A new study overturns longstanding scientific ideas regarding how
energy is distributed within muscles for powering movement. Scientists
are reporting the first clear evidence that muscle cells distribute
energy primarily by the rapid conduction of electrical charges through a
vast, interconnected network of mitochondria, the cell’s “powerhouse”, in a way that resembles the wire grid that distributes power
throughout a city. The study offers an unprecedented, detailed look at
the distribution system that rapidly provides energy throughout the
cell where it is needed for muscle contraction.
The scientists accomplished the results using state-of-the-art
imaging technologies at the National Heart, Lung, and Blood Institute
(NHLBI) and the National Cancer Institute (NCI) at the National
Institutes of Health in Bethesda, Maryland. This new information may
lead to a better understanding of many diseases linked to energy
utilization in the heart and skeletal muscle such as heart disease,
mitochondrial diseases, and muscular dystrophy, they say.
“The discovery of this mechanism for rapid distribution
of energy throughout the muscle cell will change the way scientists
think about muscle function and will open up a whole new area to
explore in health and disease,” says Robert S. Balaban, Ph.D.
This site is for information on the various Chemo treatments and Stem Cell Therapies since 1992. This journey became bitter sweet in 2014, with the passing of my beautiful and dear wife. Sherry, had fought Non - Hodgkins Lymphoma(NHL) since 1990, in and out of remissions time and time again. From T-Cell therapies(1990's) to Dual Cord Blood Transplant(2014), she was in Clinical Trials over the years. This site is for informational purpose only and is not to promote the use of certain therapies.
Thursday, July 30, 2015
New diagnostic tool Ovarian Cancer treatment
A new type of diagnostic system using sophisticated computer software
capable of analyzing and comparing cancerous tissue against a vast
databank of digital images of cancer samples could speed up treatment
for ovarian cancer.
The system, being designed by Aïcha BenTaieb, a Simon Fraser University computing science PhD student, aims to automate the identification of ovarian carcinomas for a more reliable, faster and available diagnosis. What is known is that there are five main subtypes. Effective treatment depends on identifying the subtype as soon as possible. But current methods are subjective, time-consuming and prone to error. Using information collated via computers, BenTaieb believes she has found a better way to identify these subtypes. Each ovarian cancer subtype shows individual structural and cellular characteristics. For treatment to be effectively targeted, the subtype must first be identified.
Currently, pathologists analyze tissue samples using a microscope, digital scanner and computer software. However, identification can easily be impaired by technical factors such as lighting and the pathologist’s experience.
With BenTaieb’s method, an artificial intelligence feature is integrated into the software that helps the pathologist analyze the tissue sample. This feature is trained, through a large dataset of expert annotated slides, to automatically identify the characteristic visual patterns for each subtype of carcinoma.
“We’re looking at the whole image, in different regions, in a more efficient way, using computers to extract image-based features,” BenTaieb said.
The system, being designed by Aïcha BenTaieb, a Simon Fraser University computing science PhD student, aims to automate the identification of ovarian carcinomas for a more reliable, faster and available diagnosis. What is known is that there are five main subtypes. Effective treatment depends on identifying the subtype as soon as possible. But current methods are subjective, time-consuming and prone to error. Using information collated via computers, BenTaieb believes she has found a better way to identify these subtypes. Each ovarian cancer subtype shows individual structural and cellular characteristics. For treatment to be effectively targeted, the subtype must first be identified.
Currently, pathologists analyze tissue samples using a microscope, digital scanner and computer software. However, identification can easily be impaired by technical factors such as lighting and the pathologist’s experience.
With BenTaieb’s method, an artificial intelligence feature is integrated into the software that helps the pathologist analyze the tissue sample. This feature is trained, through a large dataset of expert annotated slides, to automatically identify the characteristic visual patterns for each subtype of carcinoma.
“We’re looking at the whole image, in different regions, in a more efficient way, using computers to extract image-based features,” BenTaieb said.
Obama orders world's fastest computer
The supercomputer would be 20 times quicker than the current leading machine, which is in China.
It would be capable of making one quintillion (a billion billion) calculations per second, a figure which is known as one exaflop. A body called the National Strategic Computing Initiative (NSCI) will be set up to research and build the computer.
The US is seeking the new supercomputer, significantly faster than today's models, to perform complex simulations, aid scientific research and national security projects.
It is hoped the machine would help to analyse weather data for more accurate forecasts or assist in cancer diagnoses by analysing X-ray images.
Richard Kenway at the University of Edinburgh says he thinks the plan is "spot on" in terms of strategy, bringing together both the ambition to develop new hardware and also improved analysis of big data.
He explained the computer could aid the development of personalised medicines, tailored to specific individuals.
"Today, drugs are designed for the average human and they work OK for some people but not others," he told the BBC.
"The real challenge in precision medicine is to move from designing average drugs to designing drugs for the individual because you can know their genome and their lifestyle."
It would be capable of making one quintillion (a billion billion) calculations per second, a figure which is known as one exaflop. A body called the National Strategic Computing Initiative (NSCI) will be set up to research and build the computer.
The US is seeking the new supercomputer, significantly faster than today's models, to perform complex simulations, aid scientific research and national security projects.
It is hoped the machine would help to analyse weather data for more accurate forecasts or assist in cancer diagnoses by analysing X-ray images.
Richard Kenway at the University of Edinburgh says he thinks the plan is "spot on" in terms of strategy, bringing together both the ambition to develop new hardware and also improved analysis of big data.
He explained the computer could aid the development of personalised medicines, tailored to specific individuals.
"Today, drugs are designed for the average human and they work OK for some people but not others," he told the BBC.
"The real challenge in precision medicine is to move from designing average drugs to designing drugs for the individual because you can know their genome and their lifestyle."
Wednesday, July 29, 2015
V-Smart tech could be answer to Brain Tumor Treatment
Lauren Sciences LLC, the private New York biotechnology company
developing breakthrough V-Smart™ Nanomedicines for brain diseases,
announced today the receipt of a grant from Voices Against Brain Cancer
(VABC). The grant will support the development of a V-Smart™ drug
delivery for glioblastoma multiforme (GBM), the most
aggressive malignant primary brain tumor in humans.
The Lauren Sciences’ research team and laboratories are located at Ben-Gurion University of the Negev, where the V-Smart™ technology was invented before it was licensed to Lauren Sciences.
“V-Smart™ for GBM, formulated with a potent anti-tumor agent, has promise as an effective new treatment for GBM patients,” said Irwin Hollander, Ph.D., vice president for research and development at Lauren Sciences. “Our goal for this new V-Smart™ drug is to stop progression of, or eradicate, GBM, unlike standard treatments that in the vast majority of patients merely delay disease progression.“We anticipate future efficacy studies of V-Smart™ in GBM pre-clinical models and, thereafter, clinical studies in patients. Our goal is clinical validation and approval of this V-Smart™ for GBM.”
V-Smart™ for GBM will target and deliver a known chemotherapeutic that has proven potential to treat the brain tumor, but does not cross the blood-brain barrier (BBB) on its own. V-Smart™ Nanomedicines are designed to target and deliver therapeutics across the BBB and into selective brain cells both non-invasively and effectively.
The Lauren Sciences’ research team and laboratories are located at Ben-Gurion University of the Negev, where the V-Smart™ technology was invented before it was licensed to Lauren Sciences.
“V-Smart™ for GBM, formulated with a potent anti-tumor agent, has promise as an effective new treatment for GBM patients,” said Irwin Hollander, Ph.D., vice president for research and development at Lauren Sciences. “Our goal for this new V-Smart™ drug is to stop progression of, or eradicate, GBM, unlike standard treatments that in the vast majority of patients merely delay disease progression.“We anticipate future efficacy studies of V-Smart™ in GBM pre-clinical models and, thereafter, clinical studies in patients. Our goal is clinical validation and approval of this V-Smart™ for GBM.”
V-Smart™ for GBM will target and deliver a known chemotherapeutic that has proven potential to treat the brain tumor, but does not cross the blood-brain barrier (BBB) on its own. V-Smart™ Nanomedicines are designed to target and deliver therapeutics across the BBB and into selective brain cells both non-invasively and effectively.
New treatment options for Leukemia
Acute lymphoblastic leukemia (ALL) is the most common type of cancer in
children. It can occur in various forms, differing not only by specific
changes in the genetic material of the leukemia cells but also by their
response to therapies. Now, an international team of scientists from
Berlin, Düsseldorf, Hannover, Heidelberg, Kiel, and Zurich have
succeeded in decoding the molecular characteristics of an as yet
incurable subtype of leukemia, paving the way for new therapeutic
approaches.
The consortium team decoded the genome of the leukemic cells using sophisticated bioinformatics methods. The team found genetic aberrations in addition to the known translocation. "We are glad that we could contribute to this important project with genomic data analysis of leukemia cells to unravel some of the molecular changes in this disease", says Bodo Lange (CEO, Alacris Theranostics)."This technique provides a quantitative read out of the actual genetic program occurring in the cancer cells, which allowed us to uncover relevant molecular mechanisms cooperating to promote tumorigenesis, and to identify possible druggable targets. These findings could only be achieved through analysis of the messenger RNAs", says Marie-Laure Yaspo.
The consortium team decoded the genome of the leukemic cells using sophisticated bioinformatics methods. The team found genetic aberrations in addition to the known translocation. "We are glad that we could contribute to this important project with genomic data analysis of leukemia cells to unravel some of the molecular changes in this disease", says Bodo Lange (CEO, Alacris Theranostics)."This technique provides a quantitative read out of the actual genetic program occurring in the cancer cells, which allowed us to uncover relevant molecular mechanisms cooperating to promote tumorigenesis, and to identify possible druggable targets. These findings could only be achieved through analysis of the messenger RNAs", says Marie-Laure Yaspo.
Targeted therapy of the Brain Tumor Medulloblastoma
A targeted therapy already used to treat advanced skin cancer is also
effective against the most common subtype of the brain tumor
medulloblastoma in adults and should be considered for treatment of
newly diagnosed patients, according to research led by St. Jude
Children's Research Hospital.
The drug, called Vismodegib, is designed to block a key protein in the sonic hedgehog (SHH) signaling pathway. The pathway is normally active during fetal development and is inappropriately switched on in about 30 percent of medulloblastoma tumors, including about 60 percent of tumors in adults and 25 percent of tumors in children. Only patients with the SHH subtype responded to vismodegib; however, researchers also reported that the drug was not universally effective against all tumors in the subtype."While it was disappointing that not all medulloblastoma patients with the SHH subtype will benefit, for the right patients these results mark the beginning of a new era of targeted therapy for treatment of this tumor,"
The drug, called Vismodegib, is designed to block a key protein in the sonic hedgehog (SHH) signaling pathway. The pathway is normally active during fetal development and is inappropriately switched on in about 30 percent of medulloblastoma tumors, including about 60 percent of tumors in adults and 25 percent of tumors in children. Only patients with the SHH subtype responded to vismodegib; however, researchers also reported that the drug was not universally effective against all tumors in the subtype."While it was disappointing that not all medulloblastoma patients with the SHH subtype will benefit, for the right patients these results mark the beginning of a new era of targeted therapy for treatment of this tumor,"
Early detection of Ovarian Cancer
Early detection has come in the form of a blood test that
screens for a protein called CA-125 (Cancer Antigen 125), which is
commonly found on cancer cells in the ovary. A new study
from the University College London has found that, with regular blood
screenings for this protein, 86 percent of ovarian cancers can be found
earlier than they might be detected through ultrasound. For women at
high risk, this can be a very valuable test. Estimates indicate that there will be over 21,000 new cases of ovarian cancer in
2015. An even more startling statistic is that 14,000 are expected to
die of ovarian cancer each year. Only 20 percent of these cancers are found
at an early enough stage to cure patients long term. Compared to breast
cancer, where 90 percent of cancers are detected early,
there's a lot of room for improving early detection by figuring out who
is at risk (women with a family history of ovarian and breast cancer as
well as other genetically transmitted cancer syndromes) and then
following these women closely with a blood test to catch this disease
when the CA-125 just starts to rise. Screening tests may not be
appropriate for women of average risk but, for those in the high-risk
category, it is important to consult with health care experts familiar
with the most current screening standards.
Monday, July 27, 2015
New therapy slows spread of Brain Tumor cells
The rapid spread of a common and deadly brain tumor has been slowed
down significantly in a mouse model by cutting off the way some cancer
cells communicate, according to a team of researchers that includes UF
Health faculty. The technique improved the survival time for patients with
glioblastoma by 50 percent when tested in a mouse model, said Loic P.
Deleyrolle, Ph.D., a research assistant professor of neurosurgery in the
UofFL College of Medicine.
Researchers focused on disrupting the cell-to-cell communication that allows cancer stem cells to spread. To do that, they targeted a channel that cancer cells use to transfer molecules. By cutting off their communications pathway, the deadly cells stay in check, Deleyrolle said.
The research focused on connexin 46, a protein that is an essential component of cancer stem cells. Connexin 46 is part of intercellular channels known as a gap junction. That intercellular channel, which allows cells to exchange molecules and ions, is crucial to the growth of a glioblastoma tumor, researchers found.
"When we shut down those channels in the cancer stem cells, we can significantly reduce the tumor-forming abilities of the cells," Deleyrolle said.
Researchers focused on disrupting the cell-to-cell communication that allows cancer stem cells to spread. To do that, they targeted a channel that cancer cells use to transfer molecules. By cutting off their communications pathway, the deadly cells stay in check, Deleyrolle said.
The research focused on connexin 46, a protein that is an essential component of cancer stem cells. Connexin 46 is part of intercellular channels known as a gap junction. That intercellular channel, which allows cells to exchange molecules and ions, is crucial to the growth of a glioblastoma tumor, researchers found.
"When we shut down those channels in the cancer stem cells, we can significantly reduce the tumor-forming abilities of the cells," Deleyrolle said.
New treatment options for a Leukemia
In industrialized countries like in Europe, acute lymphoblastic leukemia
is the most common form of cancer in children. An international
research consortium lead by pediatric oncologists from the Universities
of Zurich and Hannover has now succeeded in decoding a specific form of
this leukemia, which is regarded as incurable, and in obtaining insights
for new therapeutic possibilities.
Modifications of genes that control the development and promote the growth of highly specific blood defense cells, so-called B-lymphocytes, were evident in the leukemia cells studied. The interplay between the pathogenic fusion of TCF3 with HLF and newly identified alterations triggers a previously undetected reprogramming of the leukemia cells to a very early, stem-cell-like developmental stage, which is not externally visible on the cells. "This form of leukemia might be described as a kind of 'wolf in sheep's clothing'," stresses Martin Stanulla. "These key findings could be made, in particular, by reading out the messenger molecules synthesized in the tumor cells, a powerful technique allowing not only a deeper understanding of the genetic program specifying the behavior of tumor cells, but also of therapeutic entry points" adds Marie-Laure Yaspo.
Zurich researchers tested hundreds of novel drugs. Some of them, which are still undergoing further clinical development, displayed a very positive effect. One such drug is Venetoclax, which specifically targets the protein BCL2 relevant for the programmed cell death and already worked for other cancer strains.
The development of new courses of therapy in the humanized leukemia model was supported by the Swiss National Science Foundation and the University of Zurich's clinical research focus program "Human Hemato-Lymphatic Diseases". The genetic studies were funded by the German Federal Office for Radiation Protection via the environmental research program of the German Federal Environment Ministry and by the Max Planck Institute for Molecular Genetics.
Modifications of genes that control the development and promote the growth of highly specific blood defense cells, so-called B-lymphocytes, were evident in the leukemia cells studied. The interplay between the pathogenic fusion of TCF3 with HLF and newly identified alterations triggers a previously undetected reprogramming of the leukemia cells to a very early, stem-cell-like developmental stage, which is not externally visible on the cells. "This form of leukemia might be described as a kind of 'wolf in sheep's clothing'," stresses Martin Stanulla. "These key findings could be made, in particular, by reading out the messenger molecules synthesized in the tumor cells, a powerful technique allowing not only a deeper understanding of the genetic program specifying the behavior of tumor cells, but also of therapeutic entry points" adds Marie-Laure Yaspo.
Zurich researchers tested hundreds of novel drugs. Some of them, which are still undergoing further clinical development, displayed a very positive effect. One such drug is Venetoclax, which specifically targets the protein BCL2 relevant for the programmed cell death and already worked for other cancer strains.
The development of new courses of therapy in the humanized leukemia model was supported by the Swiss National Science Foundation and the University of Zurich's clinical research focus program "Human Hemato-Lymphatic Diseases". The genetic studies were funded by the German Federal Office for Radiation Protection via the environmental research program of the German Federal Environment Ministry and by the Max Planck Institute for Molecular Genetics.
Inovio Pharmaceuticals initiates clinical trial for Prostate Cancer
Inovio Pharmaceuticals, Inc. announced today that it has
initiated a phase I trial to evaluate Inovio's DNA immunotherapy in men
with biochemically relapsed prostate cancer. The launch of this human
trial follows strong pre-clinical results revealing that INO-5150
generated robust CD8+ T cell responses in animal studies including
non-human primates. The immune responses generated by INO-5150 were
similar in character to immune responses generated by VGX-3100, Inovio's
immunotherapy for human papillomavirus (HPV) that regressed
pre-cancerous cervical lesions and eliminated HPV in a randomized,
placebo-controlled phase II trial.
INO-5150 is a novel SynCon® immunotherapy for prostate cancer targeting two antigens, prostate specific antigen (PSA) and prostate specific membrane antigen (PSMA), present in the majority of prostate cancer cells. This phase I study will evaluate the safety, tolerability, and immunogenicity of INO-5150 alone or in combination with INO-9012, Inovio's DNA-based IL-12 immune activator. The multi-centered study will also evaluate changes in PSA levels, an important biomarker in prostate cancer.
INO-5150 is a novel SynCon® immunotherapy for prostate cancer targeting two antigens, prostate specific antigen (PSA) and prostate specific membrane antigen (PSMA), present in the majority of prostate cancer cells. This phase I study will evaluate the safety, tolerability, and immunogenicity of INO-5150 alone or in combination with INO-9012, Inovio's DNA-based IL-12 immune activator. The multi-centered study will also evaluate changes in PSA levels, an important biomarker in prostate cancer.
Two cheap generic drugs can cut breast cancer deaths
The most powerful regimen against breast cancer since tamoxifen has been
discovered by researchers at the University of Oxford, and it's a
combination of two available, inexpensive generic drugs called aromatase
inhibitors and bisphosphonates.The current study combined results from 31,920 women in nine clinical
trials. It showed that taking aromatase inhibitors for five years
reduced the risk of postmenopausal women with ER-positive breast cancer
dying from their disease by 40 per cent within 10 years of starting
treatment, compared with no hormonal treatment. Women who took tamoxifen
for five years reduced their risk by 30 percent."Aromatase inhibitors remove only the tiny amount of estrogen that
remains in the circulation of women after the menopause, but that's
enough to have a substantial impact on a wide range of ER-positive
tumors" said Mitch Dowsett, the study's lead author.
Friday, July 24, 2015
End-of-Life Chemotherapy may do more harm than good
A new study finds that half of cancer patients received chemotherapy
in their final months of life, even though the therapy, which can cause
nausea, vomiting and other grueling side effects, had no chance of
curing them.
Doctors often prescribe chemo to people in the end stages of cancer in the hope that the drugs will shrink patients' tumors and make them feel better, said study co-author Holly Prigerson, co-director of the Center for Research on End-of-Life Care at Weill Cornell Medical College in New York.
Her new research, however, found no evidence that chemo improved patients' quality of life. For the healthiest, least disabled patients, quality of life actually got worse after chemo, Prigerson said. The study of 312 patients, published in JAMA Oncology, included only people expected to live six months or less.
"People put a lot of stock in treatment and they tend to overestimate the odds that treatment will work," said Timothy Quill, a professor of medicine, psychiatry and medical humanities at the University of Rochester Medical Center, who wasn't involved in the new study. "There is a real potential for harm here and making quality of life worse."
Doctors often prescribe chemo to people in the end stages of cancer in the hope that the drugs will shrink patients' tumors and make them feel better, said study co-author Holly Prigerson, co-director of the Center for Research on End-of-Life Care at Weill Cornell Medical College in New York.
Her new research, however, found no evidence that chemo improved patients' quality of life. For the healthiest, least disabled patients, quality of life actually got worse after chemo, Prigerson said. The study of 312 patients, published in JAMA Oncology, included only people expected to live six months or less.
"People put a lot of stock in treatment and they tend to overestimate the odds that treatment will work," said Timothy Quill, a professor of medicine, psychiatry and medical humanities at the University of Rochester Medical Center, who wasn't involved in the new study. "There is a real potential for harm here and making quality of life worse."
Estrogen-suppressing drugs substantially reduce Breast Cancer
A class of hormonal drugs called aromatase inhibitors substantially
reduce the risk of death in postmenopausal women with the most common
type of breast cancer, a major study of more than 30,000 women shows.
The research underlines the importance of aromatase inhibitors
in the treatment of oestrogen receptor (ER)-positive breast cancer,
and shows they reduce risk of death by significantly more than the older
hormonal treatment tamoxifen.
The study, published in The Lancet, is relevant to postmenopausal women with ER-positive breast cancer, which accounts for over 80 per cent of cases which occur after the menopause. Each trial had used both aromatase inhibitors and tamoxifen at various times during the course of treatment.
In the study, researchers from the Aromatase Inhibitors Overview Group, chaired by Professor Mitch Dowsett at The Institute of Cancer Research, London and The Royal Marsden NHS Foundation Trust - collaborated with colleagues at the Clinical Trials Service Unit at The University of Oxford, to combine the results from 31,920 women in nine clinical trials.
The study was funded by Cancer Research UK and the Medical Research Council and conducted under the umbrella of the Early Breast Cancer Trialists Collaborative Group.
Aromatase inhibitors suppress the synthesis of oestrogens and are taken by postmenopausal women with hormone-sensitive (ER-positive) breast cancer.
The study, published in The Lancet, is relevant to postmenopausal women with ER-positive breast cancer, which accounts for over 80 per cent of cases which occur after the menopause. Each trial had used both aromatase inhibitors and tamoxifen at various times during the course of treatment.
In the study, researchers from the Aromatase Inhibitors Overview Group, chaired by Professor Mitch Dowsett at The Institute of Cancer Research, London and The Royal Marsden NHS Foundation Trust - collaborated with colleagues at the Clinical Trials Service Unit at The University of Oxford, to combine the results from 31,920 women in nine clinical trials.
The study was funded by Cancer Research UK and the Medical Research Council and conducted under the umbrella of the Early Breast Cancer Trialists Collaborative Group.
Aromatase inhibitors suppress the synthesis of oestrogens and are taken by postmenopausal women with hormone-sensitive (ER-positive) breast cancer.
New 'chemotherapy booster' could treat Lung and Pancreatic Cancer
A new drug that blocks cancer's escape route from chemotherapy could
be used to treat deadly lung and pancreatic cancers, new research
reports.
Scientists have shown in human cancer cells and in mice that the drug - discovered at The Institute of Cancer Research, London, boosts the effectiveness of conventional chemotherapy.
The drug, known as CCT245737, is scheduled to begin first-in-human clinical trials in patients with lung and pancreatic cancers - two cancers with low survival rates that continue to resist currently available treatments.
The new study is published in the journal Oncotarget, and was funded by Cancer Research UK and Sareum Limited.
Scientists have shown in human cancer cells and in mice that the drug - discovered at The Institute of Cancer Research, London, boosts the effectiveness of conventional chemotherapy.
The drug, known as CCT245737, is scheduled to begin first-in-human clinical trials in patients with lung and pancreatic cancers - two cancers with low survival rates that continue to resist currently available treatments.
The new study is published in the journal Oncotarget, and was funded by Cancer Research UK and Sareum Limited.
Thursday, July 23, 2015
Roche Pharma sales strong, due to Cancer Drugs
New and old Cancer Drugs boost revenue for the Big Pharma. Total sales across the group were up 6% at constant exchange rates,
with its pharma division up 5% as sales reached CHF18.35bn ($19.21bn) in
the first six months of 2015.
Revenue was unsurprisingly buoyed by its oncology drug range, with blood cancer and arthritis treatment MabThera (rituximab) remaining its top-selling product, bringing in sales of CHF3.5bn, a growth of 6% on last year.
Its ageing breast cancer drug Herceptin (trastuzumab) and multi-cancer licensed Avastin (bevacizumab) were both a close second, recording identical sales of CHF3.26bn, up 11% and 9% respectively.
Revenue was unsurprisingly buoyed by its oncology drug range, with blood cancer and arthritis treatment MabThera (rituximab) remaining its top-selling product, bringing in sales of CHF3.5bn, a growth of 6% on last year.
Its ageing breast cancer drug Herceptin (trastuzumab) and multi-cancer licensed Avastin (bevacizumab) were both a close second, recording identical sales of CHF3.26bn, up 11% and 9% respectively.
Drug prices soar, Prompting calls for Justification
So-called
pharmaceutical cost transparency bills have been introduced in at least
six state legislatures in the last year, aiming to make drug companies
justify their prices, which are often attributed to high research and
development costs.
“If
a prescription drug demands an outrageous price tag, the public,
insurers and federal, state and local governments should have access to
the information that supposedly justifies the cost,” says the preamble
of a bill introduced in the New York State Senate in May. Pressure is mounting from elsewhere as well. The top Republican and
Democrat on the United States Senate Finance Committee last year
demanded detailed cost data from Gilead Sciences, whose hepatitis C
drugs, which cost $1,000 a pill or more, have strained the budgets of
state and federal health programs. The U.A.W. Retiree Medical Benefits
Trust tried to make Gilead, Vertex Pharmaceuticals, Celgene and other
companies report to their shareholders more about how they set prices
and the risks to their businesses from resistance to high drug prices. Even former President Bill Clinton, in a speech to pharmaceutical
executives in Philadelphia last month, said it would be in the
industry’s best interest to say more about its costs and pricing.The pharmaceutical industry has already had the veil lifted on various
practices. Drug companies now have to report the payments, including
meals and entertainment, that they make to doctors for research,
consulting and giving promotional speeches.
Shareholders of Gilead, Vertex and Celgene voted down the resolutions
proposed by the U.A.W. trust, though the trust says it reached
settlements with Eli Lilly and with two other drug companies it would
not identify.
Doctors object to High Cancer-Drug Prices
More than 100 oncologists from top cancer hospitals around the U.S.
have issued a harsh rebuke over soaring cancer-drug prices and called
for new regulations to control them.Top cancer experts called Thursday for steps to curb the rapidly
escalating price of oncology drugs, warning that the current trajectory
“will affect millions of Americans and their immediate families, often
repeatedly.”
The physicians are the latest in a growing roster of objectors to drug prices. Critics from doctors to insurers to state Medicaid officials have voiced alarm about prescription drug prices, which rose more than 12% last year in the U.S., the biggest annual increase in a decade, according to the nation’s largest pharmacy-benefit manager.
The physicians are the latest in a growing roster of objectors to drug prices. Critics from doctors to insurers to state Medicaid officials have voiced alarm about prescription drug prices, which rose more than 12% last year in the U.S., the biggest annual increase in a decade, according to the nation’s largest pharmacy-benefit manager.
In 2014, the physicians noted, every new drug approved by the Food and
Drug Administration was priced at more than $120,000 per year. And the
cost for each additional year lived by a patient has skyrocketed from
$54,000 in 1995 to $207,000 in 2013.
Wednesday, July 22, 2015
Salmonella bacteria offers hope to Pancreatic Cancer patients
This particular form of cancer, known as pancreatic ductal
adenocarcinoma, or PDAC, has not shown significant improvement in
therapy for more than 25 years, according to the study, which was published online Wednesday in the journal Cancer Immunology Research.
Surgery is rarely successful against PDAC and results in delay, but not a cure, in almost 100 percent of cases, and there's no early warning, Diamond said.
PDAC tumors secrete a thick barrier that can block drugs from acting on the cells. The cancer cells also produce huge amounts of a molecule that effectively camouflages them from the immune system, so the body can't recognize them to form a response.
In this study, researchers modified salmonella bacteria to carry a piece of DNA that creates molecules that specifically block the cancer cells from creating that camouflage. They then coupled the bacteria with an enzyme that digests the tumor's protective barrier. The enzyme effectively drops the tumor's shield, allowing the bacteria to get in and destroy the cancer cells' immunosuppressive defenses.
Surgery is rarely successful against PDAC and results in delay, but not a cure, in almost 100 percent of cases, and there's no early warning, Diamond said.
PDAC tumors secrete a thick barrier that can block drugs from acting on the cells. The cancer cells also produce huge amounts of a molecule that effectively camouflages them from the immune system, so the body can't recognize them to form a response.
In this study, researchers modified salmonella bacteria to carry a piece of DNA that creates molecules that specifically block the cancer cells from creating that camouflage. They then coupled the bacteria with an enzyme that digests the tumor's protective barrier. The enzyme effectively drops the tumor's shield, allowing the bacteria to get in and destroy the cancer cells' immunosuppressive defenses.
Tuesday, July 21, 2015
Breast Cancer survivors tend to gain more weight
Among
women with a family history of breast cancer, breast cancer survivors
tend to gain more weight than women who are free of the disease, new
research suggests.
And that added weight might increase the risk of heart disease and diabetes, as well as recurrence of the cancer, the researchers said.
The researchers compared 303 breast cancer survivors with 307 women who were cancer-free. All were participants in a study of women with a familial risk of breast and ovarian cancer. They included women with BRCA1 and BRCA2 gene mutations that can raise breast cancer risk.
"We found that breast cancer survivors, especially those with chemotherapy, gained more weight compared to cancer-free women," said lead researcher Amy Gross.
And that added weight might increase the risk of heart disease and diabetes, as well as recurrence of the cancer, the researchers said.
The researchers compared 303 breast cancer survivors with 307 women who were cancer-free. All were participants in a study of women with a familial risk of breast and ovarian cancer. They included women with BRCA1 and BRCA2 gene mutations that can raise breast cancer risk.
"We found that breast cancer survivors, especially those with chemotherapy, gained more weight compared to cancer-free women," said lead researcher Amy Gross.
those who had chemotherapy gained even
more weight. "We found that the survivors who had received chemotherapy
were twice as likely to have gained at least 11 pounds (compared to
cancer-free women)," Gross said.
Kanzius Cancer machine gets its first human trial
Researchers from the University of Pittsburgh, the MD Anderson Cancer
Center and Rice University tested the technology. Curley’s team injected
nanoparticles into human cancer cells in petri dishes, as well as into
tumors in mice, rats, rabbits and pigs. Using the Kanzius machine, they
were able to heat the nanoparticles and, as a result, kill all those
cancerous cells. Results were published in the oncology medical journal Cancer, as well as Nano Research. They were publicized around the world and featured on 60 Minutes.
Over and over again, after being injected with nanoparticles and heated
with radio waves, cancer cells died while surrounding healthy areas
remained intact.
The treatment, of course, would need to be approved by the Food and Drug Administration before it could treat patients in the U.S.
Curley has 20 researchers with expertise in
nanomaterials, radiofrequency, immune function and drug delivery
functions working in his lab at the Dan L. Duncan Cancer Center at
Baylor College of Medicine in Houston, Texas. But he’s also been doing
clinical research in Italy since 1982—the regulatory processes for human
trials there, he says, are not as arduous as they are in the U.S. He
did initial clinical trials for his early radiofrequency ablation
research in Italy in 1997, which were followed by successful clinical
trials in the U.S. a year later.
The first round of
clinical trials for the new Kanzius machine design will involve exposing
15 to 20 pancreatic and liver cancer patients to radio waves in the
Kanzius machine, primarily to prove the process will not harm them, and
to study the impact on their cancer cells. Tests will also examine how
effectively radio wave treatments work when used along with known chemo
drugs.The treatment, of course, would need to be approved by the Food and Drug Administration before it could treat patients in the U.S.
Friday, July 17, 2015
Scientists develop new class of Cancer drugs
Thomas Burris, chair of pharmacology and physiology at Saint Louis
University, has, for the first time, found a way to stop cancer cell
growth by targeting the Warburg Effect, a trait of cancer cell
metabolism that scientists have been eager to exploit. Metabolism, the ability to use energy, is a feature of all living
things. Cancer cells aggressively ramp up this process, allowing mutated
cells to grow unchecked at the expense of surrounding tissue.
“Targeting cancer metabolism has become a hot area over the past few years, though the idea is not new,” Burris said. Since the early 1900s, scientists have known that cancer cells prefer to use glucose as fuel even if they have plenty of other resources available. In fact, this is how doctors use PET (positron emission tomography) scan images to spot tumors. PET scans highlight the glucose that cancer cells have accumulated. This preference for using glucose as fuel is called the Warburg effect, or glycolysis. In his paper, Burris reports that the Warburg effect is the metabolic foundation of oncogenic (cancer gene) growth, tumor progression and metastasis as well as tumor resistance to treatment. Burris and his colleagues created a class of compounds that affect a receptor that regulates fat synthesis. The new compound, SR9243, which started as an anti-cholesterol drug candidate, turns down fat synthesis so that cells can’t produce their own fat. This also impacts the Warburg pathway, turning cancer cells into more normal cells. SR9243 suppresses abnormal glucose consumption and cuts off cancer cells’ energy supply.
When cancer cells don’t get the parts they need to reproduce through glucose or fat, they simply die.
Because the Warburg effect is not a feature of normal cells and because most normal cells can acquire fat from outside, SR9243 only kills cancer cells and remains non-toxic to healthy cells.
The drug also has a good safety profile; it is effective without causing weight loss, liver toxicity, or inflammation.
“Targeting cancer metabolism has become a hot area over the past few years, though the idea is not new,” Burris said. Since the early 1900s, scientists have known that cancer cells prefer to use glucose as fuel even if they have plenty of other resources available. In fact, this is how doctors use PET (positron emission tomography) scan images to spot tumors. PET scans highlight the glucose that cancer cells have accumulated. This preference for using glucose as fuel is called the Warburg effect, or glycolysis. In his paper, Burris reports that the Warburg effect is the metabolic foundation of oncogenic (cancer gene) growth, tumor progression and metastasis as well as tumor resistance to treatment. Burris and his colleagues created a class of compounds that affect a receptor that regulates fat synthesis. The new compound, SR9243, which started as an anti-cholesterol drug candidate, turns down fat synthesis so that cells can’t produce their own fat. This also impacts the Warburg pathway, turning cancer cells into more normal cells. SR9243 suppresses abnormal glucose consumption and cuts off cancer cells’ energy supply.
When cancer cells don’t get the parts they need to reproduce through glucose or fat, they simply die.
Because the Warburg effect is not a feature of normal cells and because most normal cells can acquire fat from outside, SR9243 only kills cancer cells and remains non-toxic to healthy cells.
The drug also has a good safety profile; it is effective without causing weight loss, liver toxicity, or inflammation.
Red Wine antioxidant may provide new Cancer Therapy
Resveratrol and Quercetin, two polyphenols that have been widely
studied for their health properties, may soon become the basis of an
important new advance in cancer treatment, primarily by improving the
efficacy and potential use of an existing chemotherapeutic cancer drug.
Resveratrol, a powerful antioxidant found in red wine and other foods, has already received much attention as a possible explanation for the “French paradox,” a low incidence of cardiovascular disease despite a diet often high in fats.
In laboratory experiments, researchers at Oregon State University have developed a system to increase the bioavailability of these compounds in the body by using “copolymers” that make them water soluble and allow their injection into the blood stream, creating levels that are far higher than could ever be obtained by diet or oral intake.
The resveratrol and quercetin then appear to reduce the cardiac toxicity of a very widely used cancer drug, Adriamycin. Although highly effective in the treatment of lymphomas, breast, ovarian and other cancers, Adriamycin can only be used for a limited time in humans because of its cardiotoxicity. The co-administration of these polyphenols might allow much more extensive use of this drug, while at the same time improving its efficacy and demonstrating the polyphenols’ own anti-cancer properties, scientists said. Findings on this research have been published in the Journal of Controlled Release, by scientists from the College of Pharmacy at Oregon State University and the School of Pharmacy at Pacific University.
Resveratrol, a powerful antioxidant found in red wine and other foods, has already received much attention as a possible explanation for the “French paradox,” a low incidence of cardiovascular disease despite a diet often high in fats.
In laboratory experiments, researchers at Oregon State University have developed a system to increase the bioavailability of these compounds in the body by using “copolymers” that make them water soluble and allow their injection into the blood stream, creating levels that are far higher than could ever be obtained by diet or oral intake.
The resveratrol and quercetin then appear to reduce the cardiac toxicity of a very widely used cancer drug, Adriamycin. Although highly effective in the treatment of lymphomas, breast, ovarian and other cancers, Adriamycin can only be used for a limited time in humans because of its cardiotoxicity. The co-administration of these polyphenols might allow much more extensive use of this drug, while at the same time improving its efficacy and demonstrating the polyphenols’ own anti-cancer properties, scientists said. Findings on this research have been published in the Journal of Controlled Release, by scientists from the College of Pharmacy at Oregon State University and the School of Pharmacy at Pacific University.
New role for Prostate Cancer protein
US scientists studying how prostate cancer cells grow say they’ve discovered a new role for a protein previously known to be involved in repairing damaged DNA.
The protein DNA-PK, first shown to repair DNA damage in the 1990s by UK scientists, has now been shown to be involved in regulating the activity of genes involved in cancer spread.
According to study leader Dr Karen Knudsen, from the Sidney Kimmel Cancer Centre, her team’s results “strongly suggest” that DNA-PK plays an important role in prostate cancer spread.
“And high levels of DNA-PK could predict which early stage tumours may go on to metastasise (spread)," she added.
Using a variety of laboratory techniques, her team showed that disrupting DNA-PK’s activity inside growing prostate cancer cells altered the levels of other key molecules that regulate cell movement, and slowed down the cancer cells’ ability to spread.
They also found higher levels of the protein in tumour samples taken from men whose prostate cancer went on to spread.
The protein DNA-PK, first shown to repair DNA damage in the 1990s by UK scientists, has now been shown to be involved in regulating the activity of genes involved in cancer spread.
According to study leader Dr Karen Knudsen, from the Sidney Kimmel Cancer Centre, her team’s results “strongly suggest” that DNA-PK plays an important role in prostate cancer spread.
“And high levels of DNA-PK could predict which early stage tumours may go on to metastasise (spread)," she added.
Using a variety of laboratory techniques, her team showed that disrupting DNA-PK’s activity inside growing prostate cancer cells altered the levels of other key molecules that regulate cell movement, and slowed down the cancer cells’ ability to spread.
They also found higher levels of the protein in tumour samples taken from men whose prostate cancer went on to spread.
Thursday, July 16, 2015
Current blood Cancer drug prices not justified
The costs associated with cancer drug prices have risen dramatically
over the past 15 years, which is of concern to many top oncologists. In a
new analysis, researchers at The University of Texas MD Anderson Cancer
Center concluded the majority of existing treatments for hematologic,
or blood, cancers are currently priced too high to be considered
cost-effective in the United States. Their findings are published in the
current issue of the journal Cancer.There have been substantial improvements in survival and quality of life
after treatment for hematologic cancers in recent years, but drug costs
have also skyrocketed. High prices have placed a significant financial
burden on patients facing these diseases, especially in light of falling
household income levels. In fact, up to 20 percent of patients may
forgo treatment or significantly compromise their treatment plan due to
high drug costs, according to a 2014 study.
The researchers were able to re-analyze 20 of the 29 studies with updated drug prices in the current U.S. market. Upon doing this, they found that 63 percent of those studies had costs per additional life-year higher than the $50,000 threshold. Several studies resulted in costs of $210,000 to $426,000 per additional life-year, many times higher than conventionally accepted levels.
This indicates that, although the drugs may have been cost-effective originally, their current prices cannot be justified based upon improved quality of life.
One of the drugs evaluated, Imatinib, was priced at $26,000 per year of therapy in 2001 and $132,000 per year in 2014. The price increase in imatinib and other drugs evaluated is not the result of new and improved versions, but instead is simply the result of rising prices charged by drug companies!
The researchers were able to re-analyze 20 of the 29 studies with updated drug prices in the current U.S. market. Upon doing this, they found that 63 percent of those studies had costs per additional life-year higher than the $50,000 threshold. Several studies resulted in costs of $210,000 to $426,000 per additional life-year, many times higher than conventionally accepted levels.
This indicates that, although the drugs may have been cost-effective originally, their current prices cannot be justified based upon improved quality of life.
One of the drugs evaluated, Imatinib, was priced at $26,000 per year of therapy in 2001 and $132,000 per year in 2014. The price increase in imatinib and other drugs evaluated is not the result of new and improved versions, but instead is simply the result of rising prices charged by drug companies!
Immunotherapy vaccine to transform Cancer Treatment
Driven by
its proprietary platform, ImPACT, Heat is developing multiple vaccines for a
number of different cancers. Vaccines have transformed polio, tetanus, chicken
pox and measles from being deadly diseases, to merely something we take a shot
for today. Cancer could become the next disease to be virtually eliminated by a
vaccine.
ImPACT genetically modifies human cancer cells to pump out antigens (biological agents that target the immune system) and proteins to create an immune response and attack a specific cancer. Not like competitor's drugs that take days, if not weeks, to work, Heat's therapy takes only a few minutes. Then the vaccine lives at the site of the tumor, continuously targeting and destroying the cancer.
Heat's vaccine platform is easy to make, stays on the shelf until needed, and can be given to anybody, regardless of their blood type or DNA makeup, which is unique in the cancer immunotherapy market.
ImPACT will direct its drugs to kill cancer cells faster with immunotherapy that activates, stimulates, and strengthens a patient's immune system to attack a deadly disease with no known cure. Besides lung cancer, Heat targets bladder cancer with HS-410, now in Phase II at 16 US clinical sites (including Johns Hopkins, known for its extensive urological work) to potentially enter a market estimated at $300 million in the next two years. Expected completion of enrollment for the bladder cancer trial is the third quarter of next year.
ImPACT genetically modifies human cancer cells to pump out antigens (biological agents that target the immune system) and proteins to create an immune response and attack a specific cancer. Not like competitor's drugs that take days, if not weeks, to work, Heat's therapy takes only a few minutes. Then the vaccine lives at the site of the tumor, continuously targeting and destroying the cancer.
Heat's vaccine platform is easy to make, stays on the shelf until needed, and can be given to anybody, regardless of their blood type or DNA makeup, which is unique in the cancer immunotherapy market.
ImPACT will direct its drugs to kill cancer cells faster with immunotherapy that activates, stimulates, and strengthens a patient's immune system to attack a deadly disease with no known cure. Besides lung cancer, Heat targets bladder cancer with HS-410, now in Phase II at 16 US clinical sites (including Johns Hopkins, known for its extensive urological work) to potentially enter a market estimated at $300 million in the next two years. Expected completion of enrollment for the bladder cancer trial is the third quarter of next year.
Tuesday, July 14, 2015
Stem cell gene therapy for eliminating HIV infection
Scientists at the UCLA Eli and Edythe Broad
Center of Regenerative Medicine and Stem Cell Research are one step
closer to engineering a tool that could one day arm the body's immune
system to fight HIV, and win. The new technique harnesses the
regenerative capacity of stem cells to generate an immune response to
the virus.
"We hope this approach could one day allow HIV-positive individuals
to reduce or even stop their current HIV drug regimen and clear the
virus from the body altogether," said Scott Kitchen, the study's lead
author and a member of the Broad Stem Cell Research Center. "We also
think this approach could possibly be extended to other diseases."
Kitchen also is a member of the UCLA AIDS Institute and an associate
professor of medicine in the division of hematology and oncology at the
David Geffen School of Medicine at UCLA.Kitchen and his colleagues were the first to report the use of an
engineered molecule called a chimeric antigen receptor, or CAR, in
blood-forming stem cells. Blood-forming stem cells are capable of turning into any type of blood cell, including T cells, the white blood cells
that are central to the immune system. In a healthy immune system, T
cells can usually rid the body of viral or bacterial infection. But HIV
is too strong and mutates too rapidly for T cells to fight against the
virus.The researchers inserted a gene for a CAR into blood-forming stem
cells in the lab. The CAR, which is a two-part receptor that recognizes
an antigen, was engineered to be carried by T cells and direct them to
locate and kill HIV-infected cells. The CAR-modified blood stem cells
were then transplanted into HIV-infected mice that had been genetically
engineered with human immune systems. (As a result, HIV infection
causes disease similar to that in humans.)
The researchers found that the CAR-carrying blood stem cells successfully turned into functional T cells that could kill HIV-infected cells in the mice. The result was a decrease in HIV levels of 80 to 95 percent.
The researchers found that the CAR-carrying blood stem cells successfully turned into functional T cells that could kill HIV-infected cells in the mice. The result was a decrease in HIV levels of 80 to 95 percent.
New drug to beat Cancer
Scientists are confident from new research that the disease can be stopped in its tracks after tests revealed how it turns from being a benign illness into a full-blown killer.Experts now believe a rogue protein causes cells to multiply and spread, attacking the body and its vital organs with devastating consequences.They say a cure - the Holy Grail of medicine - now rests with developing drugs that can eliminate this trigger.The quantum leap in understanding of a disease which kills 160,000 in the UK each year comes as American scientists start world-first tests of a drug aimed at zapping the protein.Most tumours only become lethal once they spread, a process known as metastasis.But new research on prostate cancer sufferers shows stopping the disease could be as simple as “switching off” a molecule known as DNA-PKcs.Tonight experts said this fresh understanding of cancer, which kills 160,000 in the UK each year, was almost “as good as a cure”.Dr Karen Knudsen, professor of cancer biology at Thomas Jefferson University, Philadelphia, where the research was undertaken, said: “Finding a way to halt or prevent cancer metastasis has proven elusive.We discovered that a molecule called DNA-PKcs could give us a means of knocking out major pathways that control metastasis before it begins.
Anti-stress hormone provides indication of Breast Cancer risk
A new study from Lund University in Sweden shows that women with low
levels of an anti-stress hormone have an increased risk of getting
breast cancer. The study is the first of its kind on humans and confirms
previous similar observations from animal experiments.The recent findings on a potential new marker for the risk of developing breast cancer are presented in the renowned Journal of Clinical Oncology.
The study focused on a hormone which circulates freely in the blood,
enkephalin, with pain- and anxiety-reducing properties. Enkephalin also
reinforces the immune system by directly affecting immune cells.
"This is the first time the role of enkephalin in breast cancer has been studied in humans, and the results were surprisingly clear. Among women with the lowest levels of the hormone, the risk of breast cancer was more than three times that of the women with the highest levels of the hormone. This is one of the strongest correlations between cancer risk and a freely circulating biomarker ever described", said Olle Melander and Mattias Belting, both professors at Lund University and consultant physicians at Skåne University Hospital.
The findings were possible thanks to a broad approach combining the latest knowledge within cancer and cardiovascular research at Lund University; the study was based on blood samples taken from just over 1 900 women in Malmö. The women were followed up with regard to breast cancer for an average period of 15 years.The results were adjusted for age, menopause, hormonal treatment, smoking and other factors which can affect the risk of getting breast cancer.
The current study confirms a statistical correlation between low enkephalin concentrations in the blood and increased risk of breast cancer, and it remains to be seen whether there is a causal relation showing that a low level of the hormone directly affects tumour development. The researchers also point out that geographical location and age, in spite of the adjustments in the study, may be significant. The average age of the women studied was 57.
"This is the first time the role of enkephalin in breast cancer has been studied in humans, and the results were surprisingly clear. Among women with the lowest levels of the hormone, the risk of breast cancer was more than three times that of the women with the highest levels of the hormone. This is one of the strongest correlations between cancer risk and a freely circulating biomarker ever described", said Olle Melander and Mattias Belting, both professors at Lund University and consultant physicians at Skåne University Hospital.
The findings were possible thanks to a broad approach combining the latest knowledge within cancer and cardiovascular research at Lund University; the study was based on blood samples taken from just over 1 900 women in Malmö. The women were followed up with regard to breast cancer for an average period of 15 years.The results were adjusted for age, menopause, hormonal treatment, smoking and other factors which can affect the risk of getting breast cancer.
The current study confirms a statistical correlation between low enkephalin concentrations in the blood and increased risk of breast cancer, and it remains to be seen whether there is a causal relation showing that a low level of the hormone directly affects tumour development. The researchers also point out that geographical location and age, in spite of the adjustments in the study, may be significant. The average age of the women studied was 57.
Friday, July 10, 2015
Arthritis drug could treat Blood Cancer
Researchers at the University of Sheffield found that Methotrexate
(MTX), which is one thousandth of the cost of the current drug used to
treat Myeloproliferative neoplasms (MPN), a group of blood disorders
related to leukemia, can also provide relief.
"Given that a year's course of low-dose MTX costs around $45, the
potential to repurpose MTX could provide thousands of patients with a
much needed treatment option and also generate substantial savings for
health care systems," researcher Dr. Martin Zeidler said in a statement.
"Because MTX is a World Health Organization 'Essential Medicine', this
also means that this well understood drug could be used throughout the
developing world."
The arthritis drug is commonly used at low doses to treat
inflammatory diseases including rheumatoid arthritis, Crohn's disease
and psoriasis and has few side effects. It is also used in some cancers
at much higher doses where the side effects are substantial and similar
to other chemotherapy agents.
MPNs are most often diagnosed in people in their 50s and 60s and currently treatment is limited to aspirin, removal of excess blood and mild chemotherapy. Recently, the drug Ruxolitinib has been developed and has been shown to provide relief, but at a cost of more than $ 60,000 per year per patient, it has not been approved by the National Institute for Health and Care Excellence (NICE).
Zeidler is now working with clinical colleagues at the Royal Hallamshire Hospital to examine the possibility of repurposing low-dose MTX for the treatment of blood cancers.
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MPNs are most often diagnosed in people in their 50s and 60s and currently treatment is limited to aspirin, removal of excess blood and mild chemotherapy. Recently, the drug Ruxolitinib has been developed and has been shown to provide relief, but at a cost of more than $ 60,000 per year per patient, it has not been approved by the National Institute for Health and Care Excellence (NICE).
Zeidler is now working with clinical colleagues at the Royal Hallamshire Hospital to examine the possibility of repurposing low-dose MTX for the treatment of blood cancers.
Tuesday, July 7, 2015
Mistletoe can it help in fight against Cancer ?
Sure, the mistletoe is great for those seeking stealthy kisses, but the
plant actually contains a variety of chemicals, such as phenylpropanoids
and lectins, the Independent writes; "mistletoe (extract has) a number
of pharmacological properties including stimulation of the immune system
and direct toxic effects on tumor cells." Since the 1920s, many have
used the plant to treat cancer, epilepsy, infertility, menopausal
symptoms, nervous tension, asthma, hypertension, headache, and
dermatitis.
In Europe, the semi-poisonous plant is "regularly prescribed for various types of cancers as its extract demonstrates anti-cancer activity when used against cancerous cells in the lab." Mistletoe extract enhances immune function, which increases the production of the immune cells. When administered as a form of therapy for cancer, the extracts are given by injection under the skin, into a vein or directly into a tumor. The mistletoe has demonstrated efficacy against cancer in a particular German study where researchers examined the use of the mistletoe extract brand Iscador. The researchers used Iscador in 800 patients with colorectal cancer who were all treated with chemotherapy and/or radiation therapy. Researchers found the patients treated with Iscador had fewer adverse events, better symptom relief and improved disease-free survival compared to patients who did not receive the mistletoe extract as additional therapy.
American critics have been dismissive about medical studies of the plant, calling the studies too small or improperly designed. The FDA does not recognize the use of mistletoe to treat any form of cancer, and injectable mistletoe extracts cannot be sold in the U.S.
In Europe, the semi-poisonous plant is "regularly prescribed for various types of cancers as its extract demonstrates anti-cancer activity when used against cancerous cells in the lab." Mistletoe extract enhances immune function, which increases the production of the immune cells. When administered as a form of therapy for cancer, the extracts are given by injection under the skin, into a vein or directly into a tumor. The mistletoe has demonstrated efficacy against cancer in a particular German study where researchers examined the use of the mistletoe extract brand Iscador. The researchers used Iscador in 800 patients with colorectal cancer who were all treated with chemotherapy and/or radiation therapy. Researchers found the patients treated with Iscador had fewer adverse events, better symptom relief and improved disease-free survival compared to patients who did not receive the mistletoe extract as additional therapy.
American critics have been dismissive about medical studies of the plant, calling the studies too small or improperly designed. The FDA does not recognize the use of mistletoe to treat any form of cancer, and injectable mistletoe extracts cannot be sold in the U.S.
Cancer drug 49 times more potent than Cisplatin
Tests have shown that a new cancer drug, FY26, is 49 times more potent than the clinically used treatment Cisplatin. Based on a compound of the rare precious metal osmium and
developed by researchers at the University of Warwick's Department of
Chemistry and the Warwick Cancer Research Unit, FY26 is able to shut
down a cancer cell by exploiting weaknesses inherent in their energy generation.
The researchers argue that the drug could be cheaper to produce, less harmful to healthy cells than existing treatments and has been shown to be active against cancer cells which have become resistant to platinum-based drugs. The experiments conducted by the Wellcome Trust Sanger Institute
comprising 809 cancer cell lines found that FY26 was 49 times more
potent than cisplatin. Similar results were obtained by the National
Cancer Institute USA in tests conducted on 60 cell lines.
The new drug works by forcing cancer cells to use their mitochondria, the 'power house' of a cell, to generate the energy necessary to function. While healthy cells use mitochondria to generate energy, cancer cells contain defective mitochondria which are incapable of sustaining the cell's energy requirements.
In the absence of FY26, cancer cells switch from using their defective mitochondria to using metabolic activity in their cytoplasm to generate energy. By stopping this switch of energy source, the drug causes the cancer cell to die.
Breast Cancer and mammograms widespread overdiagnosis
"This study shows that the more we look, the more you find," says Joann Elmore, a professor of medicine at the University of Washington who wrote a commentary
accompanying the study. "The more you screen, the more likely you are
to detect early precancerous abnormalities like ductal carcinoma in situ
and early-stage cancer."
It's not clear how many women are overdiagnosed; Elmore says 10 to 20 percent may be a good estimate. But with the current tests, there's no way for a woman to know if she's in that 10 to 20 percent or if she really does have a dangerous cancer. Thus most women who get a diagnosis of DCIS or early-stage invasive cancer opt for treatment, which can mean surgery, radiation or chemotherapy.
"That is so hard," Elmore says. "I really feel for those women. I need help both figuring out how to explain this to women, and I need better research helping me look at the tissue and figure out whether these women are overdiagnosed or not."
"As is the case with screening in general, the balance of benefits and harms is likely to be most favorable when screening is directed to those at high risk, provided neither too frequently nor too rarely, and sometimes followed by watchful waiting instead of immediate active treatment," they wrote.
Current guidelines from the U.S. Preventive Services Task Force recommend screening every two years for women ages 50 to 74 and that those who are younger should also consider screening depending on individual risk factors, such as family history of the disease.
It's not clear how many women are overdiagnosed; Elmore says 10 to 20 percent may be a good estimate. But with the current tests, there's no way for a woman to know if she's in that 10 to 20 percent or if she really does have a dangerous cancer. Thus most women who get a diagnosis of DCIS or early-stage invasive cancer opt for treatment, which can mean surgery, radiation or chemotherapy.
"That is so hard," Elmore says. "I really feel for those women. I need help both figuring out how to explain this to women, and I need better research helping me look at the tissue and figure out whether these women are overdiagnosed or not."
"As is the case with screening in general, the balance of benefits and harms is likely to be most favorable when screening is directed to those at high risk, provided neither too frequently nor too rarely, and sometimes followed by watchful waiting instead of immediate active treatment," they wrote.
Current guidelines from the U.S. Preventive Services Task Force recommend screening every two years for women ages 50 to 74 and that those who are younger should also consider screening depending on individual risk factors, such as family history of the disease.
Thursday, July 2, 2015
Extra weight helps Cancer patients
People with advanced colorectal cancer who are overweight or obese may
survive longer than their thinner counterparts, a new study suggests.
Researchers found that, on average, patients with a body mass index (BMI) of 25 or higher lived two and a half months longer after starting their treatment than patients with a lower BMI. People with a BMI of 25 or higher are considered overweight, and those with a BMI of 30 or higher are considered obese.
As BMI increased, the length of survival also went up, the researchers found.
"These results are surprising," Dr. Yousuf Zafar, the study's lead researcher and an associate professor of medicine at Duke University, said in a statement. "What we expected, based on prior evidence, was that those obese patients would do worse." The researchers gathered data from more than 6,000 patients with stage IV colorectal cancer who were enrolled in five cancer registry studies in the United States and Europe. All of the patients received the same drug, bevacizumab (known by the brand name Avastin) during their chemotherapy treatment.
Researchers found that, on average, patients with a body mass index (BMI) of 25 or higher lived two and a half months longer after starting their treatment than patients with a lower BMI. People with a BMI of 25 or higher are considered overweight, and those with a BMI of 30 or higher are considered obese.
As BMI increased, the length of survival also went up, the researchers found.
"These results are surprising," Dr. Yousuf Zafar, the study's lead researcher and an associate professor of medicine at Duke University, said in a statement. "What we expected, based on prior evidence, was that those obese patients would do worse." The researchers gathered data from more than 6,000 patients with stage IV colorectal cancer who were enrolled in five cancer registry studies in the United States and Europe. All of the patients received the same drug, bevacizumab (known by the brand name Avastin) during their chemotherapy treatment.
Wednesday, July 1, 2015
Gene mutations in Aplastic Anemia help optimize treament
Scientists have identified a group of genetic mutations in patients with
aplastic anemia, which likely will help doctors optimize treatment for
this rare and deadly blood condition. The study, appearing in the New England Journal of Medicine,
could lead to tailor-made treatment plans for aplastic anemia patients
as part of the emerging precision medicine movement. It is the largest
study of its kind to examine gene mutations in aplastic anemia, the
scientists note. The work involved researchers from the National Institutes of Health, the
Cleveland Clinic, Cleveland, OH, and Kanazawa University, Kanazawa,
Japan. Neal S. Young, chief of the hematology branch at the NIH's
National Heart, Lung, and Blood Institute, was the study's co-leader.
Almost 1,000 new cases of aplastic anemia occur each year in the United
States alone. Although the disease can affect anyone, children and young
adults make up the majority of cases. Stem cells in the bone marrow are
normally responsible for producing blood. In aplastic anemia, the body's immune system appears to destroy these stem cells.
In the future, genomic screening at diagnosis should allow care providers to choose the best treatment option or monitor for the emergence of clone stem cells. The unfavorable genes, DNMT3A and ASXL1, are frequently mutated in myeloid leukemia and myelodysplastic syndromes, and they are also mutated in a substantial number of older individuals without a blood disease.
In the future, genomic screening at diagnosis should allow care providers to choose the best treatment option or monitor for the emergence of clone stem cells. The unfavorable genes, DNMT3A and ASXL1, are frequently mutated in myeloid leukemia and myelodysplastic syndromes, and they are also mutated in a substantial number of older individuals without a blood disease.
Spainish scientists find new biomarkers for the prevention of Colon Cancer
Scientists from the Instituto de Investigación Biomédica (IBI)
[Institute of Biomedical Research], in Galicia (Spain), have made
progress in the identification of new biomarkers for improving
prevention of colorectal cancer. In Spain, colorectal tumours are the most common malignant form and constitute the second most frequent cause of death from cancer, after lung cancer.
It is one of the cancers against which preventive strategies could be
most effective, as generally it develops from a previous benign polyp
called adenoma, which can be detected and removed prior to evolution to
cancer. Worldwide, colon cancer
is the third most common type of cancer and the second in terms of
deaths caused, although the survival rate varies very much from country
to country. In the USA the survival rate is 62%, whereas in Europe it is
only 43%.
Within the overall structure of the project, the Galician group, led by Professor Javier Rodríguez Berrocal, is undertaking a sub-study of protein biomarkers in the serum of healthy individuals. This research will assess the efficacy of certain proteins in the early detection of colon cancer and adenomas. In a first phase, work begun in 2009 will be completed to identify potentially effective markers. In a second phase, the validity of these markers will be confirmed in a group of individuals who participate in screening programs for this type of cancer.
Within the overall structure of the project, the Galician group, led by Professor Javier Rodríguez Berrocal, is undertaking a sub-study of protein biomarkers in the serum of healthy individuals. This research will assess the efficacy of certain proteins in the early detection of colon cancer and adenomas. In a first phase, work begun in 2009 will be completed to identify potentially effective markers. In a second phase, the validity of these markers will be confirmed in a group of individuals who participate in screening programs for this type of cancer.
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