to determine precisely how widespread the problem is, she said.
"The science behind chromium-6 is evolving. EPA is already on a path toward identifying and addressing any potential health threats from excessive, long-term exposure with its new draft assessment released this past fall. This assessment still needs to be reviewed by independent scientists as an essential step toward tightening drinking water standards for chromium-6. Strong science and the law will continue to be the backbone of our decision-making at EPA. EPA takes this matter seriously and we will continue to do all that we can, using good science and the law, to protect people’s health and our environment,” Anderson said.
The EPA currently requires testing for total chromium, consisting of both chromium-3 and the toxic chromium-6, but doesn't not determine the ratio. All water facilities in the U.S. are in compliance with "existing total chromium standards" the agency announcement says.
Jackson summarized the agency's view and commitment in four points.
1) While provocative, the EWG report is a self-described “snapshot” in time and does not provide a full, long-term picture of the prevalence of chromium-6 in our drinking water. The EPA will work with state and local officials to better determine how wide-spread and prevalent this contaminant is.
2) Meanwhile, the EPA will issue guidance to all water systems on how to test for and sample drinking water specifically for chromium-6. This guidance will provide EPA-approved methods and other technical information.
3) The EPA will also offer technical expertise and assistance to the communities cited in the EWG study with the highest levels of chromium. This assistance will include providing technical experts to work with water system operators and engineers to ensure the latest testing and monitoring is being utilized.
4) Once the EPA’s chromium-6 risk assessment is finalized, the agency will work quickly to determine if new standards need to be set. Based on the current draft assessment, which has yet to undergo scientific peer review, it is likely that the EPA will tighten drinking water standards to address the health risks posed by chromium-6.
What is potentially as explosive as the EWG's reported discovery of contamination is what it says about the industry deception that delayed protection.
"Industry has sought for more than six years to delay state-mandated regulation of hexavalent chromium in tap water in California. Aerospace giant Honeywell International Inc. and others have stalled the adoption of the advisory public health goal by pressing for additional external scientific peer review," the EWG report says.
The group pressed for immediate action from the EPA.
"At least 74 million Americans in 42 states drink chromium-polluted tap water, much of it likely in the form of cancer-causing hexavalent chromium. Given the scope of exposure and the magnitude of the potential risk, the EPA should move expeditiously to establish a legal limit for the chemical in tap water and require water utilities to test for it."
While current levels may meet existing EPA, those levels are drastically out of date, the EWG's report says.
"The EPA’s inaction is but one example of the agency’s lack of resolve in protecting Americans’ tap water. The agency has not set a new, enforceable drinking water standard for any contaminant since 2001, even though the Safe Drinking Water Act requires the EPA to assess the need for standards for at least five new chemicals every five years. Three-fourths of the current standards, including for total chromium, were set in 1991 and 1992 and have not been updated since," it says.
Current standards also do not take into account maximum legal levels for contaminants that could possible affect children, newborns or a fetus. Neither do existing threshholds take into account the possibility of exposure to multiple contaminants at the same time.
Finally, it says: "EWG recommends that the EPA set a legal limit for hexavalent chromium in drinking water as quickly as possible and require all water utilities to test for it. The EPA can speed the process by streamlining the IRIS assessment. We hope that Administrator Jackson’s leadership on this critical issue will reduce cancer risk for all Americans."
The principle author of the EWG report was Rebecca Sutton, PhD. Editors were Jane Houlihan, Renee Sharp and Nils Bruzelius.
Chromium, the EWG notes, is a natural substance used in a number of manufacturing processes, including steel manufacturing, welding, the plating of metal surfaces, in pesticides that are used in pressure-treated lumber for play sets and outdoor decks, and in the making of alloys, dyes and pigments. It was used widely as an anti-corrosive agent in industrial cooling towers until a 1990 ban. Its most common use is as an essential component in the making of stainless steel and super-alloys.
Skyrocketing Cancer Treatment Costs a Concern
Oncologists Report Patients Rationing Medication, Avoiding TreatmentsWASHINGTON - (BUSINESS WIRE) - 10/9/10 - Ninety five percent of the nation's oncologists report a rise in their patients' concerns over treatment costs in the past six months, according to a survey conducted by MDLinx (www.mdlinx.com), one of the U.S.'s largest doctor portals. More than 60 percent of US oncologists regularly visit the websites of MDLinx, whose services help physicians stay current with latest and most important medical research in each specialty.
The survey of 106 U.S. oncologists was conducted from August 20 to August 30, 2010. Respondents were asked about their patients’ financial concerns over the first six months of 2010. Eighty four percent of respondents said they had invested more time and effort into the financial planning of patients' treatments in the last six months than at any time previously. Sixty-seven percent of responding doctors reported patients rationing medications or forgoing treatment due to financial and insurance coverage concerns.
Aki Tomaru, CEO of M3 USA, which owns the MDLinx site, says that oncology patients' heightened financial challenges may be the result of several factors.
"We believe that the change in the air in the United States regarding medical coverage has injected an additional measure of anxiety for what is already often the most anxious times of these people's lives," Tomaru said. "In addition, the continuing grinding effect of the worldwide economic downturn has its obvious effects as well."
Wisconsin-based oncologist Dr. Shahid Shekhani says that patients are canceling appointments, follow up visits, and even treatment due to financial concerns. “I just had a young grandmother, in her 60s, halt lung cancer treatment that would have extended her survival in order to preserve her family’s finances and her ability to leave an inheritance to her children.”
MDLinx aggregates medical articles and research from more than 1,200 peer-reviewed journals and leading news media every weekday. Its physician editors rank, sort and summarize this content into 36 medical specialty sites and more than 800 subspecialty sections. MDLinx is owned by M3 USA, a Sony Group Company. The company specializes in creating effective communication channels between physicians and industries who wish to reach them.
For more information, visit the corporate site at www.usa.m3.com.
