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


Quarta-feira, 19.08.15

Low-fat diets better than low-carb diets for weight loss, NIH study finds

Low-fat diets better than low-carb diets for weight loss, NIH study finds

Published on August 14, 2015 at 7:30 AM ·

In a recent study, restricting dietary fat led to body fat loss at a rate 68 percent higher than cutting the same number of carbohydrate calories when adults with obesity ate strictly controlled diets. Carb restriction lowered production of the fat-regulating hormone insulin and increased fat burning as expected, whereas fat restriction had no observed changes in insulin production or fat burning. The research was conducted at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. Results were published August 13 in Cell Metabolism.

"Compared to the reduced-fat diet, the reduced-carb diet was particularly effective at lowering insulin secretion and increasing fat burning, resulting in significant body fat loss," said Kevin Hall, Ph.D., NIDDK senior investigator and lead study author. "But interestingly, study participants lost even more body fat during the fat-restricted diet, as it resulted in a greater imbalance between the fat eaten and fat burned. These findings counter the theory that body fat loss necessarily requires decreasing insulin, thereby increasing the release of stored fat from fat tissue and increasing the amount of fat burned by the body."

The researchers studied 19 non-diabetic men and women with obesity in the Metabolic Clinical Research Unit at the NIH Clinical Center in Bethesda, Maryland. Participants stayed in the unit 24 hours per day for two extended visits, eating the same food and doing the same activities. For the first five days of each visit they ate a baseline balanced diet. Then for six days, they were fed diets containing 30 percent fewer calories, achieved by cutting either only total carbs or total fat from the baseline diet, while eating the same amount of protein. They switched diets during the second visit.

The researchers had previously simulated the study with a math model of human metabolism, whose body fat predictions matched the data later collected in the study. When simulating what might happen over longer periods, the model predicted relatively small differences in body fat loss with widely varying ratios of carbs to fat. Those results suggest the body may eventually minimize differences in body fat loss when diets have the same number of calories. More research is needed to assess the physiological effects of fat and carb reduction in the long term.

"This NIH study provides invaluable evidence on how different types of calories affect metabolism and body composition," said NIDDK Director Griffin P. Rodgers, M.D. "The more we learn about the complicated topic of weight loss, the better we can find ways to help people manage their health."

More than two-thirds of American adults are overweight or obese. Maintaining a healthy weight can help prevent complications related to overweight and obesity such as heart disease, type 2 diabetes and certain types of cancer, some of the leading causes of preventable death.

"Our data tell us that when it comes to body fat loss, not all diet calories are exactly equal," Hall said. "But the real world is more complicated than a research lab, and if you have obesity and want to lose weight, it may be more important to consider which type of diet you'll be most likely to stick to over time."

Source:

NIH/National Institute of Diabetes and Digestive and Kidney Diseases

 

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por cyto às 11:47

Terça-feira, 21.07.15

TSRI study reveals alternative approach to current anti-HIV strategies

 

TSRI study reveals alternative approach to current anti-HIV strategies

Published on July 9, 2015 at 8:49 AM 

AIDS Study Points to ‘Functional Cure’

HIV-infected patients remain on antiretroviral therapy for life because the virus survives over the long-term in infected dormant cells. Interruption of current types of antiretroviral therapy results in a rebound of the virus and clinical progression to AIDS.

But now, scientists from the Florida campus of The Scripps Research Institute (TSRI) have shown that, unlike other antiretroviral therapies, a natural compound called Cortistatin A reduces residual levels of virus from these infected dormant cells, establishing a near-permanent state of latency and greatly diminishing the virus' capacity for reactivation.

"Our results highlight an alternative approach to current anti-HIV strategies," said Susana Valente, a TSRI associate professor who led the study. "Prior treatment with Cortistatin A significantly inhibits and delays viral rebound in the absence of any drug. Our results suggest current antiretroviral regimens could be supplemented with a Tat inhibitor such as Cortistatin A to achieve a functional HIV-1 cure, reducing levels of the virus and preventing reactivation from latent reservoirs."

The study was published this week in the journal mBio.

Cortistatin A was isolated from a marine sponge, Corticium simplex, in 2006, and in 2008, TSRI chemist Phil Baran won the global race to synthesize the compound. A configuration of the compound, didehydro-Cortistatin A, was shown in earlier studies to target the protein Tat, which exponentially increases viral production.

The new study shows that didehydro-Cortistatin A inhibits replication in HIV-infected cells by significantly reducing levels of viral messenger RNA - the blueprints for producing proteins and more infection.

"In latently infected primary T cells isolated from nine HIV-infected subjects being treated with antiretroviral drugs, didehydro-Cortistatin A reduced viral reactivation by an average of 92.3 percent," said Guillaume Mousseau, the first author of the study and a member of the Valente lab.

The results suggest an alternative to a widely studied strategy for latent HIV eradication known as "kick and kill," which tries to purge viral reservoirs by "kicking" them out of their latency with reversing agents and stopping new rounds of infection with an immunotherapy agent to boost the body's own immune system response while on antiretroviral treatment.

"In our proposed model, didehydro-Cortistatin A inhibits the viral transcriptional activator, Tat, far more completely, delaying or even halting viral replication, reactivation and replenishment of the latent viral reservoir," said Valente.

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por cyto às 18:25

Terça-feira, 21.07.15

Patients' own genetically engineered immune cells show significant success against multiple myeloma

 

Patients' own genetically engineered immune cells show significant success against multiple myeloma

Published on July 21, 2015 at 2:37 AM 

In recent years, immunotherapy has emerged as a promising treatment for certain cancers. Now this strategy, which uses patients' own immune cells, genetically engineered to target tumors, has shown significant success against multiple myeloma, a cancer of the plasma cells that is largely incurable. The results appeared in a study published online today in Nature Medicine.

Patients received an infusion of altered immune cells known as T-cells - roughly 2.4 billion of them - after undergoing a stem cell transplantation of their own stem cells. In 16 of 20 patients with advanced disease, there was a significant clinical response. The scientists found that the T-cell therapy was generally well-tolerated and that modified immune cells traveled to the bone marrow, where myeloma tumors typically are found, and showed a long-term ability to fight the tumors. Relapse was generally associated with a loss of the engineered T-cells.

"This study suggests that treatment with engineered T-cells is not only safe but of potential clinical benefit to patients with certain types of aggressive multiple myeloma," says first author Aaron P. Rapoport, MD, the Gary Jobson Professor in Medical Oncology at the University of Maryland School of Medicine. "Our findings provide a strong foundation for further research in the field of cellular immunotherapy for myeloma to help achieve even better results for our patients."

The trial is the first published use of genetically modified T-cells for treating patients with multiple myeloma. The approach has been used to treat leukemia as well as lymphoma, according to Dr. Rapoport, who is the Director of the Blood and Marrow Transplant Program at the University of Maryland Marlene and Stewart Greenebaum Cancer Center.

More than 77,000 people in the United States have multiple myeloma, with about 24,000 new cases diagnosed each year. Patients are treated with chemotherapy and in many cases an autologous stem cell transplant, but long-term response rates are low, and median survival is three to five years.

"The majority of patients who participated in this trial had a meaningful degree of clinical benefit," Dr. Rapoport notes. "Even patients who later relapsed after achieving a complete response to treatment or didn't have a complete response had periods of disease control that I believe they would not have otherwise experienced. Some patients are still in remission after nearly three years."

The research is a collaboration between the University of Maryland School of Medicine, the Perelman School of Medicine at the University of Pennsylvania and Adaptimmune, a clinical stage biopharmaceutical company which owns the core T-cell receptor technology and funded the study. Dr. Rapoport and co-authors Edward A. Stadtmauer, MD, of the University of Pennsylvania Abramson Cancer Center, and Gwendolyn K. Binder-Scholl, PhD, of Adaptimmune, contributed equally to the research. Dr. Rapoport is the study's principal investigator.

In the clinical study, patients' T-cells were engineered to express an affinity-enhanced T-cell receptor (TCR) specific for a type of tumor antigen, or protein, known as a cancer-testis antigen (CT antigen). The target CT antigens were NY-ESO-1 and LAGE-1. Up to 60 percent of advanced myelomas have been reported to express NY-ESO-1 and/or LAGE-1, which correlates to tumor proliferation and poorer outcomes. According to Adaptimmune, the trial is the first published study of lentiviral vector mediated TCR gene expression in humans.

Of the 20 patients treated, 14 (70 percent) had a near complete or complete response three months after treatment. Median progression-free survival was 19.1 months and overall survival was 32.1 months. Two patients had a very good partial response three months post treatment. Half the patients were treated at the University of Maryland Greenebaum Cancer Center and half at the University of Pennsylvania Abramson Cancer Center. Researchers note that the response rate was better than would be expected for a standard autologous stem cell transplant. In addition, patients did not experience side effects which have been associated with another type of genetically engineered T-cells (chimeric antigen receptors, or CARS) used to treat other cancers.

The study was originally developed by Carl H. June, MD, of the University of Pennsylvania Abramson Cancer Center, and Dr. Rapoport, who have been research collaborators for 18 years.

"Multiple myeloma is a treatable but largely incurable cancer. This study reveals the promise that immunotherapy with genetically engineered T-cells holds for boosting the body's ability to attack the cancer and provide patients with better treatments and control of their disease," says E. Albert Reece, MD., PhD, MBA, vice president for medical affairs at the University of Maryland and the John Z. and Akiko K. Bowers Distinguished Professor and dean of the University of Maryland School of Medicine. "This trial is also an excellent example of significant scientific advances that result from collaborations between academic medical institutions and private industry."

Source:

University of Maryland Medical Center

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por cyto às 18:10

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

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

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

Quinta-feira, 02.07.15

CTCA at Western begins Phase Ib/II trial of 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.

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por cyto às 11:56

Sexta-feira, 26.06.15

Vaxon Biotech receives new patent in Japan for cancer vaccine candidates

Vaxon Biotech receives new patent in Japan for cancer vaccine candidates

Published on June 22, 2015 at 9:21 AM ·

The company’s worldwide cancer vaccines patent portfolio, made up of ten patent families, now comprises 24 issued patents

Vaxon Biotech, a company specialized in anti-tumor immunotherapy, today announces that it has been granted a new patent in Japan. This patent (JP application n°2012-502822) covers a series of optimized cryptic peptides to be used in the design of the Vbx-026, a new cancer vaccine for solid tumors.

This patent gives Vaxon exclusive rights in Japan and raises its worldwide portfolio to 24 issued patents.

The patent will support the development of Vbx-026, a vaccine dedicated to the treatment of cancer patients expressing the HLA-A24 molecule. This molecule is widely expressed in the Asian population, mainly in Japan, with more than 40% of the Japanese population expressing HLA-A24. The initiation of preclinical development of the Vbx-026 vaccine is planned for 2016.

“This new patent will strengthen our position in Japan, a promising market for the development of the Vbx-026 vaccine,” said Dr. Kostas Kosmatopoulos, CEO of Vaxon Biotech. “With four cancer vaccines under development, ranging from lead optimization to phase II, we have built a strong patent portfolio and we now cover the three major HLA molecules, corresponding to around 80% of cancer patients.”

Vaxon Biotech develops therapeutic vaccines against cancer, based on its proprietary technology of optimized cryptic peptides, which are protected by ten patent families. All vaccines developed by Vaxon target universal tumor antigens and therefore have wide-ranging applications in cancer treatment.

Vx-001 and Vx-006 are already in clinical trials (Vx-001 in an ongoing randomized phase II trial in eight European countries and Vx-006 in an ongoing phase I trial). Vbx-016 has successfully completed its preclinical development and is ready to enter clinical trials and Vbx-026 is at the final stage of lead optimization.

Vx-001 and Vx-006 can be used for the treatment of patients expressing HLA-A2, the most common HLA molecule in humans (40-45% of the world population). Vx-001 and Vx-006 are fully protected by a total of 17 patents granted in Europe, the US, Canada, China and Japan. These patents belong to four patent families and cover peptide optimization technology, the products derived from this technology and their use. Six of these patents belong to INSERM/IGR and have been licensed to Vaxon Biotech, while the remaining 11 are Vaxon’s own property.

Vbx-016 can be used for the treatment of patients expressing HLA-B7, a common HLA molecule (25% of the population). Vbx-016 is already protected by three patent families. Five patents are already granted in Europe, the US, China and South Korea. Additional patents are still under review. All these patents are Vaxon’s own property.

The global market for cancer vaccines is expected to grow to $4.3 billion (€3.8 billion) by 2019, with a five-year compound annual growth rate (CAGR) of 1.3%. Technological advancements, new product launches and unmet treatment needs are predicted to drive consistent growth in this market for the foreseeable future.

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por cyto às 00:58

Segunda-feira, 18.05.15

way for noninvasive detection of early stage liver cancer

Research leads way for noninvasive detection of early stage liver cancer

Published on May 15, 2015 at 9:02 AM ·

Led by Georgia State University, researchers have developed the first robust and noninvasive detection of early stage liver cancer and liver metastases, in addition to other liver diseases, such as cirrhosis and liver fibrosis.

Their findings were published Wednesday (May 13) in Proceedings of the National Academy of Sciences.

More than 700,000 people are diagnosed with liver cancer each year. It is the leading cause of cancer deaths worldwide, accounting for more than 600,000 deaths annually, according to the American Cancer Society. The rate of liver cancer in the U.S. has sharply increased because of several factors, including chronic alcohol abuse, obesity and insulin resistance.

"Liver cancers associated with high mortality rates and poor treatment responses are often diagnosed in the late stages because there is not a reliable way to detect primary liver cancer and metastasis at a size smaller than one centimeter," said Jenny Yang, lead author on the paper, Distinguished University Professor and associate director of the Center for Diagnostics and Therapeutics at Georgia State.

The liver is a common site for a variety of cancers, including melanoma, breast, pancreatic and colon cancers. Magnetic resonance imaging (MRI) is the leading imaging technique to detect disease without using radiation. MRI contrast or imaging agents aid MRI techniques to obtain tissue-specific images.

As reported by Yang, the applications of MRI contrast agents are not effective for early detection of cancerous tumors because they are hampered by uncontrolled blood circulation time, low relaxation rate or sensitivity, and low specificity. Most contrast agents, she said, are rapidly excreted from the liver, not allowing sufficient time to obtain quality imaging.

To more effectively detect cancerous tumors at an early stage, researchers from Georgia State, in collaboration with researchers from Emory University, Georgia Tech, the University of Georgia and the University of Virginia, have developed a new class of protein-based contrast agents (PRCAs) and an imaging methodology that provides robust results for the early detection of liver cancer and other liver diseases.

ProCA32, the researchers' newly developed contrast agent, allows for imaging liver tumors that measure less than 0.25 millimeters. The agent is more than 40 times more sensitive than today's commonly used and clinically approved agents used to detect tumors in the liver.

ProCA32 widens the MRI detection window and is found to be essential for obtaining high-resolution quality images of the liver. This application has important medical implications for imaging various liver diseases, the origin of cancer metastasis, monitoring cancer treatment and guiding therapeutic interventions, such as drug delivery.

"Our new agents can obtain both positive and negative contrast images within one application, providing double the accuracy and confidence of locating cancerous tumors," Yang said. "These agents are also expected to be much safer with reduced metal toxicity."

The researchers have shown proof-of-concept that ProCA32 can be used to detect cancerous liver tumors at an early stage with high sensitivity. They have also demonstrated that these new agents better aid the imaging of multiple organs, including the kidney and blood vessels, in addition to the liver and tumors.

"ProCA32 may have far-reaching implications in the diagnosis of other malignancies, which in turn would facilitate development of targeted treatment along with effective monitoring of reduction of tumor burden," Yang said. "Our agent and methodology can also be applied to study the brain and monitor treatment outcomes in a number of disorders, including stroke and recovery after stroke, Alzheimer's disease, brain tumors and gliomas,"

Source:

Georgia State University

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por cyto às 14:03


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