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Copyright © 2008-11 Prostate Cancer International, Inc.Funding for the DoD PCRP in FY 2012
Posted on June 16, 2011 by Sitemaster
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So here’s a quick status report on the potential funding for the US Department of Defense (DoD) Prostate Cancer Research Program (PCRP) for the fiscal year (FY) that begins on October 1, 2012 and runs through September 30, 2013.
As regular readers of this news blog may remember, funding for FY 2011 was renewed at the same level of $80 million as we had seen in the preceding few fiscal years. Congress has now initiated the process of looking at funding for the Department of Defense in FY 2012, and our current understanding is that there will be cuts to many of the Congressionally Directed Medical Research Program (CDMRP) initiatives, including the PCRP.
At this time, the House Appropriations Committee has proposed a 20 percent cut to the PCRP, which will mean a reduction in the total budget for PCRP from $80 million to $64 million for FY 2012. This is not good, but it could have been a lot worse. However, this is also just the first step in what may be a long process. We believe that the House of Representatives will vote on this bill some time next week. Hopefully, it will pass without any further fuss, but then we will have to wait and see what the Senate decides to do, and that could take a while.
For new readers, the PCRP is the largest single source of US government funding specifically dedicated to prostate cancer research. At its height, in FY 2001, a total of $100 million was dedicated to this initiative. Securing continuing funding for the PCRP is a critical priority for the Prostate Cancer Roundtable here in the USA. As a group, under the current economic circumstances, it is probably safe to say that the Roundtable members would be willing to live with a 20 percent budget cut of this type — even if we don’t like it! However, …
Friday, June 17, 2011
Tuesday, June 14, 2011
Two-Tiered Prostate Cancer Surveillance
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OncologyStat®One Source, Many Resources.® By Elsevier
News
Two-Tiered Prostate Cancer Surveillance Could Curb Overtreatment
Two-Tiered Prostate Cancer Surveillance Could Curb Overtreatment
J Smith
20110418
2011 May 18
Elsevier Global Medical News
Find more items about these cancer types:
ProstateTwo-Tiered Prostate Cancer Surveillance Could Curb Overtreatment
Elsevier Global Medical News. 2011 May 18, J Smith
A two-tiered system of surveillance could reduce prostate cancer deaths by half while also curbing overdiagnosis and overtreatment, according to results from a large Swedish study.
The system would allow men who test for high levels of prostate-specific antigen (more than 1.6 ng/mL) in their 40s to undergo close surveillance as they age, while the rest - approximately half of all men - would need to be tested only three times between the ages of 44 and 60 years.
The findings, released May 18 and highlighted during a press briefing at which the American Society of Clinical Oncology offered a preview of studies to be presented at its annual meeting in June, could help lead to a more "rational" screening strategy, according to the study's investigators.
While there is evidence that PSA screening can detect prostate cancer at an early, curable stage, it is viewed as problematic because of the risk of overtreatment. PSA levels are not necessarily indicative of present cancer, and a large number of men must be screened to prevent a single death.
The investigators, led by Dr. Hans Lilja of Memorial Sloan-Kettering Cancer Center in New York, conducted a case-control study nested within a cohort of 12,090 Swedish men who provided blood between 1974 and 1986. A total of 4,999 provided repeat samples 6 years later. The investigators also looked at an independent cohort of 1,167 men who provided blood at age 60 years. Men with evidence of prostate cancer metastasis or death (n = 252) were matched 3:1 with controls.
The study found that 44% of prostate cancer deaths occurred in men who had the top 10% of PSA levels (greater than 1.6 ng/mL) for their age group when they were tested for the first time between the ages of 44 and 50 years.
Men whose PSA levels remained below the median for the population in their age group saw a progressively declining rate of death or metastasis.
The investigators found that 28% of metastases or deaths from prostate cancer over the next 27 years occurred in men aged 44-50 years whose initial screens showed a PSA below the median in the population (0.7 ng/mL).
For men aged 51-55 years with a PSA lower than the median (0.8 ng/mL), the risk of metastatic prostate cancer or death was 18% over 27 years. At age 60 years, only 0.5% of deaths or metastases occurred in men with a PSA less than the median for that age (1.1 ng/mL).
The findings show that PSA levels at the time of initial screening among men aged 44-50 years can accurately predict the risk of death from prostate cancer or metastatic prostate cancer up to 30 years later. Concentrating surveillance in this group of men could allow the rest to undergo only three lifetime tests at the ages of 44, 51-55, and 60 years, the investigators concluded.
Dr. Lilja disclosed owning stock in Arctic Partners, a firm that holds patents for PSA assays.
Copyright © 2010 International Medical News Group
null
OncologyStat®One Source, Many Resources.® By Elsevier
News
Two-Tiered Prostate Cancer Surveillance Could Curb Overtreatment
Two-Tiered Prostate Cancer Surveillance Could Curb Overtreatment
J Smith
20110418
2011 May 18
Elsevier Global Medical News
Find more items about these cancer types:
ProstateTwo-Tiered Prostate Cancer Surveillance Could Curb Overtreatment
Elsevier Global Medical News. 2011 May 18, J Smith
A two-tiered system of surveillance could reduce prostate cancer deaths by half while also curbing overdiagnosis and overtreatment, according to results from a large Swedish study.
The system would allow men who test for high levels of prostate-specific antigen (more than 1.6 ng/mL) in their 40s to undergo close surveillance as they age, while the rest - approximately half of all men - would need to be tested only three times between the ages of 44 and 60 years.
The findings, released May 18 and highlighted during a press briefing at which the American Society of Clinical Oncology offered a preview of studies to be presented at its annual meeting in June, could help lead to a more "rational" screening strategy, according to the study's investigators.
While there is evidence that PSA screening can detect prostate cancer at an early, curable stage, it is viewed as problematic because of the risk of overtreatment. PSA levels are not necessarily indicative of present cancer, and a large number of men must be screened to prevent a single death.
The investigators, led by Dr. Hans Lilja of Memorial Sloan-Kettering Cancer Center in New York, conducted a case-control study nested within a cohort of 12,090 Swedish men who provided blood between 1974 and 1986. A total of 4,999 provided repeat samples 6 years later. The investigators also looked at an independent cohort of 1,167 men who provided blood at age 60 years. Men with evidence of prostate cancer metastasis or death (n = 252) were matched 3:1 with controls.
The study found that 44% of prostate cancer deaths occurred in men who had the top 10% of PSA levels (greater than 1.6 ng/mL) for their age group when they were tested for the first time between the ages of 44 and 50 years.
Men whose PSA levels remained below the median for the population in their age group saw a progressively declining rate of death or metastasis.
The investigators found that 28% of metastases or deaths from prostate cancer over the next 27 years occurred in men aged 44-50 years whose initial screens showed a PSA below the median in the population (0.7 ng/mL).
For men aged 51-55 years with a PSA lower than the median (0.8 ng/mL), the risk of metastatic prostate cancer or death was 18% over 27 years. At age 60 years, only 0.5% of deaths or metastases occurred in men with a PSA less than the median for that age (1.1 ng/mL).
The findings show that PSA levels at the time of initial screening among men aged 44-50 years can accurately predict the risk of death from prostate cancer or metastatic prostate cancer up to 30 years later. Concentrating surveillance in this group of men could allow the rest to undergo only three lifetime tests at the ages of 44, 51-55, and 60 years, the investigators concluded.
Dr. Lilja disclosed owning stock in Arctic Partners, a firm that holds patents for PSA assays.
Copyright © 2010 International Medical News Group
Abiraterone ProlongsOverall Survival
Abiraterone Prolongs Survival in Metastatic Castration-Resistant Prostate Cancer
Elsevier Global Medical News. 2011 May 25, MA Moon
Abiraterone acetate, a selective inhibitor of androgen biosynthesis, prolonged overall survival, reduced mortality risk by 35%, and delayed time to disease progression in men with metastatic castration-resistant prostate cancer who had already undergone chemotherapy, according to a report in the May 26 issue of the New England Journal of Medicine.
"The use of hormonal agents is typically not considered in patients who have received chemotherapy. These results show that continued androgen-receptor signaling contributes to disease progression, and they provide support for the evaluation of other endocrine therapies in this [advanced] stage of the disease," wrote Dr. Johann S. de Bono of the Institute of Cancer Research and Royal Marsden Hospital, Sutton (England), and his associates.
Several previous studies have demonstrated that, despite medical or surgical castration, prostate cancers continue to have sufficient levels of androgens, perhaps from synthesis within the tumor itself, to propel tumor growth. In phase I and phase II trials, abiraterone acetate - which potently blocks cytochrome P450 c17 (CYP17), an enzyme critical to testosterone synthesis - has shown promising antitumor activity even in advanced prostate cancer.
Dr. de Bono and his colleagues performed this international phase III randomized double-blind trial at 147 sites to compare daily oral therapy with four 250-mg abiraterone acetate tablets plus low-dose prednisone against placebo plus low-dose prednisone. They enrolled 1,195 men who had previously received docetaxel and showed disease progression despite ongoing androgen deprivation.
The primary end point of the study was overall survival.
At a preplanned interim analysis, active treatment was found to reduce the risk of death by 35%, compared with placebo. Mortality was 42% with active treatment, compared with 55% with placebo. Median overall survival was 14.8 months with abiraterone, compared with 10.9 months with placebo, the investigators reported (N. Engl J. Med. 2011;364:1995-2005).
This survival benefit "was consistent across all subgroups, and ... robust after adjustment for stratification factors in a multivariate analysis," they said.
Based on these findings, the trial was unblinded and patients in the placebo group were allowed to switch to active treatment.
"All the secondary end points analyzed provided support for the superiority of abiraterone acetate over placebo," Dr. de Bono and his associates said. Treatment response was greater with abiraterone whether measured by PSA levels (29% response vs. 6%) or Response Evaluation Criteria in Solid Tumors (RECIST) criteria (14% vs. 3%). Time to PSA progression was longer (10.2 months vs. 6.6 months), as was median progression-free survival on radiography (5.6 vs. 3.6 months).
Active treatment reduced the risk of disease progression by 42% when assessed by PSA levels and by 33% when assessed by radiographic imaging.
Exploratory end points, including pain palliation and time to 25% of patients having a skeletal event, also consistently favored abiraterone over placebo.
"This study validates the hypothesis that the biosyntehsis of steroid hormones downstream of CYP17 contributes to progression of castration-resistant prostate cancer in a subgroup of men for whom this disease remains driven by steroid ligands and should not be described as 'hormone refractory.' Since these men cannot be identified a priori, continuing to call this disease 'androgen independent' or 'hormone refractory' is imprecise," Dr. de Bono and his associates said.
"As our study shows, blocking androgen synthesis by inhibiting CYP17 can produce tumor responses in patients who no longer have a response to standard hormonal therapies and who had received docetaxel-based chemotherapy," they added.
Compliance with abiraterone acetate therapy was high, "and side effects were easily manageable and reversible, despite the advanced age and level of frailty of the study population," the investigators said.
Toxic effects included hypokalemia, hypertension, and fluid retention, "which were largely abrogated by the use of low-dose prednisone," they wrote.
The rates of drug discontinuation and dose reduction were low, and therapy "did not appear to increase the risk of metabolic changes or symptoms associated with chronic androgen deprivation. Nevertheless, longer follow-up is warranted to evaluate late toxic effects," they noted.
In editorial accompanying the study, Dr. Emmanuel S. Antonarakis and Dr. Mario A. Eisenberger wrote that the findings "provide a proof of principle that metastatic castration-resistant prostate cancer remains androgen-driven" (N. Engl. J. Med. 2011;364:2055-8).
The results of this phase III trial led to Food and Drug Administration approval of abiraterone [Zytiga] in late April for patients who had received docetaxel, but they also "provide sufficient evidence of efficacy to justify the use of abiraterone in all patients with metastatic castration-resistant prostate cancer (i.e., even those with no previous chemotherapy treatment)," said Dr. Antonarakis and Dr. Eisenberger, who are with the Johns Hopkins Sidney Kimmel Comprehensive Cancer Center, Baltimore.
Moreover, "it is clear ... that our knowledge of the biologic mechanisms involved in the progression of metastatic castration-resistant prostate cancer has reached a level at which the discovery of more effective targeted approaches will probably further improve outcomes," they added.
Johns Hopkins receives funding from Cougar Biotechnology and participated in this clinical trial, but Dr. Antonarakis and Dr. Eisenberger were not involved. They reported ties to Sanofi-Aventis, Millennium, Astellas, and Tokai.
This study was sponsored by Ortho Biotech Oncology Research and Development, a unit of Cougar Biotechnology, with further support provided by the Medical Research Council of the United Kingdom, the Experimental Cancer Medical Centre, the National Institute for Health Research Biomedical Research Centre, and the Prostate Cancer Foundation. Dr. de Bono is employed by the Institute of Cancer Research, where abiraterone was designed and synthesized, and which has a commercial interest in the drug. He and his associates reported ties to numerous drug and biotechnology companies.
Elsevier Global Medical News. 2011 May 25, MA Moon
Abiraterone acetate, a selective inhibitor of androgen biosynthesis, prolonged overall survival, reduced mortality risk by 35%, and delayed time to disease progression in men with metastatic castration-resistant prostate cancer who had already undergone chemotherapy, according to a report in the May 26 issue of the New England Journal of Medicine.
"The use of hormonal agents is typically not considered in patients who have received chemotherapy. These results show that continued androgen-receptor signaling contributes to disease progression, and they provide support for the evaluation of other endocrine therapies in this [advanced] stage of the disease," wrote Dr. Johann S. de Bono of the Institute of Cancer Research and Royal Marsden Hospital, Sutton (England), and his associates.
Several previous studies have demonstrated that, despite medical or surgical castration, prostate cancers continue to have sufficient levels of androgens, perhaps from synthesis within the tumor itself, to propel tumor growth. In phase I and phase II trials, abiraterone acetate - which potently blocks cytochrome P450 c17 (CYP17), an enzyme critical to testosterone synthesis - has shown promising antitumor activity even in advanced prostate cancer.
Dr. de Bono and his colleagues performed this international phase III randomized double-blind trial at 147 sites to compare daily oral therapy with four 250-mg abiraterone acetate tablets plus low-dose prednisone against placebo plus low-dose prednisone. They enrolled 1,195 men who had previously received docetaxel and showed disease progression despite ongoing androgen deprivation.
The primary end point of the study was overall survival.
At a preplanned interim analysis, active treatment was found to reduce the risk of death by 35%, compared with placebo. Mortality was 42% with active treatment, compared with 55% with placebo. Median overall survival was 14.8 months with abiraterone, compared with 10.9 months with placebo, the investigators reported (N. Engl J. Med. 2011;364:1995-2005).
This survival benefit "was consistent across all subgroups, and ... robust after adjustment for stratification factors in a multivariate analysis," they said.
Based on these findings, the trial was unblinded and patients in the placebo group were allowed to switch to active treatment.
"All the secondary end points analyzed provided support for the superiority of abiraterone acetate over placebo," Dr. de Bono and his associates said. Treatment response was greater with abiraterone whether measured by PSA levels (29% response vs. 6%) or Response Evaluation Criteria in Solid Tumors (RECIST) criteria (14% vs. 3%). Time to PSA progression was longer (10.2 months vs. 6.6 months), as was median progression-free survival on radiography (5.6 vs. 3.6 months).
Active treatment reduced the risk of disease progression by 42% when assessed by PSA levels and by 33% when assessed by radiographic imaging.
Exploratory end points, including pain palliation and time to 25% of patients having a skeletal event, also consistently favored abiraterone over placebo.
"This study validates the hypothesis that the biosyntehsis of steroid hormones downstream of CYP17 contributes to progression of castration-resistant prostate cancer in a subgroup of men for whom this disease remains driven by steroid ligands and should not be described as 'hormone refractory.' Since these men cannot be identified a priori, continuing to call this disease 'androgen independent' or 'hormone refractory' is imprecise," Dr. de Bono and his associates said.
"As our study shows, blocking androgen synthesis by inhibiting CYP17 can produce tumor responses in patients who no longer have a response to standard hormonal therapies and who had received docetaxel-based chemotherapy," they added.
Compliance with abiraterone acetate therapy was high, "and side effects were easily manageable and reversible, despite the advanced age and level of frailty of the study population," the investigators said.
Toxic effects included hypokalemia, hypertension, and fluid retention, "which were largely abrogated by the use of low-dose prednisone," they wrote.
The rates of drug discontinuation and dose reduction were low, and therapy "did not appear to increase the risk of metabolic changes or symptoms associated with chronic androgen deprivation. Nevertheless, longer follow-up is warranted to evaluate late toxic effects," they noted.
In editorial accompanying the study, Dr. Emmanuel S. Antonarakis and Dr. Mario A. Eisenberger wrote that the findings "provide a proof of principle that metastatic castration-resistant prostate cancer remains androgen-driven" (N. Engl. J. Med. 2011;364:2055-8).
The results of this phase III trial led to Food and Drug Administration approval of abiraterone [Zytiga] in late April for patients who had received docetaxel, but they also "provide sufficient evidence of efficacy to justify the use of abiraterone in all patients with metastatic castration-resistant prostate cancer (i.e., even those with no previous chemotherapy treatment)," said Dr. Antonarakis and Dr. Eisenberger, who are with the Johns Hopkins Sidney Kimmel Comprehensive Cancer Center, Baltimore.
Moreover, "it is clear ... that our knowledge of the biologic mechanisms involved in the progression of metastatic castration-resistant prostate cancer has reached a level at which the discovery of more effective targeted approaches will probably further improve outcomes," they added.
Johns Hopkins receives funding from Cougar Biotechnology and participated in this clinical trial, but Dr. Antonarakis and Dr. Eisenberger were not involved. They reported ties to Sanofi-Aventis, Millennium, Astellas, and Tokai.
This study was sponsored by Ortho Biotech Oncology Research and Development, a unit of Cougar Biotechnology, with further support provided by the Medical Research Council of the United Kingdom, the Experimental Cancer Medical Centre, the National Institute for Health Research Biomedical Research Centre, and the Prostate Cancer Foundation. Dr. de Bono is employed by the Institute of Cancer Research, where abiraterone was designed and synthesized, and which has a commercial interest in the drug. He and his associates reported ties to numerous drug and biotechnology companies.
Sunday, June 12, 2011
Finasteride & Dutasteride Raise Risk Of Hi-Gr PCa
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Finasteride And Dutasteride Raise Risk Of High-Grade Prostate Cancer, FDA Informs
Editor's Choice
Main Category: Prostate / Prostate Cancer
Also Included In: Urology / Nephrology; Regulatory Affairs / Drug Approvals
Article Date: 10 Jun 2011 - 7:00 PDT
email to a friend printer friendly opinions
Current Article Ratings:
Patient / Public: 4.6 (5 votes)
Healthcare Prof: 4.4 (5 votes)
Article Opinions: 1 posts
Although finasteride and dutasteride lower overall risk of developing prostate cancer, they raise the chances of developing high-grade prostate cancer, a more serious form of the disease, the FDA (Food and Drug Administration) has announced. The Agency adds that the risk is low; but doctors need to be aware of this.
The FDA announced that all 5-alpha reductase inhibitor (5-ARI) medications will now have new safety information about the risk of developing high-grade prostate in their labeling, in the Warnings and Precautions section.
Examples of 5-ARI class medications include finasteride (Proscar, Propecia), dutasteride (Avodart), turosteride, bexlosteride and izonsteride. They are drugs with antiandrogenic activity and are used to treat benign prostatic hyperplasia (prostate gland enlargement) and androgenic alopecia (hair loss, baldness).
The FDA evaluated two randomized controlled trials - PCPT (the Prostate Cancer Prevention Trial), which compared finasteride 5mg against placebo for 7 years, and REDUCE (Reduction by Dutasteride of Prostate Cancer Events trial), which compared dutasteride 0.5 mg against placebo for 4 years. Both trials were measuring prostate cancer risk reduction in males aged 50+ years.
Even though both studies demonstrated an overall reduction in prostate cancer risk with both drugs, they also showed a higher risk of high-grade prostate cancer.
High-grade prostate cancer (Gleason score between 8 and 10) is the most deadly form of prostate cancer. It is an aggressive cancer which grows and spreads into surrounding areas rapidly. The cancer cells are large, very difficult to treat, and frequently reappear.
The FDA stresses that patients should talk to their doctors first before deciding on whether to change or stop any prescription medication.
Finasteride is marketed by Merck. Dutasteride is marketed by GlaxoSmithKline.
Written by Christian Nordqvist
View drug information on dutasteride; Propecia; Proscar.
Copyright: Medical News Today
Finasteride And Dutasteride Raise Risk Of High-Grade Prostate Cancer, FDA Informs
Editor's Choice
Main Category: Prostate / Prostate Cancer
Also Included In: Urology / Nephrology; Regulatory Affairs / Drug Approvals
Article Date: 10 Jun 2011 - 7:00 PDT
email to a friend printer friendly opinions
Current Article Ratings:
Patient / Public: 4.6 (5 votes)
Healthcare Prof: 4.4 (5 votes)
Article Opinions: 1 posts
Although finasteride and dutasteride lower overall risk of developing prostate cancer, they raise the chances of developing high-grade prostate cancer, a more serious form of the disease, the FDA (Food and Drug Administration) has announced. The Agency adds that the risk is low; but doctors need to be aware of this.
The FDA announced that all 5-alpha reductase inhibitor (5-ARI) medications will now have new safety information about the risk of developing high-grade prostate in their labeling, in the Warnings and Precautions section.
Examples of 5-ARI class medications include finasteride (Proscar, Propecia), dutasteride (Avodart), turosteride, bexlosteride and izonsteride. They are drugs with antiandrogenic activity and are used to treat benign prostatic hyperplasia (prostate gland enlargement) and androgenic alopecia (hair loss, baldness).
The FDA evaluated two randomized controlled trials - PCPT (the Prostate Cancer Prevention Trial), which compared finasteride 5mg against placebo for 7 years, and REDUCE (Reduction by Dutasteride of Prostate Cancer Events trial), which compared dutasteride 0.5 mg against placebo for 4 years. Both trials were measuring prostate cancer risk reduction in males aged 50+ years.
Even though both studies demonstrated an overall reduction in prostate cancer risk with both drugs, they also showed a higher risk of high-grade prostate cancer.
High-grade prostate cancer (Gleason score between 8 and 10) is the most deadly form of prostate cancer. It is an aggressive cancer which grows and spreads into surrounding areas rapidly. The cancer cells are large, very difficult to treat, and frequently reappear.
The FDA stresses that patients should talk to their doctors first before deciding on whether to change or stop any prescription medication.
Finasteride is marketed by Merck. Dutasteride is marketed by GlaxoSmithKline.
Written by Christian Nordqvist
View drug information on dutasteride; Propecia; Proscar.
Copyright: Medical News Today
Friday, June 10, 2011
Androgen Ablation &Bone Metastasis
Androgen Ablation
Androgen deprivation therapy (ADT) is commonly used in the treatment of prostate cancer.53 Survival in men with nonmetastatic prostate cancer treated with ADT is long, with a median survival of greater than 7 years.54 Hence, long-term effects on bones are of particular concern. At least one study has also suggested skeletal fractures as an adverse predictor of overall survival in men with prostate cancer.55
Even at baseline, men with prostate cancer who have not received ADT have a higher incidence of osteoporosis than the general age-matched population.56 Effects of hormone treatment most likely compound the problem.21
A Danish case-control registry study compared more than 15,000 men aged older than 50 years who had fractures with 45,000 men who did not. The authors found that a diagnosis of prostate cancer was associated with an increased odds ratio (OR) for fracture of 1.8 (95% CI, 1.6-2.1) and ADT was associated with an increased OR of 1.7 (95% CI, 1.2-2.5). It was noted that the increased risk became apparent soon after diagnosis and persisted even in long-term survivors.57
Retrospective cohort studies of men who have survived prostate cancer for many years have demonstrated that ADT therapy is associated with an increase in fracture risk (Table 2).58-65 Shahinian et al performed a Surveillance, Epidemiology, and End Results (SEER) database study of 50,613 men who were diagnosed with prostate cancer between 1992 and 1997. Five years after starting treatment, 19.4% of survivors who received ADT developed a fracture at any site, whereas only 12.6% of survivors not receiving ADT developed a fracture.58 Dickman et al studied almost 18,000 men who were treated for prostate cancer with bilateral orchiectomy, and compared their fracture risk with that of approximately 360,000 healthy controls. The authors found that those who had undergone orchiectomy had a fracture risk over 10 years of 12% at the femoral neck alone, compared with 5% in the general population.60 Smith et al conducted a claims-based retrospective cohort study of 3887 men with nonmetastatic prostate cancer receiving GnRH agonists compared with 7774 who did not receive these agents. GnRH agonists were associated with an increased clinical fracture risk (7.88 clinical fractures per 100 person-years in the GnRH group vs 6.51 per 100 person-years in controls; relative risk [RR], 1.21; 95% CI, 1.14-1.29 [P < .001]).59 However, these studies are limited in that fractures were not designated as osteoporotic versus pathologic, and no relation with BMD was performed.
Androgen deprivation therapy (ADT) is commonly used in the treatment of prostate cancer.53 Survival in men with nonmetastatic prostate cancer treated with ADT is long, with a median survival of greater than 7 years.54 Hence, long-term effects on bones are of particular concern. At least one study has also suggested skeletal fractures as an adverse predictor of overall survival in men with prostate cancer.55
Even at baseline, men with prostate cancer who have not received ADT have a higher incidence of osteoporosis than the general age-matched population.56 Effects of hormone treatment most likely compound the problem.21
A Danish case-control registry study compared more than 15,000 men aged older than 50 years who had fractures with 45,000 men who did not. The authors found that a diagnosis of prostate cancer was associated with an increased odds ratio (OR) for fracture of 1.8 (95% CI, 1.6-2.1) and ADT was associated with an increased OR of 1.7 (95% CI, 1.2-2.5). It was noted that the increased risk became apparent soon after diagnosis and persisted even in long-term survivors.57
Retrospective cohort studies of men who have survived prostate cancer for many years have demonstrated that ADT therapy is associated with an increase in fracture risk (Table 2).58-65 Shahinian et al performed a Surveillance, Epidemiology, and End Results (SEER) database study of 50,613 men who were diagnosed with prostate cancer between 1992 and 1997. Five years after starting treatment, 19.4% of survivors who received ADT developed a fracture at any site, whereas only 12.6% of survivors not receiving ADT developed a fracture.58 Dickman et al studied almost 18,000 men who were treated for prostate cancer with bilateral orchiectomy, and compared their fracture risk with that of approximately 360,000 healthy controls. The authors found that those who had undergone orchiectomy had a fracture risk over 10 years of 12% at the femoral neck alone, compared with 5% in the general population.60 Smith et al conducted a claims-based retrospective cohort study of 3887 men with nonmetastatic prostate cancer receiving GnRH agonists compared with 7774 who did not receive these agents. GnRH agonists were associated with an increased clinical fracture risk (7.88 clinical fractures per 100 person-years in the GnRH group vs 6.51 per 100 person-years in controls; relative risk [RR], 1.21; 95% CI, 1.14-1.29 [P < .001]).59 However, these studies are limited in that fractures were not designated as osteoporotic versus pathologic, and no relation with BMD was performed.
Tuesday, May 31, 2011
NCCN Annual Report
Support NCCN About NCCN
More Oncology Drug Shortages
By Edward C. Li, PharmD, BCOP, Drugs and Biologics Editor
Recent news is plentiful with stories about how local hospitals and physician practices are struggling to provide their patients with drugs they critically need in today’s climate of drug shortages. In a previous eBulletin article, we described some ways to cope with the ever-expanding list of drugs that are in short supply. According to the FDA Drug Shortages website, three additional drugs (daunorubicin, thiotepa, and vincristine) have been added to the list of injectable drugs that are in short supply and used for the active treatment of cancer since that article was written. The shortage resolved for one drug previously on the list, which is carmustine. The list of oncology drugs currently experiencing a shortage stands as follows:
Bleomycin
Cisplatin
Cytarabine
Daunorubicin
Doxorubicin
Etoposide
Leucovorin/levoleucovorin
Mechlorethamine
Thiotepa
Vincristine.
As you can see, many of the drugs on this list are critical pieces of well-established chemotherapy regimens. In the short term, the US Food and Drug Administration (FDA) has some ability to help resolve some shortages. However, this ability is somewhat limited, especially if the cause of the shortage is due to circumstances beyond their control. Nonetheless, the FDA may be able to expedite the review of submissions by manufactures for a new product or manufacturing change that, if approved, may help to increase the supply of the drug that is currently experiencing a shortage. Additionally, the FDA works with manufacturers to identify sources of raw material or encourage others to increase production of the drug. Lastly, the FDA can utilize enforcement discretion to temporarily allow the importation of a drug from other countries, although the FDA has maintained that this practice is rare.1 Interestingly, it appears that the FDA is considering allowing the importation of certain oncology products (e.g., cytarabine, thiotepa).2, 3
Recently, legislation that may offer some long-term relief to this crisis was introduced to Congress. The “Preserving Access to Life Saving Medications Act (S. 296)” proposes to establish an early warning system so that manufacturers must report to the US Food and Drug Administration (FDA) on conditions that would likely result in a drug shortage. It also would provide the FDA with the power to impose financial penalties for manufacturers who fail to comply with this reporting.
As more drugs are added to the list of those in short supply, there is growing concern among the public regarding how patients are affected by these shortages. Hopefully, the actions of the FDA and Congress will relieve some of these problems and we will again see an adequate supply of these important medications.
Support NCCN About NCCN
More Oncology Drug Shortages
By Edward C. Li, PharmD, BCOP, Drugs and Biologics Editor
Recent news is plentiful with stories about how local hospitals and physician practices are struggling to provide their patients with drugs they critically need in today’s climate of drug shortages. In a previous eBulletin article, we described some ways to cope with the ever-expanding list of drugs that are in short supply. According to the FDA Drug Shortages website, three additional drugs (daunorubicin, thiotepa, and vincristine) have been added to the list of injectable drugs that are in short supply and used for the active treatment of cancer since that article was written. The shortage resolved for one drug previously on the list, which is carmustine. The list of oncology drugs currently experiencing a shortage stands as follows:
Bleomycin
Cisplatin
Cytarabine
Daunorubicin
Doxorubicin
Etoposide
Leucovorin/levoleucovorin
Mechlorethamine
Thiotepa
Vincristine.
As you can see, many of the drugs on this list are critical pieces of well-established chemotherapy regimens. In the short term, the US Food and Drug Administration (FDA) has some ability to help resolve some shortages. However, this ability is somewhat limited, especially if the cause of the shortage is due to circumstances beyond their control. Nonetheless, the FDA may be able to expedite the review of submissions by manufactures for a new product or manufacturing change that, if approved, may help to increase the supply of the drug that is currently experiencing a shortage. Additionally, the FDA works with manufacturers to identify sources of raw material or encourage others to increase production of the drug. Lastly, the FDA can utilize enforcement discretion to temporarily allow the importation of a drug from other countries, although the FDA has maintained that this practice is rare.1 Interestingly, it appears that the FDA is considering allowing the importation of certain oncology products (e.g., cytarabine, thiotepa).2, 3
Recently, legislation that may offer some long-term relief to this crisis was introduced to Congress. The “Preserving Access to Life Saving Medications Act (S. 296)” proposes to establish an early warning system so that manufacturers must report to the US Food and Drug Administration (FDA) on conditions that would likely result in a drug shortage. It also would provide the FDA with the power to impose financial penalties for manufacturers who fail to comply with this reporting.
As more drugs are added to the list of those in short supply, there is growing concern among the public regarding how patients are affected by these shortages. Hopefully, the actions of the FDA and Congress will relieve some of these problems and we will again see an adequate supply of these important medications.
Sunday, May 1, 2011
Dick: have you seen this available in the US>????? A Pill that gives men with advanced prostrate cancer an extra 4 months of life has come a
A Pill that gives men with advanced prostrate cancer an extra 4 months of life has come a step closer to being approved for use in Britain. Zytiga is a hormonal drug that cuts of the source of testosterone, which makes prostrate cancer cells grow.
Standard hormone treatments for prostrate cancer blocks production of male hormone in the testes, but recent research shows that tumours can produce their own supply, as does the adrenal gland. Zytiga block all testosterone generation. It can be used in up to 80 per cent of patients with aggressive drug resistant prostrate cancer who have run out of options after exhausting a range of anti-hormonal therapies and chemotherapy. The drug is not available for use on the NHS, but makers Johnson and Johnson have applied for licensing approval in Europe that could be granted by the end of this year. That approval looks more likely after U.S. watchdogs at the Food and Drug Administration gave the green light to the drug there nearly 2 months earlier than expected, following its successful trial. A trial on almost 800 patients in 13 countries found those taking the drug combined with conventional steroid treatment survive ed for about 15 months compared with 11 months on steroid alone.
The study was cut short so all patients could be given Zytiga clinical name abiraterone acetate - after independent monitors determined a clear survival benefit.
Around 250,000 men in the UK are living with prostrate cancer, with 37,000 new cases diagnosed each year. It is the biggest cancer killer after lung cancer, with 10,000 men dying from the disease each year. Zytiga was discovered by British scientists at the institute of Cancer Research.
Professor Johann de Bono, of the ICR said "This news will be incredibly important ot prostrate cancer patients and their families"
Standard hormone treatments for prostrate cancer blocks production of male hormone in the testes, but recent research shows that tumours can produce their own supply, as does the adrenal gland. Zytiga block all testosterone generation. It can be used in up to 80 per cent of patients with aggressive drug resistant prostrate cancer who have run out of options after exhausting a range of anti-hormonal therapies and chemotherapy. The drug is not available for use on the NHS, but makers Johnson and Johnson have applied for licensing approval in Europe that could be granted by the end of this year. That approval looks more likely after U.S. watchdogs at the Food and Drug Administration gave the green light to the drug there nearly 2 months earlier than expected, following its successful trial. A trial on almost 800 patients in 13 countries found those taking the drug combined with conventional steroid treatment survive ed for about 15 months compared with 11 months on steroid alone.
The study was cut short so all patients could be given Zytiga clinical name abiraterone acetate - after independent monitors determined a clear survival benefit.
Around 250,000 men in the UK are living with prostrate cancer, with 37,000 new cases diagnosed each year. It is the biggest cancer killer after lung cancer, with 10,000 men dying from the disease each year. Zytiga was discovered by British scientists at the institute of Cancer Research.
Professor Johann de Bono, of the ICR said "This news will be incredibly important ot prostrate cancer patients and their families"
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