According to an investigation published Online First in The Lancet Oncology, for individuals who have relapsed with the most prevalent type of leukemia, chronic lymphocytic leukemia (CLL), a novel, less toxic, treatment that combines the chemotherapy drug fludarabine and the monoclonal antibody alemtuzumab, considerably increases progression free survival (PFS) and extends the lives of individuals suffering with these disease, in comparison to only fludarabine. The study reveals that this novel medication combination could be a vital treatment for those suffering with this disease.

Lead author Thomas Elter from the University of Cologne, Cologne, Germany, said:

“Unlike common regimens used to treat CLL, the new two-drug combination spares patients from the toxicities of additional alkylating drugs. Moreover, the required dose of each drug is lower when used in combination than when the drugs are used alone, and the dosing schedule of 3 days a month is more convenient for patients than the standard regimen of three times a week for up to 12 weeks.”

As age, and co-occurring illnesses vary significantly among individuals with chronic lymphocytic leukemia, there is not one standard treatment for all patients with the disease, therefore, it is important that several further treatment options need to be available.

The phase 3 trial, randomly assigned patients with CLL across Europe and North America to two groups. One group (168 patients) received fludarabine plus alemtuzumab for a maximum of six 28-day cycles, and the other group (167) patients were assigned to fludarabine alone for the same duration.

They discovered that both progression free survival was considerably greater with the combination treatment (23.7 months) in comparison with fludarabine alone (16.5 months). In addition they found that complete response rates were also significantly improved with the combination of fludarabine plus alemtuzumab. Individuals with advanced disease and older patients also benefited from the combination treatment.

Overall, participants in both groups experienced a similar number and severity of infectious complications. The frequency of grade 3 or 4 neutropenia (low white blood cell count) was similar between both the groups, as was thrombocytopenia (abnormally low number of blood platelets), however, in the combination group anaemia was lower (9%) compared to 17% in the other group, while lymphopenia (abnormally low number of lyphocytes in the blood) was higher in the combination group 94% versus 33% in the fludarabine only group.

Even though the prevalence of serious side effects were higher in the combination group (33%) than the fludarabine only group (25%), the number of individuals who stopped treatment and deaths during treatment were similar in both groups.

Grace Rattue

Sprycel (dasatinib), a leukemia medication raises the risk of developing pulmonary arterial hypertension, the US Food and Drug Administration (FDA) announced today in a Drug Safety Communication. The FDA says doctors should check patients for signs and symptoms of underlying cardiopulmonary disease before considering prescribing Sprycel – they should also evaluate patients during treatment.

Pulmonary arterial hypertension, also known as pulmonary hypertension or PAH is a kind of high blood pressure that only affects the arteries in the lung and the right side of the patient’s heart. It starts when the pulmonary arteries and capillaries become narrowed, blocked or damaged, making it harder for blood to flow through the lungs. This raises pressure within the arteries in the lungs. Pressure builds up, making the right ventricle of the heart – the lower right chamber – have to work harder to pump blood through to the lungs. The heart muscle eventually weakens, and if left untreated may fail completely.

PAH is a serious illness that tends to get worse with time. PAH is potentially fatal.

Signs and symptoms of pulmonary arterial hypertension include fatigue, shortness of breath, swelling of the ankles and legs (and possibly other parts of the body), non-productive cough, angina pectoris, syncope, and in rare cases coughing up blood.

The FDA has received reports of patients who started on Sprycel developing PAH, in some cases after over a year on the medication. Some of the patients were on other drugs simultaneously, or had other underlying co-existing medical conditions. Some medical conditions may cause PAH-like symptoms. The FDA says that patients with symptoms who have other conditions ruled out, should be considered for a diagnosis of Sprycel-associated PAH.

If Sprycel-associated PAH is confirmed, the medication should be permanently discontinued, the FDA added.

The FDA stresses that if Sprycel treatment is discontinued, the PAH is reversible.

If you are a patient taking Sprycel and experience PAH-like symptoms, contact your doctor immediately.

The FDA is telling doctors that before initiating invasive procedures “more common etiologies of dyspnea associated with Sprycel therapy should be excluded, including pleural effusion, pulmonary edema, anemia, and lung infiltration.”

Sprycel (dasatinib) has been on the market in the USA since June 2006. Since 2006, Bristol-Myers Squibb, the makers of the medication, have received cases of PAH. However, no deaths directly related to dasatinib usage have been reported.

The company received 12 cases of PAH which were confirmed by right heart catheterization (Sprycel most likely cause). In many cases patients were taking other medications and had other underlying medical conditions.

The FDA wrote on its website:

“There may be a combination of factors contributing to the development of PAH in patients taking Sprycel. In some cases, improvements in hemodynamic and clinical parameters were observed following discontinuation of Sprycel.”

Patients and doctors are encouraged to report any serious problems to:

Tel: 1-800-332-1088
Fax: 1-800-FDA-0178
MedWatch Online
Regular Mail: Use postage-paid FDA Form 3500. Mail to: MedWatch 5600 Fishers Lane, Rockville, MD 20857

Dasatinib, chemical formula C22H26ClN7O2S, is an oral multi- BCR/ABL and Src family tyrosine kinase inhibitor approved for use in patients with chronic myelogenous leukemia (CML) after imatinib treatment and Philadelphia chromosome-positive acute lymphoblastic leukemia.

View drug information on Sprycel.

Researchers with UCLA’s Jonsson Comprehensive Cancer Center have developed and used a high-throughput molecular screening approach that identifies and characterizes chemical compounds that can target the stem cells that are responsible for creating deadly brain tumors.

Glioblastoma is one of the deadliest malignancies, typically killing patients within 12 to 18 months. These brain cancers consist of two kinds of cells, a larger, heterogeneous population of tumor cells and a smaller sub-population of stem cells, which are treatment-resistant.

The screening system was specifically designed to find drugs that can target that sub-population and prevent it from re-seeding the brain cancer, said study senior author Dr. Harley Kornblum, a Jonsson Cancer Center scientist and a professor of psychiatry and biobehavioral sciences.

“We’re pleased that we can present a different way to approach the discovery of potential new cancer drugs,” said Kornblum, who also is a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA. “And by finding these drugs, we may be able to reveal things about the biology of these cancer stem cells.”

The study appears in the Oct. 10 issue of Molecular Cancer Therapeutics, a peer-reviewed journal of the American Association of Cancer Research.

After testing more than 31,000 compounds from seven chemical libraries in an initial screen, the team came up with 694 that showed some activity against the brain cancer stem cells. After further narrowing the field down to 168 compounds, they decided to focus on four in future studies because they most successfully inhibited the brain cancer stem cells, Kornblum said.

What Kornblum and his team did in their approach was sort of a reverse of the usual screening processes. Typically, researchers doing high-throughput screening are seeking a drug to hit a specific target they know is on a cancer cell, perhaps a protein that is causing it to grow or a gene that keeps it from dying. In this case, Kornblum said, the team was basically shooting in the dark because the biology of these brain cancer stem cells is largely unknown.

“When brain cancer stem cells were first discovered, we all realized rapidly that we would need to find drugs that attack these cells specifically, because they’re resistant to our conventional therapies,” Kornblum said. “We needed a way to kill these stem cells.”

UCLA’s high-throughput screening technology is capable of screening as many as 100,000 compounds in a single day. Researchers generally develop cancer cells lines and then create an assay, a procedure in molecular biology to test or measure the activity of a drug or biochemical compound in an organic sample, in this case the cancer cells.

The cells are loaded into plates with 384 wells each and the drugs are added. The plates are about the size of the palm of an adult hand. The computerized, robotic screening system executes the process from start to finish, adding the compounds sitting in the tiny wells in the plates to the cancer cells, located in corresponding assay plates.

In this study, Kornblum and his team had a few clues to help them in narrowing down potential candidates that kill brain cancer stem cells. One method they used was based on a prior discovery by Jonsson Cancer Center researchers. The researchers had identified genes that correlate with how aggressive a brain tumor is, so Kornblum decided to try to find potential drug candidates that might reduce the expression of these genes. Another approach was to figure out which of the molecules killed brain cancer stem cells with a greater potency than they attacked other cells within glioblastoma.

To grow his cell lines, Kornblum used human tissue taken from UCLA patients diagnosed with glioblastoma. He knew that a certain method of culturing brain cancer cells resulted in a large number of brain cancer stem cells in the population. These cells were then screened with a molecular library of 31,624 compounds available through the cancer center’s Molecular Screening Shared Resource. These compounds encompass a wide range of structures and therefore have the possibility of influencing virtually all cellular functions.

“We decided on this type of approach because, although we have learned a great deal about brain cancer stem cells in the past several years, we still have not discovered enough of their biology to be sure that any single target will be the right one to hit,” Kornblum said.

Going forward, Kornblum and his team will further study the four identified “lead” compounds to see if they help reveal the biology of the brain cancer stem cells and potentially result in a new and more effective therapy for these deadly brain cancers.

“One of our goals was to determine whether some compounds selectively act on glioblastoma stem cells compared to the less tumorigenic cells from the same tumor,” the study states. “This selectivity may allow for the delineation of pathways and processes that are highly important to these cells. By making sure that a drug candidate has the potential to attack these stem cells, one might ensure the highest chance of therapeutic success.”

Researchers with UCLA’s Jonsson Comprehensive Cancer Center have developed and used a high-throughput molecular screening approach that identifies and characterizes chemical compounds that can target the stem cells that are responsible for creating deadly brain tumors.

Glioblastoma is one of the deadliest malignancies, typically killing patients within 12 to 18 months. These brain cancers consist of two kinds of cells, a larger, heterogeneous population of tumor cells and a smaller sub-population of stem cells, which are treatment-resistant.

The screening system was specifically designed to find drugs that can target that sub-population and prevent it from re-seeding the brain cancer, said study senior author Dr. Harley Kornblum, a Jonsson Cancer Center scientist and a professor of psychiatry and biobehavioral sciences.

“We’re pleased that we can present a different way to approach the discovery of potential new cancer drugs,” said Kornblum, who also is a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA. “And by finding these drugs, we may be able to reveal things about the biology of these cancer stem cells.”

The study appears in the Oct. 10 issue of Molecular Cancer Therapeutics, a peer-reviewed journal of the American Association of Cancer Research.

After testing more than 31,000 compounds from seven chemical libraries in an initial screen, the team came up with 694 that showed some activity against the brain cancer stem cells. After further narrowing the field down to 168 compounds, they decided to focus on four in future studies because they most successfully inhibited the brain cancer stem cells, Kornblum said.

What Kornblum and his team did in their approach was sort of a reverse of the usual screening processes. Typically, researchers doing high-throughput screening are seeking a drug to hit a specific target they know is on a cancer cell, perhaps a protein that is causing it to grow or a gene that keeps it from dying. In this case, Kornblum said, the team was basically shooting in the dark because the biology of these brain cancer stem cells is largely unknown.

“When brain cancer stem cells were first discovered, we all realized rapidly that we would need to find drugs that attack these cells specifically, because they’re resistant to our conventional therapies,” Kornblum said. “We needed a way to kill these stem cells.”

UCLA’s high-throughput screening technology is capable of screening as many as 100,000 compounds in a single day. Researchers generally develop cancer cells lines and then create an assay, a procedure in molecular biology to test or measure the activity of a drug or biochemical compound in an organic sample, in this case the cancer cells.

The cells are loaded into plates with 384 wells each and the drugs are added. The plates are about the size of the palm of an adult hand. The computerized, robotic screening system executes the process from start to finish, adding the compounds sitting in the tiny wells in the plates to the cancer cells, located in corresponding assay plates.

In this study, Kornblum and his team had a few clues to help them in narrowing down potential candidates that kill brain cancer stem cells. One method they used was based on a prior discovery by Jonsson Cancer Center researchers. The researchers had identified genes that correlate with how aggressive a brain tumor is, so Kornblum decided to try to find potential drug candidates that might reduce the expression of these genes. Another approach was to figure out which of the molecules killed brain cancer stem cells with a greater potency than they attacked other cells within glioblastoma.

To grow his cell lines, Kornblum used human tissue taken from UCLA patients diagnosed with glioblastoma. He knew that a certain method of culturing brain cancer cells resulted in a large number of brain cancer stem cells in the population. These cells were then screened with a molecular library of 31,624 compounds available through the cancer center’s Molecular Screening Shared Resource. These compounds encompass a wide range of structures and therefore have the possibility of influencing virtually all cellular functions.

“We decided on this type of approach because, although we have learned a great deal about brain cancer stem cells in the past several years, we still have not discovered enough of their biology to be sure that any single target will be the right one to hit,” Kornblum said.

Going forward, Kornblum and his team will further study the four identified “lead” compounds to see if they help reveal the biology of the brain cancer stem cells and potentially result in a new and more effective therapy for these deadly brain cancers.

“One of our goals was to determine whether some compounds selectively act on glioblastoma stem cells compared to the less tumorigenic cells from the same tumor,” the study states. “This selectivity may allow for the delineation of pathways and processes that are highly important to these cells. By making sure that a drug candidate has the potential to attack these stem cells, one might ensure the highest chance of therapeutic success.”

Funding for the study was provided by the Jonsson Comprehensive Cancer Center, the National Cancer Institute and the National Institute of Neurological Disorders and Stroke.

Water channels exist not only in nature – microscopical water channels are also present in the cells of the body, where they ensure that water can be transported through the protective surface of the cell. Scientists at the University of Gothenburg, Sweden, have discovered that one type of the body’s water channels can be modified such that it becomes more stable , which may be significant in the treatment of several diseases.

“It’s important to understand how the water channels, which are known as ‘aquaporins’, in the body work, since they control many of the processes in our cells and tissues. They also determine what is to be transported into and out of the cell, and they are thus highly significant in the development of new treatments for various diseases, such as eczema, cerebral oedema, obesity and cancer”, says Kristina Hedfalk of the Department of Chemistry at the University of Gothenburg.

Aquaporins are vital

There are 13 different types of aquaporins in the human body. One of these, AQP2, is found in the kidney where it is responsible for a large-volume recirculation of water from the primary urine every day. Without this, we would urinate nearly 10 litres every day. Another variant, AQP4, is found in the brain where it contributes to regulation of the osmotic pressure in the sensitive brain tissue. This regulation is particularly important in those who are affected by cerebral oedema, which is a life-threatening condition that can follow a blow to the head or a stroke.

The research group, which consists of Fredrik Oberg, Jennie Sj?¶hamn, Gerhard Fischer, Andreas Moberg, Anders Pedersen, Richard Neutze and Kristina Hedfalk, describes their studies of one of the most recently discovered aquaporins in an article in the scientific journal The Journal of Biological Chemistry. This aquaporin, AQP10, is preferentially found in the intestine, and is particularly interesting since it transports both water and sugar alcohols.

Carbohydrates stabilise the water channel

“AQP10 differs from other aquaporins by having a large carbohydrate structure of branched sugar molecules, somewhat similar to a tree, attached on its outer surface. This makes it significantly more stable. This may be because aquaporins in the intestine need to be particularly stable. What we have shown is that AQP10 retains its transport ability, even if the carbohydrate structure is removed.”

Data from a Phase II randomized, double-blind, placebo-controlled clinical trial which assessed talactoferrin (an oral immunotherapy) in individuals who had previously received treatment for non-small cell lung cancer (NSCLC) has been published and will appear in the November 1, 2011 print issue of the peer-reviewed medical journal, Journal of Clinical Oncology, Agennix AG . The report “A Randomized, Double-blind, Placebo-controlled Phase II Study of Oral Talactoferrin in Patients with Locally Advanced or Metastatic Non-Small Cell Lung Cancer That Progressed Following Chemotherapy” is P. Parikh and colleagues.

The investigation, conducted on individuals for whom one or more previous types of anti-cancer treatments for NSCLC had failed, reached its initial endpoint of improvement in overall survival. In addition the drug seemed to improve survival rates across a wide range of patient subsets, including patients with non-squamous and squamous histologies, and other crucial prognostic factors. Results from this investigation formed the foundation for the talactoferrin Phase III FORTIS-M trial that is currently in process. The Phase III trial is being carried out in individuals whose NSCLC has progressed after two or more previous treatment methods. Enrollment for the FORTIS-M investigation has been completed, with results expected in the first half of 2012.

Rajesh Malik, M.D., Chief Medical Officer, explained:

“There is a major need for effective, easy-to-use, well tolerated treatments for patients with refractory non-small cell lung cancer. The promising results from this study show the potential of talactoferrin to improve survival where previous therapies have failed, including effects across a broad range of clinically important subsets.

Talactoferrin appears to provide anti-tumor activity without many of the common toxicities associated with other treatments for non-small cell lung cancer. In addition, talactoferrin is an oral liquid that offers convenience for both patients and physicians to use. We look forward to reporting topline results from our ongoing Phase III FORTIS-M registration trial in advanced non-small cell lung cancer in the first half of 2012.”

The Phase II study enrolled 100 individuals with stage IIIB/IV NSCLC whose cancer had advanced after one or more forms of anti-cancer treatments failed. The participants where then assigned to two groups, one group received talactoferrin in addition to best supportive care and the other group received placebo plus best supportive care.

After evaluation, the results revealed that talactoferrin improved median overall survival by 65% in comparison to those in the placebo group (6.1 months vs. 3.7 months, hazard ratio = 0.68, 90% Confidence Interval: 0.47-0.98, p=0.04 [one-tailed log-rank test]), reaching the protocol-defined level of statistical significance. For those in the talactoferrin group, the six-month overall survival was 52% compared to 30% in the placebo group. Patients in the placebo group had a one-year overall survival rate of 16% compared to 29% in the talactoferrin group. Encouraging results were observed in the secondary endpoints of disease control rate and progression-free survival. The above examination was carried out with the intention to treat.

In the investigation, it was shown that talactoferrin was very well tolerated, with less side effects compared to placebo. Dyspnea (labored breathing) was the most prevalent reported (grade 3 or higher) side effect, which occurred in 26% of patients in the placebo group and 15% of those in the talactoferrin group. No serious side effects were believed to be connected to the treatment with talactoferrin.

Grace Rattue

According to a new study, published in the October issue of Molecular Cancer Therapeutics, a peer-reviewed journal of the American Association of Cancer Research, stem cells responsible for creating deadly brain tumors can be identified and characterized by chemical compounds that can target the stem cells. For the study researchers at the UCLA’s Jonsson Comprehensive Cancer Center developed and utilized a high-throughput molecular screening approach to identify and characterize these chemical compounds.

Glioblastoma is one of the deadliest forms of brain cancers usually killing people within 12 to 18 months. It consists of two different cell types, a larger heterogeneous population of tumor cells and a smaller sub-population of stem cells that are resistant to treatment.

Senior author Dr. Harley Kornblum, a Jonsson Cancer Center scientist and a professor of psychiatry and biobehavioral sciences said that the screening system was specifically designed to identify drugs able to target this sub-population and prevent it from re-seeding the brain cancer.

Kornblum, who also is a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA commented:

“We’re pleased that we can present a different way to approach the discovery of potential new cancer drugs. And by finding these drugs, we may be able to reveal things about the biology of these cancer stem cells.”

Kornblum explained that the researchers tested over 31,000 compounds from seven chemical libraries in an initial screen and discovered 694 compounds that showed some activity against the brain cancer stem cells. Following a further reduction process down to 168 compounds, they decided to concentrate on four compounds in their future studies, which proved to be the most successful in inhibiting the brain cancer stem cells.

Kornblum and his team used an approach similar to the reverse of the usual screening processes. Normally high-throughput screenings involve seeking a drug to hit a specific target that researchers know is on a cancer cell, for example a protein that is causing the target to growth or a gene preventing the target from dying, however, Kornblum and his team basically conducted their search blindfolded as there is still little knowledge of the biology of these brain cancer stem cells.

Kornblum explained:

“When brain cancer stem cells were first discovered, we all realized rapidly that we would need to find drugs that attack these cells specifically, because they’re resistant to our conventional therapies. We needed a way to kill these stem cells.”

As many as 100,000 compounds can be screened in a single day by using UCLA’s high-throughput screening technology. Researchers normally develop cancer cells lines after which they create an assay, a molecular biology procedure for testing or measuring a drugs activity or biochemical compound in an organic sample, i.e. cancer in this case.

The high-throughput screening technology consists of a computerized, robotic screening system in which cells are loaded into plates, which are approximately the size of an adult’s palm of the hand. Each plate contains 384 wells to which the drugs are added. The system executes this process from start to finish, adding the compounds sitting in the tiny wells in the plates to the cancer cells, located in corresponding assay plates.

Kornblum and his colleagues had a few hints in this study, which assisted them in the reduction process for potential candidates that kill brain cancer stem cells. One of the approaches was focused on a prior discovery made by Jonsson Cancer Center researchers who identified genes that correlate with how aggressive a brain tumor is. Kornblum set out to identify potential drug candidates that might reduce the expression of these genes. His other approach was to identify which of the molecules killed brain cancer stem cells with a greater potency than they attacked other cells within glioblastoma.

Kornblum used human tissue obtained from UCLA glioblastoma patients to grow his cell lines, knowing that a certain method of culturing brain cancer cells resulted in a large number of brain cancer stem cells in the population. He then screened these cells with a molecular library of 31,624 compounds available through the cancer center’s Molecular Screening Shared Resource. These compounds encompass a wide range of structures and are therefore likely to influence virtually all cellular functions.

Kornblum explained:

“We decided on this type of approach because, although we have learned a great deal about brain cancer stem cells in the past several years, we still have not discovered enough of their biology to be sure that any single target will be the right one to hit.”

Kornblum and his colleagues will continue to conduct further studies into the four identified “lead” compounds to establish whether they can help to reveal the biology of the brain cancer stem cells and possibly result in a new, more effective therapy for these deadly brain cancers.

The authors comment:

“One of our goals was to determine whether some compounds selectively act on glioblastoma stem cells compared to the less tumorigenic cells from the same tumor. This selectivity may allow for the delineation of pathways and processes that are highly important to these cells. By making sure that a drug candidate has the potential to attack these stem cells, one might ensure the highest chance of therapeutic success.”

The Jonsson Comprehensive Cancer Center, the National Cancer Institute and the National Institute of Neurological Disorders and Stroke funded the study.

Petra Rattue

A compound isolated from a wild, poisonous mushroom growing in a Southwest China forest appears to help a cancer killing drug fulfill its promise, researchers report.

The compound, verticillin A, sensitizes cancer cells to TRAIL, a drug which induces cancer cells to self destruct, said Dr. Kebin Liu, cancer immunologist at the Georgia Health Sciences University Cancer Center and corresponding author of the study in the journal Cancer Research.

The compound appears to keep cancer cells from developing resistance to TRAIL, short for tumor necrosis factor-related apoptosis inducing ligand. Drug resistance, intrinsic or acquired, is a major problem for cancer patients, accounting for greater than 90 percent of treatment failures in patients with metastatic disease.

“If we can make drugs work again, more people will survive,” Liu said.

Patient experience has shown cancer’s skill at desensitizing itself to the TRAIL. “It looks as though most cancer cells have found a way to become resistant and evade its action,” said Dr. Wendy Bollag, cell physiologist at GHSU and a study co-author. Tenacious cancer cells also are naturally resistant to cell suicide, which is how TRAIL works.

In mice, they found verticillin A alone was adequate to kill cancer cells, but the required dose made the mice sick, a common problem with many cancer therapies. However, when a lower dose was paired with TRAIL, it became a powerful, more tolerable recipe that killed previously resistant cells.

They also found that the compound improved the efficacy of commonly used cancer drugs etoposide and cisplatin, which also work by promoting cancer cell death but are less targeted than TRAIL. “We believe this could be a good companion drug for a lot of cancer therapies,” Liu said.

One way verticillin A appears to work is by upregulating BN1P3, a gene that promotes cell death, the researchers said. Cancer cells work to silence BN1P3 through a process called DNA methylation; verticillin A appears to modify the same process to turn the gene on.

All cells use DNA methylation but cancer cells use it differently, said Dr. Keith Robertson, cancer epigeneticist and Georgia Cancer Coalition Scholar. “Verticillin A may be working by altering methylation in a way that makes the cancer cells sensitive to TRAIL,” Robertson said.

Their studies were of metastatic human colon cancer cells, which are highly resistant to treatment, including TRAIL, both in culture as well as transplanted into mice. They did similar studies on sarcoma, lung adenocarcinoma and breast cancer.

Additional toxicity studies are needed before moving forward with clinical trials, Bollag said. The researchers also want to pursue the compound’s potential in melanoma and pancreatic cancer.

Verticillin A was isolated from mushrooms in Dr. Ping Wu’s laboratory at the Research Centre of Siyuan Natural Pharmacy and Biotoxicology at China’s Zhejiang University and brought to GHSU by former postdoctoral fellow, Dr. Feiyan Liu, the study’s first author, who studied with Kebin Liu in Augusta for two years. The Chinese university is involved in extensive studies to isolate active compounds from plants to explore their therapeutic potential and both Dr. Lius liked verticillin A’s aggressive response against cancer.

A select group of 30 volunteer patients were administered with a Ginger Root Supplement or placebo and after a month showed a promising decrease in many of the inflammation markers in the colon.

Inflammation of the colon is an indicator believed to be a precursor to colon cancer. Thus reducing inflammation is an important step in colon cancer prevention.

Suzanna M. Zick, N.D., M.P.H., a research assistant professor at the University of Michigan Medical School and colleagues, enrolled 30 patients and randomly assigned them to two grams of ginger root supplements per day or placebo for 28 days.

Zick commented that :

“We need to apply the same rigor to the sorts of questions about the effect of ginger root that we apply to other clinical trial research. Interest in this is only going to increase as people look for ways to prevent cancer that are nontoxic, and improve their quality of life in a cost-effective way.”

The study published in Cancer Prevention Research, a journal of the American Association for Cancer Research, measured standard levels of colon inflammation and saw real reductions in most of the markers, and others trending towards significant reductions.

The team says that Phase II trials are now required to validate the initial results. It’s interesting to see a herb that is not under patent, being treated with the same methodical approach used to test pharmaceutical drugs in which there is obviously a far greater vested interest in studying and proving their validity. Many doctors complain that natural medicine is unproven “witchery” but when you think into it, it’s only because there is no real financial interest or profit incentive to spending thousands testing a product which is common property.

In Summary :

–Reductions of markers like PGE2 may be a biomarker for colon cancer prevention.
–Phase II study conducted in humans requires validation.
–Natural supplement use could be potential cancer prevention strategy

Ginger may have colon cancer prevention qualities

Zick is a naturopathic doctor (N.D.), who has followed a four year degree that places traditional medical education alongside training in natural therapies, diet, nutrition and other alternative treatments. Her program is one of only eight in the US, compared with 135 regular medical schools.

The study was funded by the National Cancer Institute and University of Michigan Clinical Research Center and the Kutsche Family Memorial Endowment. The ginger extract was donated by Pure Encapsulations (Sudbury, MA).

Rupert Shepherd

“It’s not brain surgery” is a phrase often uttered to dismiss a job’s difficulty, but when the task actually is removing a brain tumor, even the slightest mistake could have serious health consequences. To help surgeons in such high-pressure situations, researchers from Prof. Adam Wax’s team at Duke University’s Fitzpatrick Institute for Photonics and Biomedical Engineering Department have proposed a way to harness the unique optical properties of gold nanoparticles to clearly distinguish a brain tumor from the healthy, and vital, tissue that surrounds it. The team will present their findings at the Optical Society’s (OSA) Annual Meeting, Frontiers in Optics (FiO) 2011, taking place in San Jose, Calif. next week.

Current techniques for outlining brain tumors vary, but all have limitations, such as the inability to perform real-time imaging without big, expensive equipment, or the toxicity and limited lifespan of certain labeling agents. Gold nanoparticles – which are so small that 500 of them end-to-end could fit across a human hair – might provide a better way to flag tumorous tissue, since they are non-toxic and relatively inexpensive to manufacture.

The Duke researchers synthesized gold, rod-shaped nanoparticles with varying length-to-width ratios. The different-sized particles displayed different optical properties, so by controlling the nanorods’ growth the team could “tune” the particles to scatter a specific frequency of light. The researchers next joined the tuned particles to antibodies that bind to growth factor receptor proteins found in unusually high concentrations on the outside of cancer cells. When the antibodies latched on to cancer cells, the gold nanoparticles marked their presence.

The team tested the method by bathing slices of tumor-containing mouse brain in a solution of gold nanoparticles merged with antibodies. Shining the tuned frequency of light on the sample revealed bright points where the tumors lurked. The tunability of the gold nanoparticles is important, says team member Kevin Seekell, because it allows researchers to choose from a window of light frequencies that are not readily absorbed by biological tissue. It might also allow researchers to attach differently tuned nanoparticles to different antibodies, providing a way to diagnose different types of tumors based the specific surface proteins the cancer cells display. Future work by the team will also focus on developing a surgical probe that can image gold nanoparticles in a living brain, Seekell says.