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Espaço de publicação e discussão sobre oncologia. GBM IMMUNOTHERAPY ONCO-VIRUS ONCOLOGY CANCER CHEMOTHERAPY RADIOTHERAPY



Sábado, 04.07.15

effect of pioglitazone and other antidiabetics on dementia

Pioglitazone drug significantly decreases risk of dementia

Published on June 23, 2015 at 2:03 PM 

Patients with type 2 diabetes have a dysfunctional sugar metabolism because the essential hormone insulin does not work effectively. Once the disease reaches an advanced stage, the body stops producing insulin altogether, which means that it has to be administered externally. Type 2 diabetes most commonly occurs in late adulthood, and it has long been known that it can affect the patient's mental health: Patients have a greater risk of developing dementia than non-diabetics. However, how does antidiabetic medication influence this risk? Neurologist Michael Heneka and the demographers Anne Fink and Gabriele Doblhammer investigated this issue in the current study. Their work is based on data from the years 2004 to 2010 provided by the German public health insurance company AOK. These data set comprises information about diseases and medication related to more than 145,000 men and women aged 60 and over.

Long-term treatment reduced dementia risk

The analysis confirmed previous findings that diabetics have an increased risk of developing dementia. However, it was also found that this risk can significantly be modified by pioglitazone. This drug is taken as tablets. It is applied in short-term as well as in long-term treatment of diabetes as long as the body is still capable of producing its own insulin.

"Treatment with pioglitazone showed a remarkable side benefit. It was able to significantly decrease the risk of dementia," says Doblhammer. "The longer the treatment, the lower the risk." Risk reduction was most noticeable when the drug was administered for at least two years. Diabetics given this treatment developed dementia less often than non-diabetics. Doblhammer: "The risk of developing dementia was around 47 percent lower than in non-diabetics, i.e. only about half as large."

Metformin - another frequently prescribed antidiabetic drug - also lowered the risk of developing dementia. However, the effect was lower than that of pioglitazone.

Protection against nerve cell damage

Pioglitazone improves the effect of the body's own insulin. Moreover, laboratory tests have long indicated that it also protects the nerve cells. The current results are therefore no surprise to neuroscientist Michael Heneka. "Pioglitazone is an anti-inflammatory drug that also inhibits the deposition of harmful proteins in the brain," he says.

However, Heneka emphasizes that the exact mechanisms are not yet understood: "Our study suggests that pioglitazone has a preventive effect. This happens when the drug is taken before symptoms of dementia manifest. Thus, it protects in particular against Alzheimer's, the most common form of dementia. The causes for this, whether pioglitazone only has this protective effect in diabetics or if it would also work in non-diabetics - all these questions have yet to be answered. The next logical step would therefore be clinical studies. These studies would specifically investigate the effect of pioglitazone and other antidiabetics on dementia."

Source:

DZNE - German Center for Neurodegenerative Diseases

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por cyto às 11:54

Sábado, 04.07.15

gene mutation linked to anaplastic oligodendroglioma

Scientists identify gene mutation linked to anaplastic oligodendroglioma

Published on June 12, 2015 at 9:23 AM · 

Scientists have identified a gene mutation linked to the development of an aggressive form of brain cancer.

Researchers found that errors in a gene known as TCF12 - which plays a key role in the formation of the embryonic brain are associated with more aggressive forms of a disease called anaplastic oligodendroglioma.

The new research is the largest ever genetic study of oligodendrogliomas, and provides important insights into their causes - and how they might be treated.

Oligodendrogliomas are fast-growing cancers that account for around 5-10 per cent of all tumours of the brain and central nervous system, and typically have a very poor prognosis.

Researchers at The Institute of Cancer Research, London, in collaboration with laboratories in France and Canada, compared the genetic sequence of 134 of these brain tumours with the DNA of healthy cells.

The study was largely funded by Investissements d'avenir and Génome Québec, with support from Cancer Research UK, and was published in the journal Nature Communications.

Researchers identified mutations in the TCF12 gene in 7.5 per cent of anaplastic oligodendrogliomas. They found that this subset of cancers grew more rapidly, and in other ways seemed more aggressive, than those where the gene was intact.

TCF12 is the genetic code for a protein that binds to DNA and controls the activity of other genes. The researchers found that mutations in TCF12 rendered the protein less able to bind to DNA, and this in turn led to a reduction in activity of other key genes - including one already associated with cancer spread, known as CHD1.

The researchers initially read the DNA sequence of 51 tumours and went on to look for TCF12 mutations in an additional group of 83.

The researchers also discovered errors in the gene IDH1 in 78 per cent of the tumours, confirming the findings of an initial scan of the data.

Finding out more about what genetic faults cause anaplastic oligodendrogliomas will allow scientists and clinicians to develop new personalised therapies that target a range of the mutations driving the disease.

Professor Richard Houlston, Professor of Molecular and Population Genetics at The Institute of Cancer Research, London, said:

"Our in-depth study has set out many of the genetic defects that cause this rare but highly aggressive form of brain cancer - including identifying a gene mutation that appears in particularly fast-growing forms.

"Anaplastic oligodendrogliomas are difficult to remove by surgery and don't respond well to other forms of treatment. We hope this new information might be used to discover new targeted therapies, offering patients a better chance at survival from this aggressive cancer."

Source:

Institute of Cancer Research

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por cyto às 11:46

Sábado, 04.07.15

Fibromyalgia now considered as a lifelong central nervous system disorder

Fibromyalgia now considered as a lifelong central nervous system disorder

Published on May 18, 2015 at 6:10 AM ·

Fibromyalgia is the second most common rheumatic disorder behind osteoarthritis and, though still widely misunderstood, is now considered to be a lifelong central nervous system disorder, which is responsible for amplified pain that shoots through the body in those who suffer from it. Daniel Clauw, M.D., professor of anesthesiology, University of Michigan, analyzed the neurological basis for fibromyalgia in a plenary session address today at the American Pain Society Annual Scientific Meeting.

"Fibromyalgia can be thought of both as a discreet disease and also as a final common pathway of pain centralization and chronification. Most people with this condition have lifelong histories of chronic pain throughout their bodies," said Clauw. "The condition can be hard to diagnose if one isn't familiar with classic symptoms because there isn't a single cause and no outward signs."

Clauw explained that fibromyalgia pain comes more from the brain and spinal cord than from areas of the body in which someone may experience peripheral pain. The condition is believed to be associated with disturbances in how the brain processes pain and other sensory information. He said physicians should suspect fibromyalgia in patients with multifocal (mostly musculoskeletal) pain that is not fully explained by injury or inflammation.

"Because pain pathways throughout the body are amplified in fibromyalgia patients, pain can occur anywhere, so chronic headaches, visceral pain and sensory hyper-responsiveness are common in people with this painful condition," said Clauw.

"This does not imply that peripheral nociceptive input does not contribute to pain experienced by fibromyalgia patients, but they do feel more pain than normally would be expected from the degree of peripheral input. Persons with fibromyalgia and other pain states characterized by sensitization will experience pain from what those without the condition would describe as touch," Clauw added.

Due to the central nervous system origins of fibromyalgia pain, Clauw said treatments with opioids or other narcotic analgesics usually are not effective because they do not reduce the activity of neurotransmitters in the brain. "These drugs have never been shown to be effective in fibromyalgia patients, and there is evidence that opioids might even worsen fibromyalgia and other centralized pain states," he said.

Clauw advises clinicians to integrate pharmacological treatments, such as gabapentinoids, trycyclics and serotonoin reuptake inhibitors, with nonpharmacological approaches like cognitive behavioral therapy, exercise and stress reduction.

"Sometimes the magnitude of treatment response for simple and inexpensive non-drug therapies exceeds that for pharmaceuticals," said Clauw. "The greatest benefit is improved function, which should be the main treatment goal for any chronic pain condition. The majority of patients with fibromyalgia can see improvement in their symptoms and lead normal lives with the right medications and extensive use of non-drug therapies."

Source:

American Pain Society (APS)

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por cyto às 11:40

Sábado, 04.07.15

Harvard Medical School scientists reveal structure of vesicular stomatitis virus protein

Harvard Medical School scientists reveal structure of vesicular stomatitis virus protein

Published on July 3, 2015 at 5:17 AM 

Viruses need us. In order to multiply, viruses have to invade a host cell and copy their genetic information. To do so, viruses encode their own replication machinery or components that subvert the host replication machinery to their advantage.

Ebola virus and rabies virus, two of the most lethal pathogens known to humans, belong to an order of RNA viruses that share a common strategy for copying their genomes inside their hosts. Other relatives include Marburg virus, measles, mumps, respiratory syncytial virus and vesicular stomatitis virus (VSV). Scientists study VSV, which causes acute disease in livestock but typically does not lead to illness in people, as a model for viruses that are harmful to humans.

Now a team from Harvard Medical School, using electron cryomicroscopy (imaging frozen specimens to reduce damage from electron radiation), has for the first time revealed the structure of a VSV protein at the atomic level. Called polymerase protein L, it is required for viral replication in this group of RNA viruses. The findings are published in Cell.

"We now have a better understanding of how RNA synthesis works for these viruses," said Sean Whelan, HMS professor of microbiology and immunobiology and senior author of the paper. "I think if you were trying to develop a viral-specific target to block the replication of one of these viruses, having the structure of the polymerase protein would help."

Scientists already know how these RNA viruses infect cells. They start by delivering a large protein RNA complex, which is viral RNA enclosed in a protein coat. The protein that copies viral RNA is polymerase protein L, which conducts all the enzymatic activities needed to synthesize RNA and then add a cap structure to its end to ensure it doesn't get destroyed by the cell--and to ensure that it can be translated into protein.

While researchers have known the atomic structures of the protein that coats the viral RNA, there are no data on protein L's atomic structure.

Antiviral drugs that target polymerase molecules are based in part on knowing their structure. That approach has been successful against HIV and herpes and hepatitis C viruses. But for the class of viruses known as nonsegmented negative-strand RNA viruses, finding the structure of polymerase protein L has been challenging.

The "L" stands for large. Larger proteins are often difficult to produce and to purify, Whelan said. Protein L is also flexible, with many functional fragments that are hard to isolate. The viruses evolved to make only small quantities of this protein.

Five years ago, using a lower-resolution form of electron microscopy in which the protein is visualized in the presence of negative stain, Whelan's team was able to detect at low resolution a structure that looked like a doughnut with three globular domains. Those earlier studies were informative, but the approach could not provide the atomic level of resolution the team ultimately needed.

Advances in electron cryomicroscopy encouraged them to try again. A team from Whelan's lab, working with a group led by Stephen Harrison, Giovanni Armenise - Harvard Professor of Basic Biomedical Science at HMS and a Howard Hughes Medical Institute (HHMI) investigator, was able to collect data from their viral samples that gave them much greater resolution. They also were able to align the images they collected into a three-dimensional model of polymerase protein L.

Into the density map obtained from these studies, members of the team built an atomic model of the polypeptide chain of VSV L protein. Solving this puzzle was a significant challenge and also involved the team of Nikolaus Grigorieff at HHMI's Janelia campus.

The result? An atomic level model of polymerase protein L's structure for VSV, which will form the basis for understanding the L protein of the other viruses in the order.

"The Ebola protein will look the same, the rabies protein will look the same, the other L proteins will look the same," Whelan said. "There will be some subtle differences reflecting the precise nature of amino acids, but we know that they're functionally and structurally the same."

Knowing the structure means scientists can explore how RNA synthesis is working in these viruses.

"It begins to suggest ways that we can perhaps pull apart other proteins that have not been so easy to express, such as the L protein in Ebola," Whelan said. "It doesn't mean we're going to have inhibitors immediately, but this is an important step, I think, towards that longer-term goal."

Source:

Harvard Medical School

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por cyto às 11:37

Sábado, 04.07.15

new protein that affects growth of secondary breast tumours in the brain

Scientists identify new protein that affects growth of secondary breast tumours in the brain

Published on July 1, 2015 at 7:19 AM 

Scientists from the University of Leeds and The Institute of Cancer Research, London, have discovered a new protein which triggers the growth of blood vessels in breast cancer tumours which have spread to the brain, a common location which breast cancer can spread to.

Dr Georgia Mavria's team in the School of Medicine at Leeds found that by withholding the DOCK4 protein in mouse models, a particular part of the blood vessel did not form as quickly, meaning tumours grew at a slower rate.

Dr Mavria said: "We want to understand how these tumours form and grow, but we still need to do more research to stop these tumours growing altogether.

"The finding gives an important indicator of how the protein affects the growth of secondary breast tumours in the brain. The discovery could also enable experts to predict which patients might be at risk of their breast cancer spreading, and develop drugs to prevent the growth of secondary tumours."

Working with Professor Chris Marshall, Professor of Cell Biology at The Institute of Cancer Research, London and the late Dr Tony Pawson at the Lunenfeld-Tanenbaum Research Institute in Toronto, researchers found that a complex of two related proteins, DOCK4 and DOCK9, is critical in the formation of the lumen, the interior space of a vessel through which blood flows.

By impeding the speed at which the lumen forms, tumours are not fed as effectively by blood vessels.

Normally, when breast cancer spreads to other parts of the body, it forces new blood vessels to form to supply it with nutrients and oxygen to help it to grow, resulting in tumours that are very difficult to treat.

Professor Marshall said: "Our study reveals new insights into how the complex process of forming blood vessels is controlled. This knowledge could lead to new approaches to preventing the blood supply to tumours and metastases. If we can find new ways to reduce the blood supply to tumours, we might be able to find new ways to slow cancer growth in future."

The research, which has been published in Nature Communications, was funded by Breast Cancer Now, Yorkshire Cancer Research and Cancer Research UK.

Dr Matthew Lam, Senior Research Communications Officer at Breast Cancer Now, said: "These findings could one day help us better identify and treat patients that might be at risk of their breast cancer spreading to the brain, a particularly common site for metastasis.

"12,000 women have their lives cut short by breast cancer in the UK each year. An understanding of what is happening on a molecular level - such as the role played by DOCK proteins - will be essential if we are to find ways to prevent secondary tumours and finally stop women dying from the disease."

Kathryn Scott, Head of Research and Innovation at Yorkshire Cancer Research, said: "Tumours need blood vessels to grow, but these blood vessels could be the cancer's weakest link because it is believed that they are less able to become resistant to drugs than the cancer cells themselves. Targeting drugs to the blood vessels that are serving the tumour rather than the tumour itself is an exciting new area of research and we are supporting a number of projects in Yorkshire which are investigating this approach."

Dr Aine McCarthy, Science Information Officer at Cancer Research UK, said: "This research shows for the first time that a molecule called DOCK4 is a key player in tumour blood vessel development and blocking it could slow tumour growth by starving the cancer cells. But the study was carried out in mice, so more research is needed to see if drugs can be developed that target the molecule and whether this approach would be safe and effective in people with cancer."

Source:

University of Leeds

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por cyto às 11:34

Sábado, 04.07.15

Umeå University researchers capture and describe 'invisible' protein structure

Umeå University researchers capture and describe 'invisible' protein structure

Published on July 3, 2015 at 6:07 AM 

A research group at Umeå University in Sweden has managed to capture and describe a protein structure that, until now, has been impossible to study. The discovery lays the base for developing designed enzymes as catalysts to new chemical reactions for instance in biotechnological applications. The result of the study is published in the journal Nature Communications.

Enzymes are extraordinary biocatalysts able to speed up the cellular, chemical reactions several million times. This increase of speed is completely necessary for all biological life, which would otherwise be limited by the slow nature of vital chemical reactions. Now, a research group at the Department of Chemistry has discovered a new aspect in enzymes that, in part, explains how enzymes manage their tasks with unmatched efficiency and selectivity.

So-called high-energy states in enzymes are regarded as necessary for catalysing of chemical reactions. A high-energy level is a protein structure only occurring temporarily and for a short period of time; and these factors collaborate until its state becomes invisible to traditional spectroscopic techniques. The Umeå researchers have managed to find a way to maintain a high-energy state in the enzyme, adenylate kinase, by mutating the protein.

"Thanks to this enrichment, we have been able to study both structure and dynamics of this state. The study shows that enzymatic high-energy states are necessary for chemical catalysis," says Magnus Wolf-Watz, research group leader at the Department of Chemistry.

The study also indicates a possibility to fine-tune the dynamics of an enzyme and this possibility can be useful for researchers in developing new enzymes for catalysis of new chemical reactions.

"Research on Bioenergy is an active field at Umeå University. An important, practical application of the new knowledge can be enzymatic digestion of useful molecules from wooden raw materials," says Magnus Wolf-Watz.

The discovery has been made possible thanks to a broad scientific approach where numerous advanced biophysical techniques have been used; Nuclear Magnetic Resonance (NMR) and x-ray crystallography being the main techniques.

"One of the strengths of Umeå University is the open cooperative climate with low or no barriers between research groups. It means that exciting research can be conducted in the borderland of differing expertise," says Magnus Wolf-Watz.

The main author of the article is Michael Kovermann who has completed his postdoctoral position at Umeå University and will shortly return to Germany for a professorship at the University of Konstanz.

Source:

Umea University

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por cyto às 11:31

Sábado, 04.07.15

way to stop growth of cancer cells by targeting the Warburg Effect

SLU researchers find way to stop growth of cancer cells by targeting the Warburg Effect

Published on June 26, 2015 at 10:55 PM 

In research published in Cancer Cell, Thomas Burris, Ph.D., 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.

Unlike recent advances in personalized medicine that focus on specific genetic mutations associated with different types of cancer, this research targets a broad principle that applies to almost every kind of cancer: its energy source.

The Saint Louis University study, which was conducted in animal models and in human tumor cells in the lab, showed that a drug developed by Burris and colleagues at Scripps Research Institute can stop cancer cells without causing damage to healthy cells or leading to other severe side effects.

The Warburg Effect

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.

Cancer's goal: to grow and divide

Cancer cells have one goal: to grow and divide as quickly as possible. And, while there are a number of possible molecular pathways a cell could use to find food, cancer cells have a set of preferred pathways.

"In fact, they are addicted to certain pathways," Burris said. "They need tools to grow fast and that means they need to have all of the parts for new cells and they need new energy."

"Cancer cells look for metabolic pathways to find the parts to grow and divide. If they don't have the parts, they just die," said Burris. "The Warburg effect ramps up energy use in the form of glucose to make chemicals required for rapid growth and cancer cells also ramp up another process, lipogenesis, that lets them make their own fats that they need to rapidly grow."

If the Warburg effect and lipogenesis are key metabolic pathways that drive cancer progression, growth, survival, immune evasion, resistance to treatment and disease recurrence, then, Burris hypothesizes, targeting glycolysis and lipogenesis could offer a way to stop a broad range of cancers.

Cutting off the energy supply

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.

Promising Results So far, SR9243 has been tested in cultured cancer cells and in human tumor cells grown in animal models. Because the Warburg pathway is a feature of almost every kind of cancer, researchers are testing it on a number of different cancer models.

"It works in a wide range of cancers both in culture and in human tumors developing in animal models," Burris said. "Some are more sensitive to it than others. In several of these pathways, cells had been reprogramed by cancer to support cancer cell growth. This returns the metabolism to that of more normal cells."

In human tumors grown in animal models, Burris said, "It worked very well on lung, prostate, and colorectal cancers, and it worked to a lesser degree in ovarian and pancreatic cancers."

It also seems to work on glioblastoma, an extremely difficult to treat form of brain cancer, though it isn't able to cross the brain/blood barrier very effectively. The challenge for researchers in this scenario will be to find a way to allow the drug to cross this barrier, the body's natural protection for the brain, which can make it difficult for drug treatments to reach their target.

And, in even more promising news, it appears that when SR9243 is used in combination with existing chemotherapy drugs, it increases their effectiveness, in a mechanism apart from SR9243's own cancer fighting ability.

Source:

Saint Louis University

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por cyto às 11:25

Sábado, 04.07.15

Nanoparticles packed with chemotherapy drug and coated with chitosan target cancer stem-like cells

 

Nanoparticles packed with chemotherapy drug and coated with chitosan target cancer stem-like cells

Published on July 1, 2015 at 7:35 AM ·

Nanoparticles packed with a clinically used chemotherapy drug and coated with an oligosaccharide derived from the carapace of crustaceans might effectively target and kill cancer stem-like cells, according to a recent study led by researchers at The Ohio State University Comprehensive Cancer Center - Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC - James). Cancer stem-like cells have characteristics of stem cells and are present in very low numbers in tumors. They are highly resistant to chemotherapy and radiation and are believed to play an important role in tumor recurrence. This laboratory and animal study showed that nanoparticles coated with the oligosaccharide called chitosan and encapsulating the chemotherapy drug doxorubicin can target and kill cancer stem-like cells six times more effectively than free doxorubicin.

"Our findings indicate that this nanoparticle delivery system increases the cytotoxicity of doxorubicin with no evidence of systemic toxic side effects in our animal model," says principal investigator Xiaoming (Shawn) He, PhD, associate professor of Biomedical Engineering and a member of the OSUCCC - James Translational Therapeutics Program.

"We believe that chitosan-decorated nanoparticles could also encapsulate other types of chemotherapy and be used to treat many types of cancer."

This study showed that chitosan binds with a receptor on cancer stem-like cells called CD44, enabling the nanoparticles to target the malignant stem-like cells in a tumor.

The nanoparticles were engineered to shrink, break open, and release the anticancer drug under the acidic conditions of the tumor microenvironment and in tumor-cell endosomes and lysosomes, which cells use to digest nutrients acquired from their microenvironment.

He and his colleagues conducted the study using models called 3D mammary tumor spheroids (i.e., mammospheres) and an animal model of human breast cancer.

The study also found that although the drug-carrying nanoparticles could bind to the variant CD44 receptors on cancerous mammosphere cells, they did not bind well to the CD44 receptors that were overexpressed on noncancerous stem cells.

Source:

Ohio State University Wexner Medical Center

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por cyto às 11:21

Sábado, 04.07.15

new immunotherapy treatment for cancer patients

 

CTCA at Western begins Phase Ib/II trial of new immunotherapy treatment for cancer patients

Published on June 27, 2015 at 2:15 AM · 

Cancer Treatment Centers of America® (CTCA) at Western Regional Medical Center (Western) in Goodyear, Arizona, has begun a new Phase Ib/II clinical trial using a new immunotherapy treatment for patients with advanced kidney, non-small cell lung cancer, pancreatic cancer and colorectal carcinoma.

This "NivoPlus" clinical trial combines an immunotherapy drug (nivolumab) with already FDA-approved chemotherapy drugs (temsirolimus, irinotecan, and a combination of irinotecan and capecitabine).

The addition of nivolumab is intended to activate the body's own immune system to improve on the results that otherwise might not be achieved from chemotherapy alone. This combination of chemotherapy and immunotherapy drugs is investigational in this study and is the third such combination clinical trial launched in the past year by CTCA® at Western.

There are anticipated to be up to 49 patients enrolled on the multi-arm NivoPlus study. The first patient received treatment on this study earlier this month.

"Some of these drug combinations are not available elsewhere, giving CTCA patients additional treatment options," said Dr. Glen Weiss, Director of Clinical Research and Medical Oncologist, CTCA at Western. "Our ultimate goal is to evaluate if these combinations yield improved results for our patients."

Nivolumab works by inhibiting a protein called PD-1, which otherwise blocks the body's immune system from attacking cancerous cells.

Nivolumab was approved by the Food and Drug Administration in December 2014 for the treatment of advanced melanoma and on March 4, 2015, for patients with previously treated metastatic squamous non-small cell lung cancer.

"Patients with these types of advanced-stage cancers have tumors that may be challenging to treat," said Dr. Vivek Khemka, Medical Oncologist, CTCA Western and NivoPlus Principal Investigator. "We are investigating whether combining nivolumab with these chemotherapy drugs will be a more powerful approach against their disease."

Recent data reported in the New England Journal of Medicine and Lancet demonstrates promising results with antibody-based immunostimulatory therapy in treating melanoma, renal cell carcinoma, non-small cell lung cancer and colorectal cancer. Data has also shown synergetic effects of utilizing cytotoxic chemotherapy in combination with immunostimulatory therapy. NivoPlus will build upon this data, extending treatment options to additional cancer types.

CTCA investigators have been actively researching the impact of immunotherapy, a topic prominently highlighted this year at the annual conferences of both the American Association for Cancer Research (AACR) and the American Society of Clinical Oncologists (ASCO).

At AACR, physicians described immunotherapy as now being considered an integral part of cancer biology and cancer treatment, and recent clinical successes were described as "stunning" and "unprecedented" in their ability to improve the care of cancer patients.

At ASCO, a full press briefing was devoted to the subject of immunotherapy, which was described by doctors as "one of the most exciting advances in oncology," enabling the body's own immune system to target cancer tumors and key to helping accelerate the pace of progress "and ultimately achieve cures for cancer."

Additionally, in 2013, Science magazine named cancer immunotherapy the scientific breakthrough of the year.

CTCA physicians are committed to bringing the latest technologies and advanced treatment options to their patients as quickly as possible. At the same time, CTCA patients are supported with therapies to reduce side effects, boost energy levels and keep them strong during treatment.

Source:

Cancer Treatment Centers of America

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por cyto às 11:18


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