Undergo TURP to ID Prostate Cancer

Tuesday, 08 December 2009

Department of Urology, Cannizzaro Hospital, Catania, Italy. To evaluate prostate cancer (PCa) detection after repeated negative saturation biopsy, 75 patients, aged 53-78 years, underwent transurethral resection of prostate (TURP) because of persistent suspicion of cancer; median PSA was 11.8 ng ml(-1) and 58 men complained lower urinary tract symptoms (LUTS). In 12 (16%) and 3 (4%) men a T1a and T1b PCa was found with median PSA and Gleason score equal to 14.2 vs 23.6 ng ml(-1) and 5.6 vs 7 ng ml(-1). In case of persistent suspicion of PCa after repeated negative saturation biopsy, TURP may be proposed, aside from the coexistence of LUTS, to rule out a PCa, in younger patients with high PSA values (>/=20 ng ml(-1)). Written by: Pepe P, Fraggetta F, Galia A, Grasso G, Aragona

Undergo TURP

McClatchy-Tribune Information Services -- Unrestricted

12-08-09

Cancer rates and deaths from the most common forms of the disease are dropping, but not nearly as fast as experts would like.

Incidence decreased about 1 percent a year from 1999 to 2006 and deaths dropped an average of 1.6 percent a year from 2001 to 2006 according to a report released today by the National Cancer Institute, the Centers for Disease Control and Prevention, the American Cancer Society and the North American Association of Central Cancer Registries.

The decreases were driven largely by drops in incidence and death linked to the most common cancers in men and women, including lung, prostate, breast and colorectal. Meanwhile, incidence of some cancers -- including kidney, liver and skin -- has gone up.

"It's very slow. I think the rate is unacceptable. It's a drop in the bucket," said Dr. Michael Caligiuri, director of Ohio State University's Comprehensive Cancer Center.

Take, for instance, colorectal cancer. Only about half of those who should be undergoing colonoscopies actually get them, he said.

Economics explains some of that, but not all, Caligiuri said.

"We need to study this. We need to talk to the people who got it done and talk to the people who didn't get it done and say, 'Why didn't you do this?'

"(Doctors) need to look at ourselves and say 'What are we doing that is preventing these other 50 percent from not getting screening?' "

Better screening and wider-spread use of optimal treatment could drive down colorectal cancer death rates much more significantly, according to the report written by Brenda Edwards of the NCI's surveillance research program.

In terms of what individuals can do, much attention in this report -- and in the field of cancer research overall -- is given to lifestyle changes, particularly reduction in obesity. Being overweight or obese is thought to contribute to a variety of cancers, including colon.

After decades of efforts to lower tobacco use, Edwards points out, reductions in lung cancer incidence have been seen.

Also yesterday, a group of experts spoke about cancer prevention efforts as part of the American Association for Cancer Research conference on the topic in Houston.

"Diet is one of those relatively few modifiable risk factors that is associated with a change in cancer incidence and tumor behavior," said John Milner, chief of the National Cancer Institute's nutritional science research group.

Thirty percent of cancers are related to dietary habits, he said.

"There's a lot we can do to prevent cancer as we become more fit and turn around the obesity epidemic," said Dr. Tim Byers, associate dean of the Colorado School of Public Health and interim director of the Colorado Cancer Center.

In addition to looking at the connection between weight and cancer, there is a lot of focus on specific dietary compounds and how they influence cancer incidence.

"There's probably not enough fish in the sea for all of us to eat as much fish as we should get," said Elaine Hardman, associate professor of medicine at Marshall University School of Medicine.

Much of Hardman's work focuses on fats found in fish and nuts.

The good news: the fats found in fish originate in plants, said Hardman, who has studied mice that are fed canola oil.

Some research is even pointing to a connection between the nutrients absorbed before birth and subsequent cancer susceptibility, she said. To see more of The Columbus Dispatch, or to subscribe to the newspaper, go to http://www.columbusdispatch.com. Copyright (c) 2009, The Columbus Dispatch, Ohio Distributed by McClatchy-Tribune Information Services. For reprints, email tmsreprints@permissionsgroup.com, call 800-374-7985 or 847-635-6550, send a fax to 847-635-6968, or write to The Permissions Group Inc., 1247 Milwaukee Ave., Suite 303, Glenview, IL 60025, USA.

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From: "jacqueline strax"
To:
Sent: Sunday, December 06, 2009 2:59 AM
Subject: [PPML] Serial biopsies are associated with an increased risk of ED
in men with prostate cancer on active surveillance.


>J Urol. 2009 Dec;182(6):2664-9.
>
> Serial prostate biopsies are associated with an increased risk of erectile
> dysfunction in men with prostate cancer on active surveillance.
>
> Fujita K, Landis P, McNeil BK, Pavlovich CP.
>
> Brady Urological Institute, The Johns Hopkins University, Baltimore,
> Maryland 21224, USA.
>
> PURPOSE: We determined whether serial prostate needle biopsies predispose
> men to erectile dysfunction and/or lower urinary tract symptoms over time.
> MATERIALS AND METHODS: Men with prostate cancer on an active surveillance
> protocol were administered the 5-item Sexual Health Inventory for Men and
> International Prostate Symptom Score questionnaires on protocol entry, and
> at a cross-sectional point in 2008. All men had at least 1, 10 to 12-core
> prostate biopsy at protocol entry and yearly surveillance biopsies
> thereafter were recommended. RESULTS: Of 333 men 231 returned the followup
> questionnaires. Correlations were found between biopsy number and erectile
> dysfunction, with increasing biopsy number associated with a decrease in
> Sexual Health Inventory for Men score (p = 0.04) and a history of 3 or
> more biopsies associated with a greater decrease in Sexual Health
> Inventory for Men score than after 2 or fewer biopsies (p = 0.02).
> Multivariable analysis for biopsy number, age, prostate volume and
> prostate specific antigen showed that only biopsy number was associated
> with decreasing Sexual Health Inventory for Men score (p = 0.02). When men
> were stratified by baseline Sexual Health Inventory for Men, those without
> preexisting erectile dysfunction (Sexual Health Inventory for Men score 22
> to 25) trended toward steeper decreases in Sexual Health Inventory for Men
> score after 3 or more biopsies (p = 0.06) than did men with baseline mild
> to moderate erectile dysfunction (Sexual Health Inventory for Men score 8
> to 21). No correlation was found between biopsy number and International
> Prostate Symptom Score. CONCLUSIONS: Serial prostate biopsies appear to
> have an adverse effect on erectile function in men with prostate cancer on
> active surveillance but do not affect lower urinary tract symptoms.
>
> best
> Jacquie Strax
> http://www.psa-rising.com
>

Low and High Fat Diets, Differences

Thursday, 03 December 2009

Urology Section, Department of Surgery, Veterans Administration, Greater Los Angeles Healthcare System; Department of Urology, University of California-Los Angeles, Los Angeles, California. A high fat Western diet and sedentary lifestyle may predispose men to prostate cancer through changes in serum hormones and growth factors. We evaluated the effect of a low fat diet on serum factors affecting prostate cancer cell growth by performing a prospective, randomized dietary intervention trial in men with prostate cancer. We randomized 18 men with prostate cancer who did not receive prior therapy to a low fat (15% kcal), high fiber, soy protein supplemented diet or a Western (40% kcal fat) diet for 4 weeks. Fasting serum was collected at baseline and after the intervention to measure prostate specific antigen, sex hormones, insulin, insulin-like growth factor I and II, insulin-like growth factor binding proteins, lipids and fatty acids. LNCaP cells (ATCC(R)) were cultured in medium containing pre-intervention and post-intervention human serum to assess the in vitro effect of the diet on prostate cancer cell proliferation. Subjects in each group were highly compliant with the dietary intervention. Serum from men in the low fat group significantly decreased the growth of LNCaP cells relative to Western diet serum (p = 0.03). There were no significant between group changes in serum prostate specific antigen, sex hormones, insulin, insulin-like growth factor I and II, and insulin-like growth factor binding proteins. Serum triglyceride and linoleic acid (omega-6) levels were decreased in the low fat group (p = 0.034 and 0.005, respectively). Correlation analysis revealed that decreased omega-6 and increased omega-3 fatty acid correlated with decreased serum stimulated LNCaP cell growth (r = 0.64, p = 0.004 and r = -0.49, p = 0.04, respectively). In this prospective, randomized dietary intervention trial a low fat diet resulted in changes in serum fatty acid levels that were associated with decreased human LNCaP cancer cell growth. Further prospective trials are indicated to evaluate the potential of low fat diets for prostate cancer prevention and treatment. Written by: Aronson WJ, Barnard RJ, Freedland SJ, Henning S, Elashoff D, Jardack PM, Cohen P, Heber D, Kobayashi N. Are you the author?

Treatment of Estrogen Deficiency after HT

Tuesday, 01 December 2009

Department of Surgery (Urology), Durham VA Medical Center and Duke Prostate Center, Duke University School of Medicine, Durham, NC 27710, USA. steve.freedland@duke.edu This email address is being protected from spam bots, you need Javascript enabled to view it Androgen deprivation therapy (ADT) is the standard of care for metastatic prostate cancer and is increasingly used to treat asymptomatic patients with prostate-specific antigen recurrence after failed primary therapy. Although effective, ADT is associated with multiple adverse effects, many of which are related to the estrogen deficiency that occurs as a result of treatment. These include increased fracture risk, hot flashes, gynecomastia, serum lipid changes and memory loss. By providing clinicians with a greater awareness of the estrogen deficiency induced adverse effects from ADT, they can proactively intervene on the physical and psychological impact these effects have on patients. Written by: Freedland SJ, Eastham J, Shore N

Value of Saturation Biopsies

Saturation biopsies for prostate cancer: current uses and future prospects - Abstract

Tuesday, 01 December 2009

Cochin Hospital, Paris Descartes University, Paris, France. Since its introduction, ultrasound-guided prostate biopsy has undergone significant evolution. Because of the low sensitivity of ultrasonography in detecting prostate cancer, tissue is sampled randomly within the gland. In an attempt to enhance cancer detection and characterization, the trend has been to increase the number of biopsy cores taken. Saturation biopsies of the prostate gland were first evaluated as a diagnostic tool. When performed as an initial procedure, saturation biopsies do not seem to improve cancer detection when compared to standard biopsy. However, saturation biopsies might be of clinical value in patients with previous negative standard biopsies but persistently rising PSA levels. As a staging tool, the use of saturation biopsies was proposed mainly to avoid overtreatment of clinically insignificant cancers. Results from clinical and autopsy studies have suggested that saturation biopsies are more accurate than standard biopsies in histological characterization of prostate cancer. Improving cancer characterization might require an increase in the number of cores taken, but knowing their precise location is paramount. Strict template guidance and three-dimensional techniques offer a more comprehensive approach than current ultrasound-guided approaches, and the advantage of precisely recording every core location. New imaging techniques, such as diffusion-weighted and spectroscopic MRI might also help in targeting prostate biopsies. Written by:

Randomized Trials of Prostate Cancer Screening by Dr. Stacy Loeb and Dr. Alan W. Partin | Reviews in Urology | Summer 2009 Since the introduction of widespread prostate-specific antigen (PSA)-based prostate cancer screening, there has been a considerable stage migration (1). Prior studies have shown that PSA screening reduces the risk of advanced disease compared with no screening (2)(3), but there were insufficient data to prove that screening saves lives. Until recently, randomized trials demonstrating Level I evidence have not been available to determine whether prostate cancer screening leads to a mortality benefit. In March 2009, the European Randomized Study of Screening for Prostate Cancer (ERSPC) and Prostate, Lung, Colorectal, and Ovarian (PLCO) trials reported on mortality results. Screening and Prostate-Cancer Mortality in a Randomized European Study Schröder FH, Hugosson J, Roobol MJ, et al. N Engl J Med 2009;360:13201328 Schröder and colleagues reported on the mortality rates in 162,243 men aged 55 to 69 years from ERSPC. Men from 7 European countries were identified through population registries and randomized into screening and control arms. It is noteworthy that PSA screening was uncommon in Europe at the time this trial was initiated, such that this represented a population with relatively low levels of prescreening. Most centers performed screening at 4-year intervals and used a serum PSA level of 3 ng/mL as the threshold for biopsy, although digital rectal examination (DRE) was primarily used as an ancillary test for men with PSA levels greater than 3 ng/mL. The mean age was 60.8 years at randomization and men in the screening arm received an average of 2.1 PSA tests per person. The cumulative incidence of prostate cancer was 8.2% in the screening arm and 4.8% in the control arm. Thus, screening compared with no screening led to an expected increase in prostate cancer incidence. At a median follow-up of approximately 9 years, prostate cancer death occurred in 214 men from the screening arm versus 326 controls (adjusted rate ratio 0.80; 95% confidence interval [CI], 0.65–0.98; P = .04) in the intent-to-screen analysis. A separate analysis of men who actually underwent screening in the first round (82% compliance) to those who did not demonstrated a 27% reduction in prostate cancer mortality. Of note, the difference in mortality emerged after 7 to 8 years, and appeared to increase over time. In addition to the reduction in mortality, the screening arm had a 41% lower rate of metastases at the time of diagnosis than the control arm. Despite the favorable mortality results, Schröder and colleagues also highlighted the potential harms of screening with respect to overdiagnosis. The prostate cancer incidence rate was 70% higher in the screening arm than the control arm. As a comparison, a systematic review of breast cancer screening similarly demonstrated a 15% to 20% relative reduction in cancer-specific mortality with mammography, with only a 30% increase in incidence (4). Overall, Schröder and colleagues estimated that 1410 men would need to be screened and an additional 48 men treated to prevent 1 prostate cancer death over 9 years. However, the number needed to treat to prevent 1 case of metastatic prostate cancer was approximately 25 compared with the ERSPC control group (F. H. Schröder, MD, personal communication, 2009), and only 15 compared with a population from Northern Ireland with virtually no screening (5). Mortality Results From a Randomized Prostate-Cancer Screening Trial Andriole GL, Crawford ED, Grubb RL 3rd, et al. N Engl J Med 2009;360:13101319 The Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial was designed by the National Cancer Institute to determine whether screening with PSA and DRE, flexible sigmoidoscopy, chest x-ray, and CA-125 with transvaginal ultrasound would reduce mortality from prostate, colorectal, lung, and ovarian cancer, respectively (6). Beginning in 1993, the prostate cancer portion of the trial randomized 76,693 men aged 55 to 74 years to screening or “usual care.” The screening protocol included annual DRE for 4 years and annual PSA testing for 6 years. Although participants were notified of abnormal test results (defined as a suspicious DRE or PSA > 4 ng/mL), the subsequent diagnostic workup and/or treatment was not mandated by the study protocol. As a result, a proportion of screened men who developed an abnormal PSA or DRE did not undergo prompt prostate biopsy (7), conditions that were designed to approximate a real-world setting. This updated report from Andriole and associates found no difference in prostate cancer mortality between men randomized to screening or no screening at 7 years (rate ratio 1.13; 95% CI, 0.75–1.70). Interestingly, prostate cancer incidence differed by only 17% between the screening and control arms at 10 years. A possible explanation underlying these findings is that 44% of participants had at least 1 PSA test within 3 years of study entry, and 52% of controls were screened (“contamination”) during the study period. Because these numbers were based upon self-report, it is possible that they represent underestimates (8) in light of the high prevalence of opportunistic PSA testing in the United States (9). Several differences between the ERSPC and PLCO studies should be highlighted, including the sample size (162,243 vs 76,693), screening intervals (every 4 years vs annual), PSA threshold for biopsy (3 ng/mL vs 4 ng/mL), and use of DRE (ancillary test vs annual for 4 years). Also, the rates of prescreening and contamination were both considerably lower in the ERSPC, and the median follow-up for prostate cancer mortality was longer (9 years vs 5–6 years). Many of these methodological differences may help to explain the disparate results between the studies. Nevertheless, the conflicting results of these trials and concerns over the benefit-to-harm ratio led Michael Barry to conclude in an accompanying editorial that PSA screening is the “controversy that refuses to die.”(10) Overall, the authors conclude based upon the ERSPC results that screening does lead to a reduction in prostate cancer mortality. Furthermore, the potential harms of screening might be reduced through more careful patient selection for both screening and treatment. In addition, the future discovery of better biomarkers for clinically significant prostate cancer and an ongoing reduction in treatment-related morbidity could further shift the risk-to-benefit ratio in favor of screening. References 1. Catalona WJ, Smith DS, Ratliff TL, Basler JW. Detection of organ-confined prostate cancer is increased through prostate-specific antigen-based screening. JAMA. 1993;270:948–954. [PubMed] 2. Aus G, Bergdahl S, Lodding P, et al. Prostate cancer screening decreases the absolute risk of being diagnosed with advanced prostate cancer-results from a prospective, population-based randomized controlled trial. Eur Urol. 2007;51:659–664. [PubMed] 3. van der Cruijsen-Koeter IW, Roobol MJ, Wildhagen MF, et al. Tumor characteristics and prognostic factors in two subsequent screening rounds with four-year interval within prostate cancer screening trial, ERSPC Rotterdam. Urology. 2006;68:615–620. [PubMed] 4. Gøtzsche PC, Nielsen M. Screening for breast cancer with mammography. Cochrane Database Syst Rev. 2006;4 CD001877. 5. van Leeuwen PJ, Connolly D, Napolitano G, et al. Metastasis-free survival in screen and clinical detected prostate cancer: a comparison between the European Randomized Study of Screening for Prostate Cancer and Northern Ireland. J Urol. 2009;181:798. Abstract 2203. 6. Prorok PC, Andriole GL, Bresalier RS, et al. Design of the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial. Control Clin Trials. 2000;21(6 suppl):273S–309S. [PubMed] 7. Pinsky PF, Andriole GL, Kramer BS, et al. Prostate biopsy following a positive screen in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. J Urol. 2005;173:746–750. discussion 750–751. [PubMed] 8. Chan EC, Vernon SW, Ahn C, Greisinger A. Do men know that they have had a prostate-specific antigen test? Accuracy of self-reports of testing at 2 sites. Am J Public Health. 2004;94:1336–1338. [PubMed] 9. Sirovich BE, Schwartz LM, Woloshin S. Screening men for prostate and colorectal cancer in the United States: does practice reflect the evidence? JAMA. 2003;289:1414–1420. [PubMed] 10. Barry MJ. Screening for prostate cancer-the controversy that refuses to die. N Engl J Med. 2009;360:1351–1354. [PubMed]