Nervous System

Up to half the number of men with prostate cancer who die do so as a direct result of the disease, rather than from other causes according to a new study presented at the National Cancer Intelligence Network conference in London.

Researchers from King’s College London looked at 50, 066 men with prostate cancer in the Thames Cancer Registry between 1997 and 2007.

Of this group, 20,181 died during the 10 years. And, of these deaths, 49 per cent were recorded as being due to the cancer itself. According to the study twelve per cent of deaths were caused by other cancers, 17 per cent from heart disease, 8 per cent were from pneumonia and 13 per cent were due to other causes.

Prostate cancer is the second most common cause of cancer death in UK men, after lung cancer. Every year around 37,000 men are diagnosed and over 10,100 men die from the disease.

Professor Henrik Moller, study author from King’s College London and head of analysis and research at the NCIN, said: “Our data show that a high proportion of men with prostate cancer die from the cancer. Our findings challenge the commonly held view that most men with prostate cancer will die with the disease rather than from it.”

Simon Chowdhury, study author and consultant oncologist at Guy’s and St Thomas’ NHS Foundation Trust, said: “This confirms that prostate cancer is a major cause of morbidity and mortality for a large number of men and the importance of ongoing and future research into this area.”

Source
King’s College London

British men lack a basic understanding of their prostate cancer risk, despite it being the cancer they are most likely to get.

Research by male cancer campaign, Everyman, found that nearly three quarters of men surveyed were unable to name age, family history or race as the top risk factors for prostate cancer, while a quarter admitted having no knowledge of any risk factors.

A third of respondents wrongly believed that drinking alcohol and smoking were the main factors related to an increased risk of getting the disease.

After age, family history is one of the strongest risk factors for prostate cancer, yet more than half (54%) of those surveyed admitted they had not considered what diseases they were more likely to get as a result of their family’s medical background.

Everyman is a campaign run by The Institute of Cancer Research (ICR) to raise funds for prostate and testicular cancer research. The ICR is currently undertaking a study to determine whether family history and genetic profiling can be used to find men at higher risk of prostate cancer, so they can be targeted for screening.

Professor Ros Eeles from the ICR said: “The PROFILE* study follows years of research into prostate cancer risk factors, including the discovery of 31 genetic variants that predispose to the disease, and the recognition that family history substantially increases men’s chances of developing the disease.

“This study will show us whether we have enough knowledge about prostate cancer genetics to find men at higher risk of the disease, and whether we should therefore start screening these men. Screening men at higher risk could potentially lead to earlier diagnoses, which would improve their chances of cure,” Professor Eeles said.

Prostate Specific Antigen (PSA) testing is the only tool currently available to screen men for prostate cancer, but it carries a significant risk of over-diagnosis and over-treatment for men who would not otherwise need it. However, these risks may be less significant in men at higher risk of the disease, so ICR scientists are looking for a way to identify this group.

Minister of State for Care Services, Paul Burstow, said: “Identifying prostate cancer sooner can mean better health outcomes. If men are at all worried, especially if they are black, have prostate cancer in the family or notice changes when they urinate, they should discuss with their GP the potential benefits of a PSA test.

“Early diagnosis is a major priority in the Government’s Cancer Strategy and will be central to achieving our aim to save at least five thousand extra lives a year from cancer. I fully support Everyman’s efforts to raise men’s awareness of prostate cancer,” said Mr Burstow.

The survey, conducted for Everyman’s Male Cancer Awareness Month, also showed a general lack of awareness around the number of men prostate cancer kills each year, with nearly two thirds underestimating the figure of 10,000 by four times or more.

Alarmingly, nearly half (46%) of respondents could not answer correctly where the prostate was, while only one in ten knew the prostate’s main function.

The Shadow Minister for Public Health, Diane Abbott, commented on the study: “It is significant that men know so little about these issues and the government needs to give more thought to how and where they target public awareness campaigns in order to reach men.

“We must improve awareness of the signs and symptoms of cancer among the public and GPs. Improved services in primary care are essential, and those men affected must be referred to hospital specialists sooner and begin treatment earlier,” said Ms Abbott.

* The PROFILE study will eventually be conducted in three centres – London, Oxford and Cambridge – but is now only open in London. Men aged between 40 and 69 with a family history of prostate cancer are invited to participate.

Source
The Institute of Cancer Research

Cancer is crafty. When one avenue driving its growth is blocked by drugs targeting that path, the malignancy often creates a detour, finding an alternative route to get around the roadblock.

In a study at UCLA’s Jonsson Comprehensive Cancer Center, researchers found that when a common type of prostate cancer was treated with conventional hormone ablation therapy blocking androgen production or androgen receptor (AR) function which drives growth of the tumor the cancer was able to adapt and compensate by activating a survival cell signaling pathway, effectively circumventing the roadblock put up by this treatment.

The findings could have important clinical implications as this type of prostate cancer, in which the PTEN tumor suppressor gene is inactivated, accounts for about 40 to 50 percent of primary prostate cancers and 70 to 90 percent of cancers that become resistant to hormone therapy, called castration resistant prostate cancers. Based on this study, these prostate cancers could be more effectively treated using a combination of drugs that target the AR cell signaling pathway and the compensating survival pathway, called the PI3K/AKT/mTOR pathway, said study senior author Dr. Hong Wu, a professor of molecular and medical pharmacology and a Jonsson Cancer Center researcher.

The study appears in the June 14, 2011 of the peer-reviewed journal Cancer Cell.

“The most significant take home message from this study is that certain prostate cancers can resist androgen deprivation therapy by activating an alternate pathway to drive its growth,” Wu said. “We found that these two pathways are talking to each other, almost like regulatory circuitry, and helping each other get around attempts to kill the cancer. When we suppress one of these pathways, it essentially feeds the other.”

Wu characterized the findings as surprising. What they discovered, she said, bucked conventional wisdom about the way PTEN negative or PTEN null prostate cancer operates.

“Most of the hypotheses have suggested that PTEN regulates the function of the androgen receptor pathway, which is opposite of what we show here,” said Wu, who also is a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA. “We had thought that when PTEN was lost, it activated the androgen receptor pathway, driving cancer growth. What we’ve found suggests that if PTEN is lost in cancer cells, then the cancer cells become androgen receptor-independent and rely on the PI3K pathway for growth and survival.”

Wu’s study showed that PTEN loss suppresses AR signaling and that leads cancer cells to become less dependent on the androgen receptor for survival. This is important, Wu said, because it addresses a key mechanism of resistance. Certain prostate cancers may resist hormone therapy and if you withdraw androgen as treatment, it enhances the activity of the PI3K pathway, which then takes over driving cancer growth. Both pathways must be hit to stifle growth of the cancer.

The study has important implications for those prostate patients with late stage disease, who often become resistant to hormone ablation therapy, said David J. Mulholland, a postdoctoral fellow in Wu’s lab and first author of the study. Men who die of prostate cancer are those that become resistant to therapy and, as a consequence, their disease can spread or metastasize to other places, most often the bones.

“What we’ve shown here is a mechanism that could explain why anti-androgen therapy may fail in some patients,” Mulholland said. “Their cancer cells adapted to the low androgen receptor function and compensated by activating a survival pathway. It was a surprising result to show that these cells could continue to live without the androgen receptor signaling. Combining drugs that hit both pathways will be much more effective than using one drug alone.”

The study was modeled in a mouse model created by the Wu laboratory in which PTEN and AR are absent in the epithelium. The findings were replicated using samples from cancerous prostates removed from patients, work done in collaboration with researchers at UCLA and the Specialized Program of Research Excellence (SPORE) in prostate cancer.

“We found similar result in both cases,” Wu said. “The human cancers may behave the same way as the mouse models.”

There are new generations of AR inhibitors that are potentially more effective than their predecessors being tested now in clinical trials. There also are drugs being tested that inhibit the PI3K pathway, which is commonly activated in a variety of cancers. Clinical trials currently are being designed at UCLA that will combine these types of drugs to cut off both the primary path and escape routes that prostate cancers use to survive.

Prostate cancer is the most common malignancy in men. More than 217,000 American men will be diagnosed with the disease this year. Of those, more than 32,000 will die.

The five-year study was funded by the National Institutes of Health, the Department of Defense, the Prostate Cancer Foundation, the California Institute for Regenerative Medicine and Jean Perkins Foundation.

Source: University of California, Los Angeles (UCLA)

The American Urological Association (AUA) is pleased to announce its support for the Prostate Research, Outreach, Screening, Testing, Access and Treatment Effectiveness (PROSTATE) Act of 2011, H.R. 2159, introduced in the U.S. House of Representatives today by Representatives Edolphus Towns (D-NY-10) and Paul Broun, MD (R-GA-10). Companion legislation, S. 1190, was also introduced in the Senate today by Senators Jon Tester (D-MT) and Roy Blunt (R-MO). The AUA worked closely with lawmakers to assist in the development of this critical legislation, which was previously introduced in 2010.

Prostate cancer is the second-leading cause of cancer death in men. More than 217,000 men were diagnosed with prostate cancer in 2010, and more than 32,000 died from the disease. There are significant racial disparities in regard to prostate cancer: African American men are not only more likely to develop the disease, but are also more than twice as likely to die from it.

Significant national resources are focused on prostate cancer, but federal agencies should determine to what extent they can coordinate the numerous prostate cancer and healthcare programs, actively encourage the translation of research into practice and identify and implement best practices. The PROSTATE Act can help foster a more integrated and coordinated focus on effective prevention, diagnosis and treatment of this disease.

Specifics of this budget-neutral bill include:

– Establish an Interagency Prostate Cancer Coordination and Education Task Force composed of agencies from the U.S. Department of Health and Human Services (HHS) and the U.S. Department of Defense (DoD) and led by the U.S. Department of Veterans Affairs (VA), which will identify and catalog prostate cancer activities across these agencies; develop a strategy to improve the research portfolio; eliminate duplication between agencies; identify best practices; expand collaboration; increase patient and medical community participation; and develop a coordinated message related to awareness of and treatment for prostate cancer.

– Encourage the VA, DoD and HHS to coordinate and intensify prostate cancer research, including improvements or alternatives to the prostate-specific antigen (PSA) test and additional tests to distinguish indolent from aggressive disease; advance the understanding of the etiology of the disease; establish clinical registries for prostate cancer; and assess appropriate imaging modalities.

– Establish a grant program to build upon existing knowledge gained from comparative effectiveness research, and recognize and address the racial and ethnic disparities in the incidence and mortality rates of prostate cancer.

– Establish four-year telehealth pilot projects in a variety of geographic areas, including rural, that contain high proportions of medically underserved populations. Such projects will promote efficient use of specialist care through better coordination of primary care and physician extender teams in underserved areas and more effectively employ tumor boards to better counsel patients.

– Develop a coordinated national education campaign to align messages to the public concerning prostate cancer screening, diagnosis and cancer. The national campaign shall ensure materials are readily available in communities with racial disparities in the incidence and mortality of prostate cancer.

“We would like to thank Reps. Towns and Broun, as well as Sens. Tester and Blunt, for their leadership in introducing the PROSTATE Act and taking a stand to help combat prostate cancer,” said AUA President Sushil Lacy, MD. “This bill helps bring much-needed focus on the diagnosis, treatment and prevention of this common cancer affecting men today.”

The PROSTATE Act of 2011 was introduced in the House by Representatives Towns and Broun with the following original cosponsors: Andre Carson (D-IN-07), Marcia Fudge (D-OH-11), Jim Gerlach (R-PA-06), Steve Israel (D-NY-02), Eddie Bernice Johnson (D-TX-30), Peter King (R-NY-03), Barbara Lee (D-CA-09), Mike McIntyre (D-NC-07), Gwen Moore (D-WI-04), Eleanor Holmes Norton (D-DC), Charles Rangel (D-NY-15), Laura Richardson (D-CA-37), Frederica Wilson (D-FL-17) and Bennie Thompson (D-MS-02).

The bill was also introduced in the Senate by Senators Tester and Blunt, with Saxby Chambliss (R-GA), Jeff Sessions (R-AL) and Ron Wyden (D-OR) as cosponsors.

Source:

American Urological Association

Study Finding Could Result in Use of Combination Therapies to Fight Disease

Cancer is crafty. When one avenue driving its growth is blocked by drugs targeting that path, the malignancy often creates a detour, finding an alternative route to get around the roadblock.

In a study at UCLA’s Jonsson Comprehensive Cancer Center, researchers found that when a common type of prostate cancer was treated with conventional hormone ablation therapy blocking androgen production or androgen receptor (AR) function – which drives growth of the tumor – the cancer was able to adapt and compensate by activating a survival cell signaling pathway, effectively circumventing the roadblock put up by this treatment.

The findings could have important clinical implications as this type of prostate cancer, in which the PTEN tumor suppressor gene is inactivated, accounts for about 40 to 50 percent of primary prostate cancers and 70 to 90 percent of cancers that become resistant to hormone therapy, called castration resistant prostate cancers. Based on this study, these prostate cancers could be more effectively treated using a combination of drugs that target the AR cell signaling pathway and the compensating survival pathway, called the PI3K/AKT/mTOR pathway, said study senior author Dr. Hong Wu, a professor of molecular and medical pharmacology and a Jonsson Cancer Center researcher.

The study appears in the June 14, 2011 of the peer-reviewed journal Cancer Cell.

“The most significant take home message from this study is that certain prostate cancers can resist androgen deprivation therapy by activating an alternate pathway to drive its growth,” Wu said. “We found that these two pathways are talking to each other, almost like regulatory circuitry, and helping each other get around attempts to kill the cancer. When we suppress one of these pathways, it essentially feeds the other.”

Wu characterized the findings as surprising. What they discovered, she said, bucked conventional wisdom about the way PTEN negative or PTEN null prostate cancer operates.

“Most of the hypotheses have suggested that PTEN regulates the function of the androgen receptor pathway, which is opposite of what we show here,” said Wu, who also is a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA. “We had thought that when PTEN was lost, it activated the androgen receptor pathway, driving cancer growth. What we’ve found suggests that if PTEN is lost in cancer cells, then the cancer cells become androgen receptor-independent and rely on the PI3K pathway for growth and survival.”

Wu’s study showed that PTEN loss suppresses AR signaling and that leads cancer cells to become less dependent on the androgen receptor for survival. This is important, Wu said, because it addresses a key mechanism of resistance. Certain prostate cancers may resist hormone therapy and if you withdraw androgen as treatment, it enhances the activity of the PI3K pathway, which then takes over driving cancer growth. Both pathways must be hit to stifle growth of the cancer.

The study has important implications for those prostate patients with late stage disease, who often become resistant to hormone ablation therapy, said David J. Mulholland, a postdoctoral fellow in Wu’s lab and first author of the study. Men who die of prostate cancer are those that become resistant to therapy and, as a consequence, their disease can spread or metastasize to other places, most often the bones.

“What we’ve shown here is a mechanism that could explain why anti-androgen therapy may fail in some patients,” Mulholland said. “Their cancer cells adapted to the low androgen receptor function and compensated by activating a survival pathway. It was a surprising result to show that these cells could continue to live without the androgen receptor signaling. Combining drugs that hit both pathways will be much more effective than using one drug alone.”

The study was modeled in a mouse model created by the Wu laboratory in which PTEN and AR are absent in the epithelium. The findings were replicated using samples from cancerous prostates removed from patients, work done in collaboration with researchers at UCLA and the Specialized Program of Research Excellence (SPORE) in prostate cancer.

“We found similar result in both cases,” Wu said. “The human cancers may behave the same way as the mouse models.”

There are new generations of AR inhibitors that are potentially more effective than their predecessors being tested now in clinical trials. There also are drugs being tested that inhibit the PI3K pathway, which is commonly activated in a variety of cancers. Clinical trials currently are being designed at UCLA that will combine these types of drugs to cut off both the primary path and escape routes that prostate cancers use to survive.

Prostate cancer is the most common malignancy in men. More than 217,000 American men will be diagnosed with the disease this year. Of those, more than 32,000 will die.

The five-year study was funded by the National Institutes of Health, the Department of Defense, the Prostate Cancer Foundation, the California Institute for Regenerative Medicine and Jean Perkins Foundation. .

Source:
Kim Irwin
Director, Media Relations
UCLA’s Jonsson Comprehensive Cancer Center
Broad Stem Cell Research Center

Decision Resources, one of the world’s leading research and advisory firms for pharmaceutical and healthcare issues, finds that nearly half of surveyed urologists view the approval of Dendreon’s Provenge as a breakthrough in the treatment of prostate cancer, compared with 31 percent of surveyed oncologists. However, oncologists prescribe the agent more frequently than urologists. In 12 months, according to surveyed physicians’ estimates, only 15 percent of patients with asymptomatic or minimally symptomatic metastatic castrate-resistant prostate cancer (MCRPC) will receive Provenge, despite the views of many surveyed physicians that the launch of Provenge represents a breakthrough in the treatment of prostate cancer.

Following its approval last year by the U.S. Food and Drug Administration (FDA) for asymptomatic and minimally symptomatic MCRPC, Provenge became the first available therapeutic cancer vaccine in any oncology indication in a major pharmaceutical market.

In their selection of patients for treatment with Provenge, surveyed clinicians-who indicate that the agent’s high cost presents a major barrier to its wider use-prefer to treat younger or good performance status patients. Illustrating the fact that Provenge’s high cost is indeed a barrier to its uptake, surveyed physicians would treat a higher proportion (one quarter) of their patients if reimbursement were widely available. However, the findings also reveal that many treating physicians will still use docetaxel (Sanofi’s Taxotere, generics) as their preferred treatment option, even in asymptomatic or minimally symptomatic MCRPC patients.

The new U.S. Physician & Payer Forum report entitled U.S. Physician & Payer Perspectives on Provenge, the First Therapeutic Cancer Vaccine: The Proof is in the Prescribing finds that surveyed clinicians who have prescribed Provenge are much more likely than those who have not prescribed it to consider the drug a breakthrough. Additionally, physicians indicate they are highly motivated by the pursuit of biomarkers as 92 percent of surveyed oncologists say they would be more likely to use Provenge if they could predict which patients are most likely to benefit from treatment with the agent.

“The majority of surveyed clinicians express satisfaction with Provenge’s impact on overall survival, although only a small proportion indicate they are very satisfied,” said Decision Resources Senior Analyst Ramya Kollipara, Ph.D. “And although efficacy is the main driver of use, particularly for surveyed oncologists, about one-quarter of surveyed clinicians believe that the FDA should not have granted approval to Provenge based on its modest efficacy. Cost was stated as the most significant limiting factor amongst surveyed physicians.”

The report also finds that although Provenge is not covered by all surveyed managed care organizations (MCOs), it is covered by most MCOs, and coverage is expected to increase slightly by 2012. Among surveyed MCO pharmacy directors, 70 percent of the largest commercial plans and 75 percent of Medicare Advantage Plans include coverage of Provenge. The majority of surveyed MCO pharmacy directors whose plans exclude Provenge believe that the agent’s premium price per course of treatment is not justified by its improvement in MOS.

Source:

Decision Resources, Inc.

View drug information on Provenge; Taxotere.

University of Leeds researchers, funded by Cancer Research UK, have used a library of DNA to create a vaccine that could be used to treat cancer, according to a study published in Nature Medicine.

Before now, ‘gene therapy’ vaccines have often delivered just one gene to stimulate the immune system. It produces a protein, called an antigen, which activates the immune system to destroy cancer cells.

It has been difficult to develop successful cancer vaccines because each tumour has specific proteins and identifying the right antigens has been a huge challenge.

Scientists have also tried to boost the effectiveness of vaccines by using several genes to increase the chances of producing successful antigens. But a worry has always been that the immune system’s response would be too strong for the body to handle.

But now researchers, working with the Mayo Clinic in Rochester, US, have solved this problem in experiments involving mice.

The team used doses of a vaccine made from a virus which contained a ‘library’ of DNA, containing multiple fragments of genes and therefore many possible antigens. This approach did not send the immune system into overdrive, which had been a concern. Instead the range of DNA meant the vaccine was able to target the tumour through many routes.

Importantly, the DNA library was harvested from the same organ as the tumour. This meant that the immune system ‘self-selected’ the cancer antigens to respond to and did not react against other healthy parts of the body. Also, the process of self-selection was triggered when the vaccine was injected into the bloodstream, an approach to vaccination that is far more practical than injecting directly into tumours.

The researchers delivered a library of DNA taken from healthy prostate tissue in mice. When delivered in a virus, the vaccine successfully treated mice with prostate cancer.

University of Leeds’ Professor Alan Melcher, co-author of the study, said: “This is the first time we’ve been able to use a whole library of DNA in a viral vaccine successfully.

“The biggest challenge in immunology is developing antigens that can target the tumour without causing harm elsewhere.

“By using DNA from the same part of the body as the tumour, inserted into a virus, we may be able to solve that problem.”

The vaccine was made by putting the DNA library inside a vesicular stomatitis virus (VSV), which stimulates an immune response that can then track down and kill tumour cells.

Professor Peter Johnson, Cancer Research UK’s chief clinician, said: “This is an interesting and significant study which could really broaden out the field of immunotherapy research.

“Although the vaccine didn’t trigger the immune system to overreact and cause serious side effects in mice, it will need to be further developed and tested in humans before we can tell whether this technique could one day be used to treat cancer patients.”

Notes:

The study was funded by the US National Institutes of Health, Cancer Research UK, The Richard M. Schulze Family Foundation, Mayo Clinic, and a private grant.

The paper: Broad Antigenic Coverage Induced by Viral cDNA Library-based Vaccination Cures Established Tumors. Kottke et al. Nature Medicine. 19 June 2011. DOI 10.1038/nm.2390).

Source:
Paula Gould

University of Leeds

Mutations that cause Parkinson’s disease prevent cells from destroying defective mitochondria, according to a study published online May 10 in the Journal of Cell Biology.

Defects in the ubiquitin ligase Parkin are linked to early-onset cases of this neurodegenerative disorder. The wild-type protein promotes the removal of impaired mitochondria by a specialized version of the autophagy pathway called mitophagy, delivering mitochondria to the lysosomes for degradation. Mitochondria are often dysfunctional in Parkinson’s disease, but how Parkin stimulates mitophagy and whether the pathway goes wrong during pathogenesis is unknown.

A team of researchers led by Tso-Pang Yao (Duke University) found that cells expressing mutant forms of Parkin failed to clear their mitochondria after the organelles were damaged. Different mutations blocked mitophagy at distinct steps: mitochondria accumulated in the perinuclear region of cells expressing Parkin lacking its ubiquitin ligase activity, for example. The researchers found that ubiquitination of defective mitochondria by Parkin normally recruits the autophagy proteins HDAC6 and p62 to clear these mitochondrial aggregates.

Depolymerizing microtubules or inhibiting the dynein motor protein blocked aggregation and prevented mitochondrial turnover. Transport to the perinuclear region was also blocked by a mutation in Parkin, indicating that this stage of mitophagy is also regulated by the protein.

The clearance of defective mitochondria is therefore similar to the removal of damaged proteins, another autophagic process that goes wrong in Parkinson’s disease resulting in the accumulation of toxic protein aggregates. Both pathways rely on microtubules, HDAC6, and p62, says Yao, providing a common link between the two main features of the neurodegenerative disorder.

Source:
Rita Sullivan
Rockefeller University Press

Abbott announced that the U.S. Food and D

IsoRay Inc. (AMEX: ISR), announced today a new dual therapy study using Cesium-131 brachytherapy (internal radiation therapy) and external beam radiation. Multiple sites have now received Institutional Review Board (IRB) approval for this study which will examine the efficacy of combining intensity modulated radiation (IMRT) with Cesium-131 brachytherapy to treat intermediate and high risk early stage prostate cancer.

Published studies have suggested that the combination of brachytherapy and external beam radiation treatments demonstrate a significant benefit for those patients at risk of failure due to significant cancer that has spread outside the prostate. Cesium-131 has been so successful as a sole therapy for low and intermediate prostate cancers that many physicians are interested in its use in conjunction with other treatments like external beam radiation therapy for cases that are at high risk of failure.

The study is expected to demonstrate that the partnership of these two therapies will enhance treatment by lowering the required dosage of both applications resulting in improved outcomes for high risk cases and potentially lessening side effects normally associated with prostate cancer treatments. The study will also evaluate PSA response and its return to baseline or normal levels. PSA is a protein produced in the prostate. High levels of PSA typically indicate the presence of prostate cancer.

The two key primary investigators are Dr. John Sylvester, Lakewood Ranch Oncology Center in Florida, and Dr. Brian Moran, Director of the Chicago Prostate Center. Dr Sylvester, a nationally recognized expert who is one of the three clinicians who wrote the most recent ABS (American Brachytherapy Society) guidelines used by prostate cancer brachytherapists worldwide, says,” The Cesium-131 monotherapy trial we participated in has published* a 98% success rate in early stage cancer patients. We are excited about this new protocol for intermediate and high risk patients. We expect excellent cancer free survival rates and even less urinary side effects than past combination therapy protocols.”

Dr. Moran, also an author of the monotherapy study, is recognized nationwide as an expert on brachytherapy and prostate cancer. Dr. Moran has high expectations for the dual therapy study. “We have already seen exceptional results using Cesium-131 as a monotherapy. Given its importance in providing improved outcomes for patients, we expect this study will yield exciting results in a dual therapy setting,” he said.

One in six men will be diagnosed with prostate cancer during their lifetimes. It is the second leading cause of cancer deaths among American men claiming more than 30,000 lives annually. Only lung cancer claims the lives of more men each year.

IsoRay CEO Dwight Babcock says the study represents another important step forward. “Cesium-131 is already demonstrating its vital role in fighting early and intermediate stage prostate cancers. Cesium-131′s full potential in aggressively treating cancers throughout the body has yet to be realized. We expect this study will add to the growing body of evidence demonstrating Cesium-131′s vital role as an effective treatment with important quality of life benefits,” he explained.

IsoRay is the exclusive manufacturer of Cesium-131. The pioneering brachytherapy treatment represents one of the most important advancements in internal radiation therapy in 20 years. Cesium-131 allows for the internal radiation treatment of many different cancers because of its unique combination of high energy (its distinctive tissue penetrating capability reaching just far enough to treat the cancer) and its 9.7 day half-life (its matchless speed in giving off therapeutic radiation). The treatment can be deployed using several delivery methods including single seed applicators, implantable strands and mesh, and several new implantable devices. In addition to its CMS codes, Cesium-131 is FDA-cleared for the treatment of prostate, lung, ocular melanoma, brain, breast, colorectal, and head and neck cancer as other cancers throughout the body.

*Abstract published in Brachytherapy, Volume 10, Supplement 1, S27 – S28, 2011.

Source:

IsoRay