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Shorter regimen can prevent GVHD
Credit: Chad McNeeley
Combining a couple of “promising” treatment approaches can prevent graft-vs-host disease (GVHD) as well as conventional therapy, researchers have reported in the Journal of Clinical Oncology.
They combined a 4-day myeloablative conditioning regimen of busulfan and fludarabine with 2 days of high-dose cyclophosphamide after transplant.
Typically, patients receive 6 months of immunosuppressive therapy to reduce their risk of GVHD.
The conditioning regimen and post-transplant cyclophosphamide have been tested separately in other studies and have good track records in controlling cancer and preventing severe GVHD.
Those successes led Leo Luznik, MD, of the Johns Hopkins University School of Medicine in Baltimore, Maryland, and his colleagues to combine the 2 therapies.
The team tested the combination in 92 patients with high-risk hematologic malignancies. Diagnoses included acute and chronic leukemias, multiple myeloma, non-Hodgkin lymphoma, and myelodysplastic syndromes. Patients had a median age of 49 (range, 21-65).
All patients received 40 mg/m2/day of intravenous (IV) fludarabine immediately before busulfan on all 4 days of conditioning. The busulfan dose of 130 mg/m2 IV daily was adjusted based on pharmacokinetics.
One or 2 days of rest were allowed before patients received a T-cell-replete bone marrow allograft. Forty-five patients had a matched, related donor, and 47 had a matched, unrelated donor.
Patients received 50 mg/kg/day of IV cyclophosphamide for 2 days, with the first dose starting 62 to 72 hours after the start of allograft infusion.
At 100 days after transplant, 51% of patients had developed grade 2-4 acute GVHD, and 15% had grade 3-4 acute GVHD. Fourteen percent of patients developed chronic GVHD.
The 2-year overall survival rate was 67%, and 2-year event-free survival was 62%.
Dr Luznik said he was encouraged by the low rate of chronic GVHD with the regimen. And he noted that percentages of acute GVHD are similar to those seen with the standard 6-month regimen of immunosuppressive drugs.
Reducing the post-transplant treatment to 2 days with cyclophosphamide, he said, “also allows for the earlier integration of other treatments.”
For example, immunotherapies used to eradicate any remaining cancer could be started much sooner with this regimen, said study author Christopher Kanakry, MD, of the Sidney Kimmel Cancer Center at Johns Hopkins.
“If you give patients immune cells to eradicate any remaining cancer cells that might be present,” he said, “those immune cells would not be prevented from doing their job by ongoing immune suppression drugs that are being used in patients treated with conventional transplant approaches.”
Dr Luznik said the researchers’ next step will be a phase 3 trial comparing this regimen to another experimental approach to prevent GVHD or to the more traditional 6-month immunosuppressive therapy.
Funding for this study was provided by Otsuka Pharmaceutical Co., Ltd. and the National Institutes of Health. 
Credit: Chad McNeeley
Combining a couple of “promising” treatment approaches can prevent graft-vs-host disease (GVHD) as well as conventional therapy, researchers have reported in the Journal of Clinical Oncology.
They combined a 4-day myeloablative conditioning regimen of busulfan and fludarabine with 2 days of high-dose cyclophosphamide after transplant.
Typically, patients receive 6 months of immunosuppressive therapy to reduce their risk of GVHD.
The conditioning regimen and post-transplant cyclophosphamide have been tested separately in other studies and have good track records in controlling cancer and preventing severe GVHD.
Those successes led Leo Luznik, MD, of the Johns Hopkins University School of Medicine in Baltimore, Maryland, and his colleagues to combine the 2 therapies.
The team tested the combination in 92 patients with high-risk hematologic malignancies. Diagnoses included acute and chronic leukemias, multiple myeloma, non-Hodgkin lymphoma, and myelodysplastic syndromes. Patients had a median age of 49 (range, 21-65).
All patients received 40 mg/m2/day of intravenous (IV) fludarabine immediately before busulfan on all 4 days of conditioning. The busulfan dose of 130 mg/m2 IV daily was adjusted based on pharmacokinetics.
One or 2 days of rest were allowed before patients received a T-cell-replete bone marrow allograft. Forty-five patients had a matched, related donor, and 47 had a matched, unrelated donor.
Patients received 50 mg/kg/day of IV cyclophosphamide for 2 days, with the first dose starting 62 to 72 hours after the start of allograft infusion.
At 100 days after transplant, 51% of patients had developed grade 2-4 acute GVHD, and 15% had grade 3-4 acute GVHD. Fourteen percent of patients developed chronic GVHD.
The 2-year overall survival rate was 67%, and 2-year event-free survival was 62%.
Dr Luznik said he was encouraged by the low rate of chronic GVHD with the regimen. And he noted that percentages of acute GVHD are similar to those seen with the standard 6-month regimen of immunosuppressive drugs.
Reducing the post-transplant treatment to 2 days with cyclophosphamide, he said, “also allows for the earlier integration of other treatments.”
For example, immunotherapies used to eradicate any remaining cancer could be started much sooner with this regimen, said study author Christopher Kanakry, MD, of the Sidney Kimmel Cancer Center at Johns Hopkins.
“If you give patients immune cells to eradicate any remaining cancer cells that might be present,” he said, “those immune cells would not be prevented from doing their job by ongoing immune suppression drugs that are being used in patients treated with conventional transplant approaches.”
Dr Luznik said the researchers’ next step will be a phase 3 trial comparing this regimen to another experimental approach to prevent GVHD or to the more traditional 6-month immunosuppressive therapy.
Funding for this study was provided by Otsuka Pharmaceutical Co., Ltd. and the National Institutes of Health.
Credit: Chad McNeeley
Combining a couple of “promising” treatment approaches can prevent graft-vs-host disease (GVHD) as well as conventional therapy, researchers have reported in the Journal of Clinical Oncology.
They combined a 4-day myeloablative conditioning regimen of busulfan and fludarabine with 2 days of high-dose cyclophosphamide after transplant.
Typically, patients receive 6 months of immunosuppressive therapy to reduce their risk of GVHD.
The conditioning regimen and post-transplant cyclophosphamide have been tested separately in other studies and have good track records in controlling cancer and preventing severe GVHD.
Those successes led Leo Luznik, MD, of the Johns Hopkins University School of Medicine in Baltimore, Maryland, and his colleagues to combine the 2 therapies.
The team tested the combination in 92 patients with high-risk hematologic malignancies. Diagnoses included acute and chronic leukemias, multiple myeloma, non-Hodgkin lymphoma, and myelodysplastic syndromes. Patients had a median age of 49 (range, 21-65).
All patients received 40 mg/m2/day of intravenous (IV) fludarabine immediately before busulfan on all 4 days of conditioning. The busulfan dose of 130 mg/m2 IV daily was adjusted based on pharmacokinetics.
One or 2 days of rest were allowed before patients received a T-cell-replete bone marrow allograft. Forty-five patients had a matched, related donor, and 47 had a matched, unrelated donor.
Patients received 50 mg/kg/day of IV cyclophosphamide for 2 days, with the first dose starting 62 to 72 hours after the start of allograft infusion.
At 100 days after transplant, 51% of patients had developed grade 2-4 acute GVHD, and 15% had grade 3-4 acute GVHD. Fourteen percent of patients developed chronic GVHD.
The 2-year overall survival rate was 67%, and 2-year event-free survival was 62%.
Dr Luznik said he was encouraged by the low rate of chronic GVHD with the regimen. And he noted that percentages of acute GVHD are similar to those seen with the standard 6-month regimen of immunosuppressive drugs.
Reducing the post-transplant treatment to 2 days with cyclophosphamide, he said, “also allows for the earlier integration of other treatments.”
For example, immunotherapies used to eradicate any remaining cancer could be started much sooner with this regimen, said study author Christopher Kanakry, MD, of the Sidney Kimmel Cancer Center at Johns Hopkins.
“If you give patients immune cells to eradicate any remaining cancer cells that might be present,” he said, “those immune cells would not be prevented from doing their job by ongoing immune suppression drugs that are being used in patients treated with conventional transplant approaches.”
Dr Luznik said the researchers’ next step will be a phase 3 trial comparing this regimen to another experimental approach to prevent GVHD or to the more traditional 6-month immunosuppressive therapy.
Funding for this study was provided by Otsuka Pharmaceutical Co., Ltd. and the National Institutes of Health.
A safer gene therapy for SCID-X1?
Credit: Chad McNeeley
A new gene therapy appears safe and effective for boys with X-linked severe combined immunodeficiency syndrome (SCID-X1).
Early data from a small trial suggest the treatment may not pose a risk of leukemia, which was seen in previous trials of gene therapy in SCID-X1 patients.
The new therapy is a self-inactivating γ-retrovirus designed to deliver its payload while minimizing the chance of inadvertently activating
oncogenes that could lead to leukemia.
Researchers described results with this therapy in The New England Journal of Medicine.
The team enrolled 9 boys with SCID-X1. They received bone marrow-derived CD34+ cells transduced with the self-inactivating γ-chain vector, without preparative conditioning.
Eight boys are still alive after 12.1 to 38.7 months of follow-up, with no SCID-X1-associated infections. One child died of an overwhelming infection that was present at the time gene therapy began.
Gene therapy alone generated functioning immune systems in 7 of the patients.
Genetic studies of the boys’ new T cells revealed that the viral vector did not lead to an expansion of cells with vector insertions near known oncogenes, raising cautious hopes about the vector’s long-term safety.
The researchers said they will continue to monitor the patients for any signs of treatment-related leukemia for 15 years.
In prior European trials, which were the first to demonstrate gene therapy’s potential to successfully cure a disease, leukemia appeared 2 to 5 years after treatment. This outcome was one of several events that, together, slowed clinical progress in gene therapy for many years.
“Our goal was to take the molecular data from the prior trial and use it to produce a vector that would remain effective and, at the same time, reduce the risk of leukemia,” said David A. Williams, MD, of the Dana-Farber/Boston Children’s Cancer and Blood Disorders Center in Massachusetts.
“The efficacy data from our study is clear: The vector does work to correct the disease. And by a surrogate endpoint, we have improved the treatment’s safety, although it’s too early to say that we’ve completely eliminated the long-term risk of leukemia.”
After a single round of treatment, 6 of 7 boys for whom the gene therapy was successful had achieved the trial’s primary efficacy endpoints—a T-cell count greater than 300 cells per microliter of blood and T-cell proliferation in response to stimulation with phytohemagglutinin.
The seventh boy received a second round of gene therapy and remains healthy despite having relatively low T-cell counts. The eighth surviving patient was successfully treated with a conventional hematopoietic stem cell transplant after gene therapy failed to stimulate T-cell production.
Credit: Chad McNeeley
A new gene therapy appears safe and effective for boys with X-linked severe combined immunodeficiency syndrome (SCID-X1).
Early data from a small trial suggest the treatment may not pose a risk of leukemia, which was seen in previous trials of gene therapy in SCID-X1 patients.
The new therapy is a self-inactivating γ-retrovirus designed to deliver its payload while minimizing the chance of inadvertently activating
oncogenes that could lead to leukemia.
Researchers described results with this therapy in The New England Journal of Medicine.
The team enrolled 9 boys with SCID-X1. They received bone marrow-derived CD34+ cells transduced with the self-inactivating γ-chain vector, without preparative conditioning.
Eight boys are still alive after 12.1 to 38.7 months of follow-up, with no SCID-X1-associated infections. One child died of an overwhelming infection that was present at the time gene therapy began.
Gene therapy alone generated functioning immune systems in 7 of the patients.
Genetic studies of the boys’ new T cells revealed that the viral vector did not lead to an expansion of cells with vector insertions near known oncogenes, raising cautious hopes about the vector’s long-term safety.
The researchers said they will continue to monitor the patients for any signs of treatment-related leukemia for 15 years.
In prior European trials, which were the first to demonstrate gene therapy’s potential to successfully cure a disease, leukemia appeared 2 to 5 years after treatment. This outcome was one of several events that, together, slowed clinical progress in gene therapy for many years.
“Our goal was to take the molecular data from the prior trial and use it to produce a vector that would remain effective and, at the same time, reduce the risk of leukemia,” said David A. Williams, MD, of the Dana-Farber/Boston Children’s Cancer and Blood Disorders Center in Massachusetts.
“The efficacy data from our study is clear: The vector does work to correct the disease. And by a surrogate endpoint, we have improved the treatment’s safety, although it’s too early to say that we’ve completely eliminated the long-term risk of leukemia.”
After a single round of treatment, 6 of 7 boys for whom the gene therapy was successful had achieved the trial’s primary efficacy endpoints—a T-cell count greater than 300 cells per microliter of blood and T-cell proliferation in response to stimulation with phytohemagglutinin.
The seventh boy received a second round of gene therapy and remains healthy despite having relatively low T-cell counts. The eighth surviving patient was successfully treated with a conventional hematopoietic stem cell transplant after gene therapy failed to stimulate T-cell production.
Credit: Chad McNeeley
A new gene therapy appears safe and effective for boys with X-linked severe combined immunodeficiency syndrome (SCID-X1).
Early data from a small trial suggest the treatment may not pose a risk of leukemia, which was seen in previous trials of gene therapy in SCID-X1 patients.
The new therapy is a self-inactivating γ-retrovirus designed to deliver its payload while minimizing the chance of inadvertently activating
oncogenes that could lead to leukemia.
Researchers described results with this therapy in The New England Journal of Medicine.
The team enrolled 9 boys with SCID-X1. They received bone marrow-derived CD34+ cells transduced with the self-inactivating γ-chain vector, without preparative conditioning.
Eight boys are still alive after 12.1 to 38.7 months of follow-up, with no SCID-X1-associated infections. One child died of an overwhelming infection that was present at the time gene therapy began.
Gene therapy alone generated functioning immune systems in 7 of the patients.
Genetic studies of the boys’ new T cells revealed that the viral vector did not lead to an expansion of cells with vector insertions near known oncogenes, raising cautious hopes about the vector’s long-term safety.
The researchers said they will continue to monitor the patients for any signs of treatment-related leukemia for 15 years.
In prior European trials, which were the first to demonstrate gene therapy’s potential to successfully cure a disease, leukemia appeared 2 to 5 years after treatment. This outcome was one of several events that, together, slowed clinical progress in gene therapy for many years.
“Our goal was to take the molecular data from the prior trial and use it to produce a vector that would remain effective and, at the same time, reduce the risk of leukemia,” said David A. Williams, MD, of the Dana-Farber/Boston Children’s Cancer and Blood Disorders Center in Massachusetts.
“The efficacy data from our study is clear: The vector does work to correct the disease. And by a surrogate endpoint, we have improved the treatment’s safety, although it’s too early to say that we’ve completely eliminated the long-term risk of leukemia.”
After a single round of treatment, 6 of 7 boys for whom the gene therapy was successful had achieved the trial’s primary efficacy endpoints—a T-cell count greater than 300 cells per microliter of blood and T-cell proliferation in response to stimulation with phytohemagglutinin.
The seventh boy received a second round of gene therapy and remains healthy despite having relatively low T-cell counts. The eighth surviving patient was successfully treated with a conventional hematopoietic stem cell transplant after gene therapy failed to stimulate T-cell production.
Microscopy advances net Nobel Prize
Credit: Max Planck Institute
for Biophysical Chemistry
Three scientists have received the 2014 Nobel Prize in Chemistry for aiding the development of super-resolved fluorescence microscopy.
For a long time, optical microscopy was held back by a presumed limitation: that it would never obtain a better resolution than half the wavelength
of light.
Working separately, this year’s Nobel Laureates in Chemistry circumvented this limitation and brought optical microscopy into the nanodimension.
Now, scientists can monitor the interplay between individual molecules inside cells, watch disease-related proteins aggregate, and track cell division at the nanolevel.
For enabling these advances, Eric Betzig, PhD, of the Howard Hughes Medical Institute in Ashburn, Virginia; Stefan W. Hell, PhD, of the Max Planck Institute for Biophysical Chemistry in Göttingen, Germany; and William E. Moerner, PhD, of Stanford University in California, received the prize. The prize amount was SEK 8 million, to be shared equally among the Laureates.
The work in brief
In 1873, the microscopist Ernst Abbe stipulated a physical limit for the maximum resolution of traditional optical microscopy—0.2 micrometers. Drs Moerner, Hell, and Betzig were able to bypass this limit.
Dr Hell developed stimulated emission depletion (STED) microscopy. This method employs 2 laser beams. One stimulates fluorescent molecules to glow, and another cancels out all fluorescence except for that in a nanometer-sized volume.
Scanning over the sample, nanometer for nanometer, yields an image with a resolution better than Abbe’s stipulated limit.
Drs Betzig and Moerner laid the foundation for another method, single-molecule microscopy. This method relies upon the possibility to turn the fluorescence of individual molecules on and off.
Scientists image the same area multiple times, letting just a few interspersed molecules glow each time. Superimposing these images yields a dense super-image resolved at the nanolevel. In 2006, Dr Betzig used this method for the first time.
For more details on the Nobel Laureates and their work, visit Nobelprize.org.
Credit: Max Planck Institute
for Biophysical Chemistry
Three scientists have received the 2014 Nobel Prize in Chemistry for aiding the development of super-resolved fluorescence microscopy.
For a long time, optical microscopy was held back by a presumed limitation: that it would never obtain a better resolution than half the wavelength
of light.
Working separately, this year’s Nobel Laureates in Chemistry circumvented this limitation and brought optical microscopy into the nanodimension.
Now, scientists can monitor the interplay between individual molecules inside cells, watch disease-related proteins aggregate, and track cell division at the nanolevel.
For enabling these advances, Eric Betzig, PhD, of the Howard Hughes Medical Institute in Ashburn, Virginia; Stefan W. Hell, PhD, of the Max Planck Institute for Biophysical Chemistry in Göttingen, Germany; and William E. Moerner, PhD, of Stanford University in California, received the prize. The prize amount was SEK 8 million, to be shared equally among the Laureates.
The work in brief
In 1873, the microscopist Ernst Abbe stipulated a physical limit for the maximum resolution of traditional optical microscopy—0.2 micrometers. Drs Moerner, Hell, and Betzig were able to bypass this limit.
Dr Hell developed stimulated emission depletion (STED) microscopy. This method employs 2 laser beams. One stimulates fluorescent molecules to glow, and another cancels out all fluorescence except for that in a nanometer-sized volume.
Scanning over the sample, nanometer for nanometer, yields an image with a resolution better than Abbe’s stipulated limit.
Drs Betzig and Moerner laid the foundation for another method, single-molecule microscopy. This method relies upon the possibility to turn the fluorescence of individual molecules on and off.
Scientists image the same area multiple times, letting just a few interspersed molecules glow each time. Superimposing these images yields a dense super-image resolved at the nanolevel. In 2006, Dr Betzig used this method for the first time.
For more details on the Nobel Laureates and their work, visit Nobelprize.org.
Credit: Max Planck Institute
for Biophysical Chemistry
Three scientists have received the 2014 Nobel Prize in Chemistry for aiding the development of super-resolved fluorescence microscopy.
For a long time, optical microscopy was held back by a presumed limitation: that it would never obtain a better resolution than half the wavelength
of light.
Working separately, this year’s Nobel Laureates in Chemistry circumvented this limitation and brought optical microscopy into the nanodimension.
Now, scientists can monitor the interplay between individual molecules inside cells, watch disease-related proteins aggregate, and track cell division at the nanolevel.
For enabling these advances, Eric Betzig, PhD, of the Howard Hughes Medical Institute in Ashburn, Virginia; Stefan W. Hell, PhD, of the Max Planck Institute for Biophysical Chemistry in Göttingen, Germany; and William E. Moerner, PhD, of Stanford University in California, received the prize. The prize amount was SEK 8 million, to be shared equally among the Laureates.
The work in brief
In 1873, the microscopist Ernst Abbe stipulated a physical limit for the maximum resolution of traditional optical microscopy—0.2 micrometers. Drs Moerner, Hell, and Betzig were able to bypass this limit.
Dr Hell developed stimulated emission depletion (STED) microscopy. This method employs 2 laser beams. One stimulates fluorescent molecules to glow, and another cancels out all fluorescence except for that in a nanometer-sized volume.
Scanning over the sample, nanometer for nanometer, yields an image with a resolution better than Abbe’s stipulated limit.
Drs Betzig and Moerner laid the foundation for another method, single-molecule microscopy. This method relies upon the possibility to turn the fluorescence of individual molecules on and off.
Scientists image the same area multiple times, letting just a few interspersed molecules glow each time. Superimposing these images yields a dense super-image resolved at the nanolevel. In 2006, Dr Betzig used this method for the first time.
For more details on the Nobel Laureates and their work, visit Nobelprize.org.
Price increases drive spending on cancer drugs
Credit: Steven Harbour
The recent surge in spending on oral anticancer drugs in the US exceeds the increase in use of these drugs, new research shows.
Average quarterly national spending on oral oncologics increased 37% during the period studied, from $940 million in the first quarter of 2006 to $1.4 billion in the third quarter of 2011.
But the average quarterly use of these drugs in the same time period increased by only 10%.
This suggests price increases are a significant driver of spending trends.
Rena M. Conti, PhD, of the University of Chicago in Illinois, and her colleagues examined recent trends in spending and use of oral oncologics and disclosed their findings in Health Affairs.
Of the 47 drugs analyzed, most were targeted agents (30%), hormonal agents (26%), and alkylating agents (19%).
The researchers observed a significant increase in national spending on oral oncologics from 2006 to 2011—an estimated average quarterly increase of $20 million.
This was driven by brand-name, patent-protected drugs, but the use of these drugs climbed a comparatively small amount. Average quarterly spending of patent-protected drugs increased 61%, and average quarterly use increased 30% between 2006 and the period from September 2010 to September 2011.
“This is an exciting time, an era of breakthrough cancer drugs,” Dr Conti said. “Some of these medications have extended the lives of many people with certain types of cancer. However, spending on these brand-name oral oncologics is outstripping national spending on all pharmaceuticals and all medical care spending generally.”
The researchers also discovered that when oncologics lose patent protection, spending takes a nosedive. The use of newly off-patent drugs increased by 16%, but average quarterly spending on those drugs fell by 65%.
Another finding was that US spending on targeted anticancer agents increased from 35% of all oral cancer drugs in 2006 to nearly 60% in 2011.
Meanwhile, spending on hormonal agents decreased from 42% of total spending to 19%, spending on antimetabolites increased from 11% to 12%, and spending on alkylating agents decreased from 10% to 8%.
Credit: Steven Harbour
The recent surge in spending on oral anticancer drugs in the US exceeds the increase in use of these drugs, new research shows.
Average quarterly national spending on oral oncologics increased 37% during the period studied, from $940 million in the first quarter of 2006 to $1.4 billion in the third quarter of 2011.
But the average quarterly use of these drugs in the same time period increased by only 10%.
This suggests price increases are a significant driver of spending trends.
Rena M. Conti, PhD, of the University of Chicago in Illinois, and her colleagues examined recent trends in spending and use of oral oncologics and disclosed their findings in Health Affairs.
Of the 47 drugs analyzed, most were targeted agents (30%), hormonal agents (26%), and alkylating agents (19%).
The researchers observed a significant increase in national spending on oral oncologics from 2006 to 2011—an estimated average quarterly increase of $20 million.
This was driven by brand-name, patent-protected drugs, but the use of these drugs climbed a comparatively small amount. Average quarterly spending of patent-protected drugs increased 61%, and average quarterly use increased 30% between 2006 and the period from September 2010 to September 2011.
“This is an exciting time, an era of breakthrough cancer drugs,” Dr Conti said. “Some of these medications have extended the lives of many people with certain types of cancer. However, spending on these brand-name oral oncologics is outstripping national spending on all pharmaceuticals and all medical care spending generally.”
The researchers also discovered that when oncologics lose patent protection, spending takes a nosedive. The use of newly off-patent drugs increased by 16%, but average quarterly spending on those drugs fell by 65%.
Another finding was that US spending on targeted anticancer agents increased from 35% of all oral cancer drugs in 2006 to nearly 60% in 2011.
Meanwhile, spending on hormonal agents decreased from 42% of total spending to 19%, spending on antimetabolites increased from 11% to 12%, and spending on alkylating agents decreased from 10% to 8%.
Credit: Steven Harbour
The recent surge in spending on oral anticancer drugs in the US exceeds the increase in use of these drugs, new research shows.
Average quarterly national spending on oral oncologics increased 37% during the period studied, from $940 million in the first quarter of 2006 to $1.4 billion in the third quarter of 2011.
But the average quarterly use of these drugs in the same time period increased by only 10%.
This suggests price increases are a significant driver of spending trends.
Rena M. Conti, PhD, of the University of Chicago in Illinois, and her colleagues examined recent trends in spending and use of oral oncologics and disclosed their findings in Health Affairs.
Of the 47 drugs analyzed, most were targeted agents (30%), hormonal agents (26%), and alkylating agents (19%).
The researchers observed a significant increase in national spending on oral oncologics from 2006 to 2011—an estimated average quarterly increase of $20 million.
This was driven by brand-name, patent-protected drugs, but the use of these drugs climbed a comparatively small amount. Average quarterly spending of patent-protected drugs increased 61%, and average quarterly use increased 30% between 2006 and the period from September 2010 to September 2011.
“This is an exciting time, an era of breakthrough cancer drugs,” Dr Conti said. “Some of these medications have extended the lives of many people with certain types of cancer. However, spending on these brand-name oral oncologics is outstripping national spending on all pharmaceuticals and all medical care spending generally.”
The researchers also discovered that when oncologics lose patent protection, spending takes a nosedive. The use of newly off-patent drugs increased by 16%, but average quarterly spending on those drugs fell by 65%.
Another finding was that US spending on targeted anticancer agents increased from 35% of all oral cancer drugs in 2006 to nearly 60% in 2011.
Meanwhile, spending on hormonal agents decreased from 42% of total spending to 19%, spending on antimetabolites increased from 11% to 12%, and spending on alkylating agents decreased from 10% to 8%.
Risk-directed therapy improves survival in ALL
Credit: St Jude Biomedical
Communications
Risk-directed therapy can level the playing field for patients with BCR-ABL1-like acute lymphoblastic leukemia (ALL), new research suggests.
Using minimal residual disease (MRD) and other risk factors to guide treatment intensity allowed patients withBCR-ABL1-like ALL to have survival rates comparable to those of other B-ALL patients.
The research also revealed that not all BCR-ABL1-like ALL patients have high-risk disease.
Ching-Hon Pui, MD, of St Jude Children’s Research Hospital in Memphis, Tennessee, and his colleagues reported these results in the Journal of Clinical Oncology.
Patients with BCR-ABL1-like ALL tend to have poor outcomes, so Dr Pui and his colleagues evaluated the utility of risk-directed therapy in these and other B-ALL patients.
The team assessed patients enrolled in the Total Therapy XV study between 2000 and 2007. They were 1 to 18 years of age at diagnosis. There were 344 subjects with adequate samples for gene expression profiling.
Forty patients (11.6%) had BCR-ABL1-like ALL. They were significantly more likely than other study participants to be male, have Down syndrome, and have higher MRD levels on day 19 and at the end of induction.
The researchers monitored patients and adjusted their treatment intensity based on MRD at days 19 and 42. The treatment regimen was described in JAMA in 2009.
The MRD monitoring combined with conventional risk factors, such as patient age and white blood count at diagnosis, demonstrated that BCR-ABL1-like ALL is not a uniformly high-risk disease.
Forty percent of BCR-ABL1-like ALL patients were actually classified as having low-risk disease because they had other favorable clinical or biological features and no MRD at the end of remission induction.
The other 60% were classified as having standard-risk or high-risk disease. The group included 6 patients who underwent transplant.
There were no significant differences in event-free or overall survival in patients with BCR-ABL1-like ALL and the other ALL patients. At 5 years, event-free survival was 90.0% ± 4.7% and 88.4% ± 1.9%, respectively. And 5-year overall survival was 92.5% ± 4.2% and 95.1% ± 1.3%, respectively.
When available, more sophisticated genetic testing should be used to identify which of the B-ALL patients with high levels of MRD have the BCR-ABL1-like ALL subtype, Dr Pui said. Many of these patients have genetic alterations that make them responsive to tyrosine kinase inhibitors (TKIs) and possibly other targeted therapies.
For example, in this study, the researchers evaluated genetic abnormalities in 25 BCR-ABL1-like ALL patients. Eleven had a genomic rearrangement of CRLF2, 6 had fusion transcripts responsive to ABL TKIs or JAK inhibitors, and 7 had mutations involving the Ras signaling pathway.
“In the future, genetic testing will likely be used at diagnosis to identify [BCR-ABL1-like ALL] and direct patients to the best targeted therapy,” Dr Pui said, “possibly including some drugs that are currently experimental.”
Credit: St Jude Biomedical
Communications
Risk-directed therapy can level the playing field for patients with BCR-ABL1-like acute lymphoblastic leukemia (ALL), new research suggests.
Using minimal residual disease (MRD) and other risk factors to guide treatment intensity allowed patients withBCR-ABL1-like ALL to have survival rates comparable to those of other B-ALL patients.
The research also revealed that not all BCR-ABL1-like ALL patients have high-risk disease.
Ching-Hon Pui, MD, of St Jude Children’s Research Hospital in Memphis, Tennessee, and his colleagues reported these results in the Journal of Clinical Oncology.
Patients with BCR-ABL1-like ALL tend to have poor outcomes, so Dr Pui and his colleagues evaluated the utility of risk-directed therapy in these and other B-ALL patients.
The team assessed patients enrolled in the Total Therapy XV study between 2000 and 2007. They were 1 to 18 years of age at diagnosis. There were 344 subjects with adequate samples for gene expression profiling.
Forty patients (11.6%) had BCR-ABL1-like ALL. They were significantly more likely than other study participants to be male, have Down syndrome, and have higher MRD levels on day 19 and at the end of induction.
The researchers monitored patients and adjusted their treatment intensity based on MRD at days 19 and 42. The treatment regimen was described in JAMA in 2009.
The MRD monitoring combined with conventional risk factors, such as patient age and white blood count at diagnosis, demonstrated that BCR-ABL1-like ALL is not a uniformly high-risk disease.
Forty percent of BCR-ABL1-like ALL patients were actually classified as having low-risk disease because they had other favorable clinical or biological features and no MRD at the end of remission induction.
The other 60% were classified as having standard-risk or high-risk disease. The group included 6 patients who underwent transplant.
There were no significant differences in event-free or overall survival in patients with BCR-ABL1-like ALL and the other ALL patients. At 5 years, event-free survival was 90.0% ± 4.7% and 88.4% ± 1.9%, respectively. And 5-year overall survival was 92.5% ± 4.2% and 95.1% ± 1.3%, respectively.
When available, more sophisticated genetic testing should be used to identify which of the B-ALL patients with high levels of MRD have the BCR-ABL1-like ALL subtype, Dr Pui said. Many of these patients have genetic alterations that make them responsive to tyrosine kinase inhibitors (TKIs) and possibly other targeted therapies.
For example, in this study, the researchers evaluated genetic abnormalities in 25 BCR-ABL1-like ALL patients. Eleven had a genomic rearrangement of CRLF2, 6 had fusion transcripts responsive to ABL TKIs or JAK inhibitors, and 7 had mutations involving the Ras signaling pathway.
“In the future, genetic testing will likely be used at diagnosis to identify [BCR-ABL1-like ALL] and direct patients to the best targeted therapy,” Dr Pui said, “possibly including some drugs that are currently experimental.”
Credit: St Jude Biomedical
Communications
Risk-directed therapy can level the playing field for patients with BCR-ABL1-like acute lymphoblastic leukemia (ALL), new research suggests.
Using minimal residual disease (MRD) and other risk factors to guide treatment intensity allowed patients withBCR-ABL1-like ALL to have survival rates comparable to those of other B-ALL patients.
The research also revealed that not all BCR-ABL1-like ALL patients have high-risk disease.
Ching-Hon Pui, MD, of St Jude Children’s Research Hospital in Memphis, Tennessee, and his colleagues reported these results in the Journal of Clinical Oncology.
Patients with BCR-ABL1-like ALL tend to have poor outcomes, so Dr Pui and his colleagues evaluated the utility of risk-directed therapy in these and other B-ALL patients.
The team assessed patients enrolled in the Total Therapy XV study between 2000 and 2007. They were 1 to 18 years of age at diagnosis. There were 344 subjects with adequate samples for gene expression profiling.
Forty patients (11.6%) had BCR-ABL1-like ALL. They were significantly more likely than other study participants to be male, have Down syndrome, and have higher MRD levels on day 19 and at the end of induction.
The researchers monitored patients and adjusted their treatment intensity based on MRD at days 19 and 42. The treatment regimen was described in JAMA in 2009.
The MRD monitoring combined with conventional risk factors, such as patient age and white blood count at diagnosis, demonstrated that BCR-ABL1-like ALL is not a uniformly high-risk disease.
Forty percent of BCR-ABL1-like ALL patients were actually classified as having low-risk disease because they had other favorable clinical or biological features and no MRD at the end of remission induction.
The other 60% were classified as having standard-risk or high-risk disease. The group included 6 patients who underwent transplant.
There were no significant differences in event-free or overall survival in patients with BCR-ABL1-like ALL and the other ALL patients. At 5 years, event-free survival was 90.0% ± 4.7% and 88.4% ± 1.9%, respectively. And 5-year overall survival was 92.5% ± 4.2% and 95.1% ± 1.3%, respectively.
When available, more sophisticated genetic testing should be used to identify which of the B-ALL patients with high levels of MRD have the BCR-ABL1-like ALL subtype, Dr Pui said. Many of these patients have genetic alterations that make them responsive to tyrosine kinase inhibitors (TKIs) and possibly other targeted therapies.
For example, in this study, the researchers evaluated genetic abnormalities in 25 BCR-ABL1-like ALL patients. Eleven had a genomic rearrangement of CRLF2, 6 had fusion transcripts responsive to ABL TKIs or JAK inhibitors, and 7 had mutations involving the Ras signaling pathway.
“In the future, genetic testing will likely be used at diagnosis to identify [BCR-ABL1-like ALL] and direct patients to the best targeted therapy,” Dr Pui said, “possibly including some drugs that are currently experimental.”
Program for poor can boost hospital profits
Credit: Petr Kratochvil
A federal program designed to help the poor may actually be used to help US hospitals increase their profits, according to research published in Health Affairs.
Researchers examined enrollment in the 340B program, which provides deep discounts on outpatient drug purchases.
They found that hospitals and clinics that joined the program since 2004 currently serve more affluent and well-insured communities than those that qualified for the program in previous years.
This supports the idea that the program is changing from one that serves patients in need to one that enriches hospitals and their affiliated clinics, according to the researchers.
“This study provides the first nationally representative empirical evidence suggesting that the program’s original intent is being eroded by the actions of certain hospitals,” said study author Rena M. Conti, PhD, of the University of Chicago in Illinois.
This study follows work by Dr Conti and Peter B. Bach, MD, of Memorial Sloan-Kettering Cancer Center in New York, that was published in JAMA last year.
The JAMA study explained how 340B-qualified hospital-affiliated clinics can boost profits thanks to discounts on expensive anticancer drugs. The facilities receive the discounts under the expectation that the savings will be passed on to poor patients.
“Hospitals qualify for the program based on the poverty of their inpatient census only,” Dr Conti said. “The affiliated clinics are the only 340B institutions not required to pass the discounts off to patients or their insurers, nor do they have to report to the government exactly how these profits are used to serve the poor. Insurers’ and their patients’ payments for outpatient drug treatment don’t reflect the discounts the hospital receives.”
The 340B program, which began in 1992, was designed to help selected hospitals and their outpatient clinics serve low-income and uninsured patients by providing discounts of 30% to 50% on outpatient drugs.
About a decade ago, enrollment in 340B began to increase rapidly. Now, more than a third of the 4375 US non-federal hospitals are 340B-qualified. Recent Congressional and news reports suggest that, for selected hospitals, profits off the 340B program can be significant.
For their new study, Drs Conti and Bach examined the populations served by hospitals and clinics qualifying for 340B before and after the decade-long growth spurt. They matched data for all hospitals and clinics registered with the 340B program to socioeconomic data from the US Census Bureau.
The results showed that communities served by hospital-affiliated clinics joining the program in 2004 or later tended to have higher household incomes, much less unemployment, and higher rates of health insurance.
The researchers said their findings are consistent with recent complaints that, rather than serving vulnerable communities, the 340B program is being used to increase profits for hospitals and their affiliated clinics.
Credit: Petr Kratochvil
A federal program designed to help the poor may actually be used to help US hospitals increase their profits, according to research published in Health Affairs.
Researchers examined enrollment in the 340B program, which provides deep discounts on outpatient drug purchases.
They found that hospitals and clinics that joined the program since 2004 currently serve more affluent and well-insured communities than those that qualified for the program in previous years.
This supports the idea that the program is changing from one that serves patients in need to one that enriches hospitals and their affiliated clinics, according to the researchers.
“This study provides the first nationally representative empirical evidence suggesting that the program’s original intent is being eroded by the actions of certain hospitals,” said study author Rena M. Conti, PhD, of the University of Chicago in Illinois.
This study follows work by Dr Conti and Peter B. Bach, MD, of Memorial Sloan-Kettering Cancer Center in New York, that was published in JAMA last year.
The JAMA study explained how 340B-qualified hospital-affiliated clinics can boost profits thanks to discounts on expensive anticancer drugs. The facilities receive the discounts under the expectation that the savings will be passed on to poor patients.
“Hospitals qualify for the program based on the poverty of their inpatient census only,” Dr Conti said. “The affiliated clinics are the only 340B institutions not required to pass the discounts off to patients or their insurers, nor do they have to report to the government exactly how these profits are used to serve the poor. Insurers’ and their patients’ payments for outpatient drug treatment don’t reflect the discounts the hospital receives.”
The 340B program, which began in 1992, was designed to help selected hospitals and their outpatient clinics serve low-income and uninsured patients by providing discounts of 30% to 50% on outpatient drugs.
About a decade ago, enrollment in 340B began to increase rapidly. Now, more than a third of the 4375 US non-federal hospitals are 340B-qualified. Recent Congressional and news reports suggest that, for selected hospitals, profits off the 340B program can be significant.
For their new study, Drs Conti and Bach examined the populations served by hospitals and clinics qualifying for 340B before and after the decade-long growth spurt. They matched data for all hospitals and clinics registered with the 340B program to socioeconomic data from the US Census Bureau.
The results showed that communities served by hospital-affiliated clinics joining the program in 2004 or later tended to have higher household incomes, much less unemployment, and higher rates of health insurance.
The researchers said their findings are consistent with recent complaints that, rather than serving vulnerable communities, the 340B program is being used to increase profits for hospitals and their affiliated clinics.
Credit: Petr Kratochvil
A federal program designed to help the poor may actually be used to help US hospitals increase their profits, according to research published in Health Affairs.
Researchers examined enrollment in the 340B program, which provides deep discounts on outpatient drug purchases.
They found that hospitals and clinics that joined the program since 2004 currently serve more affluent and well-insured communities than those that qualified for the program in previous years.
This supports the idea that the program is changing from one that serves patients in need to one that enriches hospitals and their affiliated clinics, according to the researchers.
“This study provides the first nationally representative empirical evidence suggesting that the program’s original intent is being eroded by the actions of certain hospitals,” said study author Rena M. Conti, PhD, of the University of Chicago in Illinois.
This study follows work by Dr Conti and Peter B. Bach, MD, of Memorial Sloan-Kettering Cancer Center in New York, that was published in JAMA last year.
The JAMA study explained how 340B-qualified hospital-affiliated clinics can boost profits thanks to discounts on expensive anticancer drugs. The facilities receive the discounts under the expectation that the savings will be passed on to poor patients.
“Hospitals qualify for the program based on the poverty of their inpatient census only,” Dr Conti said. “The affiliated clinics are the only 340B institutions not required to pass the discounts off to patients or their insurers, nor do they have to report to the government exactly how these profits are used to serve the poor. Insurers’ and their patients’ payments for outpatient drug treatment don’t reflect the discounts the hospital receives.”
The 340B program, which began in 1992, was designed to help selected hospitals and their outpatient clinics serve low-income and uninsured patients by providing discounts of 30% to 50% on outpatient drugs.
About a decade ago, enrollment in 340B began to increase rapidly. Now, more than a third of the 4375 US non-federal hospitals are 340B-qualified. Recent Congressional and news reports suggest that, for selected hospitals, profits off the 340B program can be significant.
For their new study, Drs Conti and Bach examined the populations served by hospitals and clinics qualifying for 340B before and after the decade-long growth spurt. They matched data for all hospitals and clinics registered with the 340B program to socioeconomic data from the US Census Bureau.
The results showed that communities served by hospital-affiliated clinics joining the program in 2004 or later tended to have higher household incomes, much less unemployment, and higher rates of health insurance.
The researchers said their findings are consistent with recent complaints that, rather than serving vulnerable communities, the 340B program is being used to increase profits for hospitals and their affiliated clinics.
Mental health challenges fairly common in cancer patients
chemotherapy
Credit: Rhoda Baer
In a large German study, investigators found that nearly a third of cancer patients experienced some form of clinically relevant mental health
challenge.
Of the more than 2100 cancer patients interviewed, 32% had experienced a clinically meaningful level of mental or emotional distress in the previous 4 weeks.
This prevalence is higher than that observed in the general population, and the difference is primarily due to a higher rate of anxiety and adjustment disorders.
The incidence of mental health issues varied by cancer type. The highest was among patients with breast cancer (42%) and head and neck cancer (41%), followed by malignant melanoma (39%).
The lowest prevalence was seen among patients with prostate cancer (22%), stomach cancers (21%), and pancreatic cancer (20%).
These results appear in the Journal of Clinical Oncology.
“These findings reinforce that, as doctors, we need to be very aware of signs and symptoms of mental and emotional distress,” said lead study author Anja Mehnert, PhD, of the University of Leipzig in Germany.
“We must encourage patients to seek evaluation, support, and treatment if necessary, as there are long-term risks often associated with more severe, untreated mental health disorders. This research also sheds light on which patients we should watch more closely.”
Dr Mehnert and her colleagues conducted this study in 2141 cancer patients who were 18 to 75 years of age. The team conducted face-to-face interviews in hospitals, outpatient cancer care centers, and rehabilitation centers in Germany.
Interview answers were immediately entered into a computer based-diagnostic program. The test assessed various psychological symptoms over the previous 4-week period. Patients’ diagnoses were classified according to the Diagnostic and Statistical Manual of Mental Disorders, the standard classification used by mental health professionals.
The patients had a range of cancer types, with the most common being breast cancer (44%), prostate cancer (15%), and colorectal cancer (14%). The average time since cancer diagnosis was 13.5 months, and 51% of the participants were women.
The researchers found that 32% of patients experienced at least one clinically meaningful mental health issue (defined in the study as a mental health disorder). This is a higher prevalence than in the general population, in which 18% to 20% of people are estimated to have a clinically meaningful mental disorder.
In the 4-week period prior to the interview, 11.5% of patients experienced an anxiety disorder. Eleven percent met the criteria for an adjustment disorder, a predominantly mixed anxiety-depressive syndrome that persisted for at least 4 weeks in response to a significant life change. And 6.5% of patients had signs of a mood disorder such as major depression.
The 11.5% rate of anxiety disorders—such as phobia, panic, or generalized anxiety disorder—was slightly higher than in the general population (9%), while the prevalence of other mental health diagnoses was similar to rates in the general population.
It is likely that the prevalence of adjustment disorders (11%), which is rarely assessed in general population surveys, significantly contributed to the overall higher prevalence rate of mental disorders in this population of patients with cancer.
Dr Mehnert said it was surprising that patients with a more treatable malignancy, such as breast cancer, experienced more distress than people with cancers that are more challenging to treat, such as stomach and pancreatic cancers. So more research is needed to interpret these findings.
The investigators believe the study’s results may be useful for planning future support programs for cancer patients, and they can provide additional information to guide programs for people with specific cancer types.
The team also believes the findings can likely be generalized to patients in the US because the prevalence of mental health diagnoses is similar between the 2 countries.
chemotherapy
Credit: Rhoda Baer
In a large German study, investigators found that nearly a third of cancer patients experienced some form of clinically relevant mental health
challenge.
Of the more than 2100 cancer patients interviewed, 32% had experienced a clinically meaningful level of mental or emotional distress in the previous 4 weeks.
This prevalence is higher than that observed in the general population, and the difference is primarily due to a higher rate of anxiety and adjustment disorders.
The incidence of mental health issues varied by cancer type. The highest was among patients with breast cancer (42%) and head and neck cancer (41%), followed by malignant melanoma (39%).
The lowest prevalence was seen among patients with prostate cancer (22%), stomach cancers (21%), and pancreatic cancer (20%).
These results appear in the Journal of Clinical Oncology.
“These findings reinforce that, as doctors, we need to be very aware of signs and symptoms of mental and emotional distress,” said lead study author Anja Mehnert, PhD, of the University of Leipzig in Germany.
“We must encourage patients to seek evaluation, support, and treatment if necessary, as there are long-term risks often associated with more severe, untreated mental health disorders. This research also sheds light on which patients we should watch more closely.”
Dr Mehnert and her colleagues conducted this study in 2141 cancer patients who were 18 to 75 years of age. The team conducted face-to-face interviews in hospitals, outpatient cancer care centers, and rehabilitation centers in Germany.
Interview answers were immediately entered into a computer based-diagnostic program. The test assessed various psychological symptoms over the previous 4-week period. Patients’ diagnoses were classified according to the Diagnostic and Statistical Manual of Mental Disorders, the standard classification used by mental health professionals.
The patients had a range of cancer types, with the most common being breast cancer (44%), prostate cancer (15%), and colorectal cancer (14%). The average time since cancer diagnosis was 13.5 months, and 51% of the participants were women.
The researchers found that 32% of patients experienced at least one clinically meaningful mental health issue (defined in the study as a mental health disorder). This is a higher prevalence than in the general population, in which 18% to 20% of people are estimated to have a clinically meaningful mental disorder.
In the 4-week period prior to the interview, 11.5% of patients experienced an anxiety disorder. Eleven percent met the criteria for an adjustment disorder, a predominantly mixed anxiety-depressive syndrome that persisted for at least 4 weeks in response to a significant life change. And 6.5% of patients had signs of a mood disorder such as major depression.
The 11.5% rate of anxiety disorders—such as phobia, panic, or generalized anxiety disorder—was slightly higher than in the general population (9%), while the prevalence of other mental health diagnoses was similar to rates in the general population.
It is likely that the prevalence of adjustment disorders (11%), which is rarely assessed in general population surveys, significantly contributed to the overall higher prevalence rate of mental disorders in this population of patients with cancer.
Dr Mehnert said it was surprising that patients with a more treatable malignancy, such as breast cancer, experienced more distress than people with cancers that are more challenging to treat, such as stomach and pancreatic cancers. So more research is needed to interpret these findings.
The investigators believe the study’s results may be useful for planning future support programs for cancer patients, and they can provide additional information to guide programs for people with specific cancer types.
The team also believes the findings can likely be generalized to patients in the US because the prevalence of mental health diagnoses is similar between the 2 countries.
chemotherapy
Credit: Rhoda Baer
In a large German study, investigators found that nearly a third of cancer patients experienced some form of clinically relevant mental health
challenge.
Of the more than 2100 cancer patients interviewed, 32% had experienced a clinically meaningful level of mental or emotional distress in the previous 4 weeks.
This prevalence is higher than that observed in the general population, and the difference is primarily due to a higher rate of anxiety and adjustment disorders.
The incidence of mental health issues varied by cancer type. The highest was among patients with breast cancer (42%) and head and neck cancer (41%), followed by malignant melanoma (39%).
The lowest prevalence was seen among patients with prostate cancer (22%), stomach cancers (21%), and pancreatic cancer (20%).
These results appear in the Journal of Clinical Oncology.
“These findings reinforce that, as doctors, we need to be very aware of signs and symptoms of mental and emotional distress,” said lead study author Anja Mehnert, PhD, of the University of Leipzig in Germany.
“We must encourage patients to seek evaluation, support, and treatment if necessary, as there are long-term risks often associated with more severe, untreated mental health disorders. This research also sheds light on which patients we should watch more closely.”
Dr Mehnert and her colleagues conducted this study in 2141 cancer patients who were 18 to 75 years of age. The team conducted face-to-face interviews in hospitals, outpatient cancer care centers, and rehabilitation centers in Germany.
Interview answers were immediately entered into a computer based-diagnostic program. The test assessed various psychological symptoms over the previous 4-week period. Patients’ diagnoses were classified according to the Diagnostic and Statistical Manual of Mental Disorders, the standard classification used by mental health professionals.
The patients had a range of cancer types, with the most common being breast cancer (44%), prostate cancer (15%), and colorectal cancer (14%). The average time since cancer diagnosis was 13.5 months, and 51% of the participants were women.
The researchers found that 32% of patients experienced at least one clinically meaningful mental health issue (defined in the study as a mental health disorder). This is a higher prevalence than in the general population, in which 18% to 20% of people are estimated to have a clinically meaningful mental disorder.
In the 4-week period prior to the interview, 11.5% of patients experienced an anxiety disorder. Eleven percent met the criteria for an adjustment disorder, a predominantly mixed anxiety-depressive syndrome that persisted for at least 4 weeks in response to a significant life change. And 6.5% of patients had signs of a mood disorder such as major depression.
The 11.5% rate of anxiety disorders—such as phobia, panic, or generalized anxiety disorder—was slightly higher than in the general population (9%), while the prevalence of other mental health diagnoses was similar to rates in the general population.
It is likely that the prevalence of adjustment disorders (11%), which is rarely assessed in general population surveys, significantly contributed to the overall higher prevalence rate of mental disorders in this population of patients with cancer.
Dr Mehnert said it was surprising that patients with a more treatable malignancy, such as breast cancer, experienced more distress than people with cancers that are more challenging to treat, such as stomach and pancreatic cancers. So more research is needed to interpret these findings.
The investigators believe the study’s results may be useful for planning future support programs for cancer patients, and they can provide additional information to guide programs for people with specific cancer types.
The team also believes the findings can likely be generalized to patients in the US because the prevalence of mental health diagnoses is similar between the 2 countries.
FDA allows access to pathogen inactivation system
The US Food and Drug Administration (FDA) has authorized the use of a pathogen inactivation system in regions of the US and its territories affected by outbreaks of Chikungunya and dengue virus.
The INTERCEPT Blood System for platelets is used for the preparation and storage of whole blood-derived and apheresis platelets.
The system can inactivate a range of viruses, bacteria, and parasites to reduce the risk of transmission via platelet transfusion. It can also prevent transfusion-associated graft-vs-host disease and reduce the risk of other adverse effects due to transfusion of contaminating donor leukocytes.
The INTERCEPT Blood System for platelets has not been granted full FDA approval. The agency has approved use of the system via an investigational device exemption (IDE).
This allows for early access to a device not yet approved in the US when no satisfactory alternative is available to treat patients with serious or life-threatening conditions.
The INTERCEPT Blood System for platelets will initially be available to sites in Puerto Rico that agree to participate in a clinical study. Depending on the scope of participation there, the system may be made available to sites in other areas where cases of Chikungunya and dengue have been reported, such as Florida and Texas.
“We are pleased to provide US blood centers and hospitals early access to INTERCEPT for the treatment of platelet components in light of the escalating threat of Chikungunya and dengue transfusion-transmitted infections,” said Carol Moore, of Cerus Corporation, the company developing the INTERCEPT system.
“With this expeditious approval of our IDE, we hope to initiate our first study site before year-end.”
About the system
The INTERCEPT Blood System for platelets is based on the premise that platelets don’t require functional DNA or RNA, but pathogens and contaminating leukocytes do. The system deploys proprietary molecules that, when activated, bind to and block the replication of DNA and RNA in the blood.
The system uses amotosalen HCl (a photoactive compound) and long-wavelength ultraviolet illumination to photochemically treat platelet components, rendering susceptible pathogens incapable of replicating and causing disease.
Published studies have demonstrated INTERCEPT inactivation of >6.4 log of Chikungunya and >5.3 log of dengue infectious titers, both in excess of observed titers in asymptomatic donors.
The INTERCEPT platelet system has been approved in Europe since 2002 and is currently used at more than 100 blood centers in 20 countries. The system is under regulatory review in the US, Canada, Brazil, and China.
About dengue and Chikungunya
Dengue virus is endemic to the Caribbean region. Local transmission of Chikungunya virus was detected in the Caribbean for the first time in February 2014. Both viruses are spread by species of mosquitoes common in tropical climates and regions within the continental US.
As of September 30, 2014, the Centers for Disease Control and Prevention has reported 11 confirmed locally transmitted cases of Chikungunya in
Florida, 421 cases in Puerto Rico, and 45 cases in the US Virgin Islands. Local transmission of dengue has also been reported in Texas and Florida.
Chikungunya virus causes high fevers, joint pain and swelling, headaches, and a rash. Symptoms have been reported to persist for up to 2 years in chronic cases. Rarely, Chikungunya can be fatal.
Symptoms of dengue include high fever, headaches, joint and muscle pain, vomiting, and a rash. In some cases, dengue infection is life-threatening due to dengue hemorrhagic fever, which causes bleeding from the nose, gums, or under the skin.
The US Food and Drug Administration (FDA) has authorized the use of a pathogen inactivation system in regions of the US and its territories affected by outbreaks of Chikungunya and dengue virus.
The INTERCEPT Blood System for platelets is used for the preparation and storage of whole blood-derived and apheresis platelets.
The system can inactivate a range of viruses, bacteria, and parasites to reduce the risk of transmission via platelet transfusion. It can also prevent transfusion-associated graft-vs-host disease and reduce the risk of other adverse effects due to transfusion of contaminating donor leukocytes.
The INTERCEPT Blood System for platelets has not been granted full FDA approval. The agency has approved use of the system via an investigational device exemption (IDE).
This allows for early access to a device not yet approved in the US when no satisfactory alternative is available to treat patients with serious or life-threatening conditions.
The INTERCEPT Blood System for platelets will initially be available to sites in Puerto Rico that agree to participate in a clinical study. Depending on the scope of participation there, the system may be made available to sites in other areas where cases of Chikungunya and dengue have been reported, such as Florida and Texas.
“We are pleased to provide US blood centers and hospitals early access to INTERCEPT for the treatment of platelet components in light of the escalating threat of Chikungunya and dengue transfusion-transmitted infections,” said Carol Moore, of Cerus Corporation, the company developing the INTERCEPT system.
“With this expeditious approval of our IDE, we hope to initiate our first study site before year-end.”
About the system
The INTERCEPT Blood System for platelets is based on the premise that platelets don’t require functional DNA or RNA, but pathogens and contaminating leukocytes do. The system deploys proprietary molecules that, when activated, bind to and block the replication of DNA and RNA in the blood.
The system uses amotosalen HCl (a photoactive compound) and long-wavelength ultraviolet illumination to photochemically treat platelet components, rendering susceptible pathogens incapable of replicating and causing disease.
Published studies have demonstrated INTERCEPT inactivation of >6.4 log of Chikungunya and >5.3 log of dengue infectious titers, both in excess of observed titers in asymptomatic donors.
The INTERCEPT platelet system has been approved in Europe since 2002 and is currently used at more than 100 blood centers in 20 countries. The system is under regulatory review in the US, Canada, Brazil, and China.
About dengue and Chikungunya
Dengue virus is endemic to the Caribbean region. Local transmission of Chikungunya virus was detected in the Caribbean for the first time in February 2014. Both viruses are spread by species of mosquitoes common in tropical climates and regions within the continental US.
As of September 30, 2014, the Centers for Disease Control and Prevention has reported 11 confirmed locally transmitted cases of Chikungunya in
Florida, 421 cases in Puerto Rico, and 45 cases in the US Virgin Islands. Local transmission of dengue has also been reported in Texas and Florida.
Chikungunya virus causes high fevers, joint pain and swelling, headaches, and a rash. Symptoms have been reported to persist for up to 2 years in chronic cases. Rarely, Chikungunya can be fatal.
Symptoms of dengue include high fever, headaches, joint and muscle pain, vomiting, and a rash. In some cases, dengue infection is life-threatening due to dengue hemorrhagic fever, which causes bleeding from the nose, gums, or under the skin.
The US Food and Drug Administration (FDA) has authorized the use of a pathogen inactivation system in regions of the US and its territories affected by outbreaks of Chikungunya and dengue virus.
The INTERCEPT Blood System for platelets is used for the preparation and storage of whole blood-derived and apheresis platelets.
The system can inactivate a range of viruses, bacteria, and parasites to reduce the risk of transmission via platelet transfusion. It can also prevent transfusion-associated graft-vs-host disease and reduce the risk of other adverse effects due to transfusion of contaminating donor leukocytes.
The INTERCEPT Blood System for platelets has not been granted full FDA approval. The agency has approved use of the system via an investigational device exemption (IDE).
This allows for early access to a device not yet approved in the US when no satisfactory alternative is available to treat patients with serious or life-threatening conditions.
The INTERCEPT Blood System for platelets will initially be available to sites in Puerto Rico that agree to participate in a clinical study. Depending on the scope of participation there, the system may be made available to sites in other areas where cases of Chikungunya and dengue have been reported, such as Florida and Texas.
“We are pleased to provide US blood centers and hospitals early access to INTERCEPT for the treatment of platelet components in light of the escalating threat of Chikungunya and dengue transfusion-transmitted infections,” said Carol Moore, of Cerus Corporation, the company developing the INTERCEPT system.
“With this expeditious approval of our IDE, we hope to initiate our first study site before year-end.”
About the system
The INTERCEPT Blood System for platelets is based on the premise that platelets don’t require functional DNA or RNA, but pathogens and contaminating leukocytes do. The system deploys proprietary molecules that, when activated, bind to and block the replication of DNA and RNA in the blood.
The system uses amotosalen HCl (a photoactive compound) and long-wavelength ultraviolet illumination to photochemically treat platelet components, rendering susceptible pathogens incapable of replicating and causing disease.
Published studies have demonstrated INTERCEPT inactivation of >6.4 log of Chikungunya and >5.3 log of dengue infectious titers, both in excess of observed titers in asymptomatic donors.
The INTERCEPT platelet system has been approved in Europe since 2002 and is currently used at more than 100 blood centers in 20 countries. The system is under regulatory review in the US, Canada, Brazil, and China.
About dengue and Chikungunya
Dengue virus is endemic to the Caribbean region. Local transmission of Chikungunya virus was detected in the Caribbean for the first time in February 2014. Both viruses are spread by species of mosquitoes common in tropical climates and regions within the continental US.
As of September 30, 2014, the Centers for Disease Control and Prevention has reported 11 confirmed locally transmitted cases of Chikungunya in
Florida, 421 cases in Puerto Rico, and 45 cases in the US Virgin Islands. Local transmission of dengue has also been reported in Texas and Florida.
Chikungunya virus causes high fevers, joint pain and swelling, headaches, and a rash. Symptoms have been reported to persist for up to 2 years in chronic cases. Rarely, Chikungunya can be fatal.
Symptoms of dengue include high fever, headaches, joint and muscle pain, vomiting, and a rash. In some cases, dengue infection is life-threatening due to dengue hemorrhagic fever, which causes bleeding from the nose, gums, or under the skin.
A single cell can cause MPNs
Credit: Aaron Logan
Scientists have found that a single cell containing the JAK2-V617F mutation can cause myeloproliferative neoplasms (MPNs) in mice.
The team isolated hematopoietic stem cells (HSCs) from malignant MPNs and transplanted a single cell with mutated JAK2 into groups of healthy mice.
A subset of the mice developed MPNs, which also bore the JAK2 mutation.
The researchers described this work in The Journal of Experimental Medicine.
Pontus Lundberg, PhD, of University Hospital Basel in Switzerland, and his colleagues performed several sets of experiments in which they transplanted JAK2-V617F-expressing cells in dilutions of wild-type bone marrow cells.
In the 1:125 dilution experiment, 24% of mice (4/17) developed polycythemia vera (PV). In the 1:250 dilution experiment, 44% of mice developed either PV or essential thrombocythemia (ET).
The researchers were interested to find that erythrocytosis and thrombocytosis were mutually exclusive in individual mice.
Additional investigation revealed that MPN development did not depend on the acquisition of additional somatic mutations.
To confirm their findings, the researchers then transplanted a single JAK2-V617F-expressing HSC into a total of 113 mice in 4 independent experiments.
Only 1 mouse developed an ET phenotype. Two other mice had transient high chimerism in erythrocytes and/or platelets, but they did not develop ET or PV.
Furthermore, transplanting bone marrow from the mouse with the ET phenotype into secondary recipients did not result in an MPN phenotype.
The researchers also analyzed JAK2-V617F-expressing HSCs in further detail, and they found these HSCs promoted cell division and increased DNA damage.
Higher JAK2-V617F expression was associated with a short-term HSC signature and increased myeloid bias. Lower JAK2-V617F expression was associated with the capacity to stably engraft in secondary recipients.
Dr Lundberg and his colleagues said this research shows that JAK2-V617F has complex effects on HSC biology and that MPNs can develop from a single JAK2-V617F-expressing cell.
Credit: Aaron Logan
Scientists have found that a single cell containing the JAK2-V617F mutation can cause myeloproliferative neoplasms (MPNs) in mice.
The team isolated hematopoietic stem cells (HSCs) from malignant MPNs and transplanted a single cell with mutated JAK2 into groups of healthy mice.
A subset of the mice developed MPNs, which also bore the JAK2 mutation.
The researchers described this work in The Journal of Experimental Medicine.
Pontus Lundberg, PhD, of University Hospital Basel in Switzerland, and his colleagues performed several sets of experiments in which they transplanted JAK2-V617F-expressing cells in dilutions of wild-type bone marrow cells.
In the 1:125 dilution experiment, 24% of mice (4/17) developed polycythemia vera (PV). In the 1:250 dilution experiment, 44% of mice developed either PV or essential thrombocythemia (ET).
The researchers were interested to find that erythrocytosis and thrombocytosis were mutually exclusive in individual mice.
Additional investigation revealed that MPN development did not depend on the acquisition of additional somatic mutations.
To confirm their findings, the researchers then transplanted a single JAK2-V617F-expressing HSC into a total of 113 mice in 4 independent experiments.
Only 1 mouse developed an ET phenotype. Two other mice had transient high chimerism in erythrocytes and/or platelets, but they did not develop ET or PV.
Furthermore, transplanting bone marrow from the mouse with the ET phenotype into secondary recipients did not result in an MPN phenotype.
The researchers also analyzed JAK2-V617F-expressing HSCs in further detail, and they found these HSCs promoted cell division and increased DNA damage.
Higher JAK2-V617F expression was associated with a short-term HSC signature and increased myeloid bias. Lower JAK2-V617F expression was associated with the capacity to stably engraft in secondary recipients.
Dr Lundberg and his colleagues said this research shows that JAK2-V617F has complex effects on HSC biology and that MPNs can develop from a single JAK2-V617F-expressing cell.
Credit: Aaron Logan
Scientists have found that a single cell containing the JAK2-V617F mutation can cause myeloproliferative neoplasms (MPNs) in mice.
The team isolated hematopoietic stem cells (HSCs) from malignant MPNs and transplanted a single cell with mutated JAK2 into groups of healthy mice.
A subset of the mice developed MPNs, which also bore the JAK2 mutation.
The researchers described this work in The Journal of Experimental Medicine.
Pontus Lundberg, PhD, of University Hospital Basel in Switzerland, and his colleagues performed several sets of experiments in which they transplanted JAK2-V617F-expressing cells in dilutions of wild-type bone marrow cells.
In the 1:125 dilution experiment, 24% of mice (4/17) developed polycythemia vera (PV). In the 1:250 dilution experiment, 44% of mice developed either PV or essential thrombocythemia (ET).
The researchers were interested to find that erythrocytosis and thrombocytosis were mutually exclusive in individual mice.
Additional investigation revealed that MPN development did not depend on the acquisition of additional somatic mutations.
To confirm their findings, the researchers then transplanted a single JAK2-V617F-expressing HSC into a total of 113 mice in 4 independent experiments.
Only 1 mouse developed an ET phenotype. Two other mice had transient high chimerism in erythrocytes and/or platelets, but they did not develop ET or PV.
Furthermore, transplanting bone marrow from the mouse with the ET phenotype into secondary recipients did not result in an MPN phenotype.
The researchers also analyzed JAK2-V617F-expressing HSCs in further detail, and they found these HSCs promoted cell division and increased DNA damage.
Higher JAK2-V617F expression was associated with a short-term HSC signature and increased myeloid bias. Lower JAK2-V617F expression was associated with the capacity to stably engraft in secondary recipients.
Dr Lundberg and his colleagues said this research shows that JAK2-V617F has complex effects on HSC biology and that MPNs can develop from a single JAK2-V617F-expressing cell.
Survey shows lack of adherence to safety guidelines
Credit: Bill Branson
Healthcare professionals do not consistently follow the recommended safe handling practices for antineoplastic drugs, according to a survey published in the Journal of Occupational and Environmental Hygiene.
Researchers surveyed more than 2000 healthcare workers and found that a majority do not always use the recommended personal protective equipment when they are administering antineoplastic drugs.
Furthermore, some respondents reported spills or leaks of a drug during administration, and a small percentage said they had experienced skin
contact with an antineoplastic drug.
“Chemotherapy drugs save lives of cancer patients but also can result in adverse health outcomes in workers who are exposed to these drugs, including cancer, reproductive problems, and organ damage when recommended safe handling guidelines are not followed,” said John Howard, MD, director of the National Institute for Occupational Safety and Health (NIOSH).
NIOSH researchers conducted this study, which included 2069 healthcare personnel who completed the 2011 Health and Safety Practices Survey of Healthcare Workers.
Results showed that, despite the longstanding availability of authoritative safe handling guidelines (ASHP, NIOSH, ONS, OSHA), recommended exposure controls were not always used.
For example, 80% of respondents said they do not always wear 2 pairs of chemotherapy gloves, and 15% said they don’t always wear a single pair.
Forty-two percent of respondents said they don’t always wear a nonabsorbent gown with a closed front and tight-fitting cuffs, and 12% had taken home potentially contaminated clothing.
Twelve percent of respondents reported a spill or leak of an antineoplastic drug during administration, and 4% reported skin contact with an antineoplastic drug.
Six percent of respondents said they primed intravenous tubing with an antineoplastic drug instead of a non-drug containing liquid, and 12% said the pharmacy department followed this practice.
Taking these and other findings into account, the researchers concluded that better risk communication is needed to ensure that employers and employees are fully aware of the hazards and the availability of precautionary measures to minimize exposure to antineoplastic drugs.
Credit: Bill Branson
Healthcare professionals do not consistently follow the recommended safe handling practices for antineoplastic drugs, according to a survey published in the Journal of Occupational and Environmental Hygiene.
Researchers surveyed more than 2000 healthcare workers and found that a majority do not always use the recommended personal protective equipment when they are administering antineoplastic drugs.
Furthermore, some respondents reported spills or leaks of a drug during administration, and a small percentage said they had experienced skin
contact with an antineoplastic drug.
“Chemotherapy drugs save lives of cancer patients but also can result in adverse health outcomes in workers who are exposed to these drugs, including cancer, reproductive problems, and organ damage when recommended safe handling guidelines are not followed,” said John Howard, MD, director of the National Institute for Occupational Safety and Health (NIOSH).
NIOSH researchers conducted this study, which included 2069 healthcare personnel who completed the 2011 Health and Safety Practices Survey of Healthcare Workers.
Results showed that, despite the longstanding availability of authoritative safe handling guidelines (ASHP, NIOSH, ONS, OSHA), recommended exposure controls were not always used.
For example, 80% of respondents said they do not always wear 2 pairs of chemotherapy gloves, and 15% said they don’t always wear a single pair.
Forty-two percent of respondents said they don’t always wear a nonabsorbent gown with a closed front and tight-fitting cuffs, and 12% had taken home potentially contaminated clothing.
Twelve percent of respondents reported a spill or leak of an antineoplastic drug during administration, and 4% reported skin contact with an antineoplastic drug.
Six percent of respondents said they primed intravenous tubing with an antineoplastic drug instead of a non-drug containing liquid, and 12% said the pharmacy department followed this practice.
Taking these and other findings into account, the researchers concluded that better risk communication is needed to ensure that employers and employees are fully aware of the hazards and the availability of precautionary measures to minimize exposure to antineoplastic drugs.
Credit: Bill Branson
Healthcare professionals do not consistently follow the recommended safe handling practices for antineoplastic drugs, according to a survey published in the Journal of Occupational and Environmental Hygiene.
Researchers surveyed more than 2000 healthcare workers and found that a majority do not always use the recommended personal protective equipment when they are administering antineoplastic drugs.
Furthermore, some respondents reported spills or leaks of a drug during administration, and a small percentage said they had experienced skin
contact with an antineoplastic drug.
“Chemotherapy drugs save lives of cancer patients but also can result in adverse health outcomes in workers who are exposed to these drugs, including cancer, reproductive problems, and organ damage when recommended safe handling guidelines are not followed,” said John Howard, MD, director of the National Institute for Occupational Safety and Health (NIOSH).
NIOSH researchers conducted this study, which included 2069 healthcare personnel who completed the 2011 Health and Safety Practices Survey of Healthcare Workers.
Results showed that, despite the longstanding availability of authoritative safe handling guidelines (ASHP, NIOSH, ONS, OSHA), recommended exposure controls were not always used.
For example, 80% of respondents said they do not always wear 2 pairs of chemotherapy gloves, and 15% said they don’t always wear a single pair.
Forty-two percent of respondents said they don’t always wear a nonabsorbent gown with a closed front and tight-fitting cuffs, and 12% had taken home potentially contaminated clothing.
Twelve percent of respondents reported a spill or leak of an antineoplastic drug during administration, and 4% reported skin contact with an antineoplastic drug.
Six percent of respondents said they primed intravenous tubing with an antineoplastic drug instead of a non-drug containing liquid, and 12% said the pharmacy department followed this practice.
Taking these and other findings into account, the researchers concluded that better risk communication is needed to ensure that employers and employees are fully aware of the hazards and the availability of precautionary measures to minimize exposure to antineoplastic drugs.