Solucion impotencia

Cancer Research UK scientists have discovered a molecular flag that predicts survival from prostate cancer at diagnosis, reveals a study published in the British Journal of Cancer.

The research led by pathologists based at the University of Liverpool measured the levels of a protein called heat shock protein27 (Hsp27) in prostate tissue samples taken from 553 men at the time they were diagnosed with prostate cancer. During a 15year followup, the research showed that those men who tested positive for Hsp27 at diagnosis were almost twice as likely to die from prostate cancer, than men who did not have the protein.

These findings suggest that Hsp27 could be used as a potential test to distinguish men with the aggressive forms of the cancer that need immediate treatment from men with slowgrowing forms of prostate cancer, and with which they can live with for many years. At the moment, there are no reliable tests to make this distinction.

Lead author, Professor Chris Foster, a Cancer Research UKfunded scientist at the University of Liverpools School of Cancer Studies, said “We have identified a link between the presence of Hsp27 at diagnosis and a lower survival rate for prostate cancer. Our study shows that this protein marker currently found in tissue samples can give us a reliable and accurate indication of whether individual cancers will become aggressive. Currently, we are working on developing this finding into a blood test to monitor men with prostate cancer in order to determine when their individual disease needs treatment.”

Hsp27 is a key component of signalling pathways that control the movement of cells around the body. The study also suggests that new drugs could be developed to block these signals and halt the spread of prostate cancer cells.

Professor Foster added “If further research shows that blocking these cell message systems is successful, it could provide a new treatment for aggressive forms of prostate cancer.”

Dr Lesley Walker, director of cancer information at Cancer Research UK, said “These results are an important step towards tackling the longstanding question of how to treat men with prostate cancer once it has been diagnosed. The need for treatment varies greatly between patients men with nonaggressive cancer can live with it for many years without needing therapy, while aggressive cancers require prompt treatment with combinations of surgery, radiotherapy and chemotherapy. But it is very difficult to distinguish who has which type of cancer.

“A marker molecule which identifies aggressive prostate cancer would help us target active treatment to patients who need it avoiding unnecessary therapy, which can have side effects, to those who dont.” She added “The next stage would be to test this protein in large clinical trials to decide if how useful it could be for diagnosis or treatment.”

Notes

*Hsp27 expression at diagnosis predicts poor clinical outcome in prostate cancer independent of ETSgene rearrangement. British Journal of Cancer. CS Foster et al.

Prostate Cancer

Prostate cancer is the most common cancer in men in the UK, with around 34,000 new cases diagnosed every year. Around 10,000 men die from the disease each year in the UK.

Higher selenium levels in the blood may worsen prostate cancer in some men who already have the disease, according to a study by researchers at DanaFarber Cancer Institute and the University of California, San Francisco.

A higher risk of moreaggressive prostate cancer was seen in men with a certain genetic variant found in about 75 percent of the prostate cancer patients in the study. In those subjects, having a high level of selenium in the blood was associated with a twofold greater risk of poorer outcomes than men with the lowest amounts of selenium. By contrast, the 25 percent of men with a different variant of the same gene and who had high selenium levels were at 40 percent lower risk of aggressive disease. The variants are slightly different forms of a gene that instructs cells to make manganese superoxide dismutase (SOD2), an enzyme that protects the body against harmful oxygen compounds.

The research findings suggest that “if you already have prostate cancer, it may be a bad thing to take selenium,” says Philip Kantoff, MD, director of DanaFarbers Lank Center for Genitourinary Oncology and senior author of the study that is published by the Journal of Clinical Oncology on its website now and later will be in a print journal. The lead author is June Chan, ScD, of the University of California, San Francisco.

The unexpected results are the first to raise concern about this potentially harmful consequence of taking supplemental selenium. Kantoff says, “These findings are interesting particularly in light of the recent negative results from the SELECT prevention study, which asked if selenium could protect against prostate cancer.”

The new study reveals the strong interaction between selenium and SOD2 to influence the biology of prostate cancer, a finding that these investigators had shown in a previous study. The authors say the current research demonstrated that variations in the make up of the SOD2 gene dramatically alter the effects of selenium on the risk of aggressive prostate cancer.

Selenium is a mineral found widely in rocks and dirt. Small amounts of selenium are essential for health 40 to 70 micrograms is the recommended daily intake. In recent years, supplemental selenium has been sold and promoted as a means of preventing prostate cancer, largely based on observational studies that found higher risk of prostate cancer incidence and mortality in areas of the country that are naturally low in selenium.

However, research aimed at confirming the benefits of selenium supplementation have been mixed. Recently, the SELECT study, which involved 35,000 men, was halted early when, after more than five years, it showed that the supplements didnt affect the incidence of prostate cancer.

Previous studies had found that the risk of developing prostate cancer was modified by a strong interaction between SOD2 and selenium. The new research was designed to look at the effect of this interaction on men already diagnosed with prostate cancer.

Scientists examined banked blood samples, DNA, and medical records of 489 male DanaFarber patients diagnosed between 1994 and 2001 with localized or locally advanced prostate cancer. Their mean age was 62, and their mean PSA (prostatespecific antigen) measurement was 6.0 ng/mL. About half the men were assessed as having a good disease risk, onethird had an intermediate risk, and the remaining onesixth were at poor risk. The researchers measured the level of selenium in the blood and, using the stored DNA, they determined the SOD2 genotype the specific form of the SOD2 gene carried by each patient.

Simply having a high level of selenium was associated with a slightly elevated risk of aggressive prostate cancer. But the risk was much more strongly affected by the interaction of selenium levels and whether the patient had a certain variant of the SOD2 gene. Men with the highest selenium levels and the “AA” form of the SOD2 gene were 40 percent less likely to have been diagnosed with aggressive prostate cancer than the men with same gene form but low levels of selenium.

But for men carrying the “V” form of the gene, selenium had the opposite effect. In these men, those with the highest levels of selenium in their blood were about twice as likely to have an aggressive type of prostate cancer as their counterparts with low selenium levels.

The study couldnt determine whether any of the men had been taking selenium supplements or not. But the researchers noted that men in the large SELECT prevention trial had a much higher average selenium level than those in the current study.

“Among the 25 percent of men with the AA genotype, having greater selenium levels may protect against aggressive disease,” the authors concluded. “However, for the 75 percent of men who carry a V allele, higher selenium levels might increase the likelihood of having worse characteristics.”

Therefore, they add, it is important to know which type of SOD2 gene a man has when considering the risks and potential benefits of taking selenium supplements. Additionally, the authors say the effects of the interaction between the SOD2 genotype and selenium may help explain apparently conflicting results of previous studies.

The results may seem counterintuitive to the public, who have been told for years that antioxidants can help people live longer, healthier lives with a lowered risk of cancer. However, Kantoff says, “There is some precedent to this research has suggested that antioxidants could be protective if you dont have cancer, but once you do, then antioxidants may be a bad thing.”

In addition to Kantoff and Chan, other authors of the paper include William Oh, MD, Wanling Xie, PhD, Meredith Regan, ScD, and Miyako Abe, PhD, of DanaFarber; Meir J. Stampfer DrPH, MD, of Brigham and Womens Hospital and the Harvard School of Public Health, and Irena King, PhD, of the Fred Hutchinson Cancer Research Center, Seattle.

The work was supported by grants from the National Cancer Institute and several foundations and charitable organizations.

DanaFarber Cancer Institute is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the DanaFarber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute.

FIRMAGON® (degarelix) a new fastacting hormone treatment for advanced prostate cancer is being offically launched in the UK yesterday at the British Association of Urological Surgeons Annual Meeting in Glasgow.

Prostate cancer is the most common cancer in men, and over 35,000 cases a year (1) are diagnosed in the UK , with 10,239 men dying in 2007.(2)

Prostate cancer is fuelled by the male hormone testosterone. The most widely used hormone treatments slow cancer cell growth by lowering production of testosterone in the testicles.

FIRMAGON® is given as a simple injection beneath the skin and acts in a unique way by forming a self gelling depot. It rapidly blocks hormone receptors in the pituitary gland, taking almost immediate effect. This is unlike existing hormone treatments which take up to four weeks to reduce testosterone to the required levels.(3)

Trials have shown that the new drug can reduce levels of the male hormone, testosterone, below 0.5ng/ml within three days in more than 96 per cent of patients (4). This makes FIRMAGON ® as effective as surgery to remove the testicles,

Mr John Anderson , consultant urological surgeon at the Royal Hallamshire Hospital says This is an important new step for the treatment of advanced hormonedependent prostate cancer, with FIRMAGON ® offering a new option and hope for many patients.Our goal is to achieve fast and sustained reduction in tesosterone levels and FIRMAGON® offers a rapid impact which is comparable to the immediacy achieved by surgery.

FIRMAGON® can also improve quality of life for patients by avoiding the initial surges in testosterone associated with the most common treatment currently used.Testosterone surges in some patients with advanced disease can cause tumours to grow rapidly resulting in increased pain, obstruction of the urethra and in severe cases paralysis due to spinal cord compression.(5, 6) Doctors currently prescribe antiandrogen therapy alongside hormone treatments to combat this, but this approach, means additional complication and is associated with the possibility of more side effects.

FIRMAGON ® doesnt cause these initial hormone surges (7) and so doctors dont have to prescribe antiandrogen therapy to conteract this, avoiding associated side effects and offering an effective monotherapy.

In clinical trials FIRMAGON® is generally welltolerated. The most common side effects in clinical trials were due to the expected physiological effects of testosterone suppression,(such as hot flushes and weight increase) or injection site pain or reddening .(8)

A new free DVD Progress for a Healthy Lifestyle A Guide for Men on Hormone Therapy for Prostate Cancer aimed at patients has been produced by Ferring Pharmaceuticals who hold the marketing authorisation for FIRMAGON®, in partnership with the British Urooncology Group and ProstateUK, to promote a holistic approach to living with prostate cancer. The DVD features information about hormone treatment but also gives advice on healthy lifestyle inlcuidng excercise and how to eat a prostatehealthy diet with recipes from celebrity chef Brian Turner. It also includes practical advice from top medical experts on how to cope with some of the issues of living with hormone therapy such as sex problems and hot flushes. It also features an interview with BBC radio DJ “Whispering” Bob Harris, who has received treatment for prostate cancer.

For more information about Firmagon®, prostate cancer, diet and exercise, please go to the Prostate UK website prostateuk.org/

References

(1) Incidence on prostate cancer in UK

(2) Statistics on deaths from prostate cancer in 2007

(3) 2007 Update of ASCO Practice Guideline for the Initial Hormonal Management of AndrogenSensitive Metastatic, Recurrent, or Progressive Prostate Cancer Guideline Summary

(4) BocconGibod L, Klotz L, Schroder FH et al. Degarelix compared to leuprolide depot 7.5mg in a 12 month randomised open lable parrallel group phase III study in prostate cancer patients.Abstract 537 presented at the 23rd EAU Congress, Milan, Italy 2008.

(5) Labrie F, Dupont A, Belanger A, et al Flutamide eliminates the risk of disease flare in prostatic cancer patients treated with a luteinizing hormonereleasing hormone agonist. J Urol 138804806, 1987.

(6) elRayes BF, Hussain MH Hormonal therapy for prostate cancer Past, present and future. Expert Rev Anticancer Ther 23747, 2002.

(7) Anderson J et al. Management of advanced prostate cancer, can we improve on androgen deprivation therapy/ BJU International 2008; 101 (12)14971501.

GPC Biotech AG (FRANKFURT GPC) (XETRA GPC) announced that data from the double blind, randomized satraplatin Phase 3 trial, the SPARC trial (Satraplatin and Prednisone Against Refractory Cancer), were presented at the 2009 American Society for Clinical Oncology (ASCO) Annual Meeting in Orlando, Florida. The SPARC trial evaluated satraplatin plus prednisone versus placebo plus prednisone in 950 patients with castraterefractory prostate cancer (CRPC) who had progressed after initial chemotherapy. The data presented are retrospective analyses of the SPARC trial evaluating correlations between overall survival (OS) and pain at baseline, pain progression, and progressionfree survival (PFS) at three months.

One presentation (”Use of pain at baseline and pain progression to predict overall survival in patients with docetaxel pretreated metastatic castrationrefractory prostate cancer results from the SPARC trial,” Sartor et al, Abstract #5148), analyzed the docetaxelpretreated population (n=488) in two separate ways

The first analysis compared OS in those patients who had no pain (Present Pain Intensity (PPI) score less than or equal to 1) vs. those with pain (PPI greater than or equal to 2) at time of entry to the trial.

The second analysis compared OS in those patients who experienced pain progression versus progression by prespecified measures other than pain (as judged by the blinded Independent Review Committee (IRC)).

Shorter OS time was observed in docetaxelpretreated patients who had pain at baseline compared to those who did not. The median survival of patients with baseline pain (n=178) was 44 weeks versus 72 weeks for patients without baseline pain (n=287) [stratified hazard ratio 0.59 (95% CI 0.480.74), stratified logrank p less than 0.0001]. The IRC found that 414 docetaxelpretreated patients (84.8%) progressed as of the data cutoff date for the SPARC study. Of these, the median survival of patients showing pain progression (n=196) was 47 weeks, compared to 71 weeks for nonpain progressors (n=292) [stratified hazard ratio 0.71 (95% CI 0.570.87), stratified logrank p=0.0022]. Thus, pain at baseline, as well as pain progression, were prognostic indicators of OS in the docetaxelpretreated patient population.

A second presentation (”Correlation of progressionfree survival and overall survival in men with metastatic castrationresistant prostate cancer who failed firstline chemotherapy results from the SPARC trial,” Halabi et al, Abstract #5150) evaluated whether PFS at three months was predictive of OS and explored the statistical dependencies between PFS and OS. Of the 853 men alive at three months postrandomization, 477 (56%) had already progressed. The median survival for this group was 34.5 weeks versus 78.7 weeks in men who had not progressed at the same three months timepoint. [hazard ratio 2.16 (95% CI=1.842.55), pvalue less than 0.001]. The dependence between PFS and OS was 0.29 (95% confidence limits=0.240.33, pvalue less than 0.00001). Thus PFS at three months was predictive of OS. Additional studies will be needed to assess the clinical relevance of the individual components of progression as defined in the SPARC trial to OS.

Data from other Phase I and Phase II clinical trials evaluating satraplatin in combination with other cancer therapeutic drugs were published in the 2009 ASCO Annual Meeting Proceedings
Phase II trial of bevacizumab and oral satraplatin and prednisone in docetaxel pretreated metastatic castrate resistant prostate cancer Vaishampayan et al (Abstract #e16028).
Dose finding study of the combination of satraplatin and gemcitabine in patients with advanced solid tumors Di Paola et al (Abstract #e13534).
A phase I study investigating the combination of orally bioavailable platinum and nonparticle albuminbound paclitaxel in advanced solid tumors Deshpande et al (Abstract #e13501).

About Satraplatin

Satraplatin, an investigational drug, is a member of the platinum family of compounds. Platinumbased drugs are a critical part of modern chemotherapy treatments and are used to treat a wide variety of cancers. All platinum drugs currently on the market require intravenous administration. Satraplatin is an oral compound that clinical trial patients are able to take at home. GPC Biotech has a license agreement with Yakult Honsha Co. Ltd. under which Yakult has exclusive commercialization rights to satraplatin for Japan. GPC Biotech is currently in discussions with Yakult regarding further development and registrational efforts for satraplatin. GPC Biotech inlicensed satraplatin from Spectrum Pharmaceuticals, Inc.

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