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prostate cancer mortality

  • High Norwegian prostate cancer mortality: evidence of over-reporting.

    This study aimed to determine the level of misattribution of prostate cancer deaths in Norway based on the county of Vestfold in the years 2009-2014.

    The study included 328 patients registered as dead from prostate cancer (PCD; part I of death certificate), 126 patients with prostate cancer as other significant condition at death (OCD; part II of death certificate) and 310 patients who died with a diagnosis of prostate cancer not registered on the death certificate (PC-DCneg) in Vestfold County in 2009-2014.

    Published January 17, 2018
  • Prostate Cancer: Prevalence - Incidence - Mortality

    Prostate Cancer has been the most common noncutaneous malignancy in U.S. men since 1984, now accounting for one quarter of all such cancers.

    • Adenocarcinoma of the prostate is the most common cancer in men and the second leading cause of cancer related deaths in men.
    • The detection and treatment of this condition has been revolutionized by the introduction of serum prostate specific antigen [PSA] testing as part of the evaluation for this disease.
    • Refinements in surgical techniques and the application of radiotherapy allow for the treatment of clinically localized disease with decreased morbidity. The choice of therapy is guided by clinical factors and patient preferences, as well as tumor characteristics. Androgen blockade is still the foundation for treating advanced disease. 

    Incidence - United States:

    • There will be an estimated 220,000 new cases of prostate cancer this year and 29,200 prostate cancer related deaths. After the abrupt rise in prostate cancer diagnosis with the introduction of PSA and the detection of disease in the prevalence population [cull effect] the yearly incidence is somewhat stable. The death rate has been gradually decreasing over the past several years, yet it is too early to say if this is a direct result of early detection and treatment.  
    • Prostate cancer incidence varies by race/ethnicity, with African-Americans at highest risk.  The years in which peak rates were observed can be differentiated by race: 1992 for whites (237.8 per 100,000 men) and 1993 for African-Americans in (343.1 per 100,000).
    • African-American men have the highest reported incidence of prostate cancer in the world, with a relative incidence of 1.6 compared with white men in the United States.  
    • Although African-Americans have experienced a greater decline in mortality than white men since the early 1990s, their death rates remain more than 2.4 times higher than whites.
    • There are currently no data that clearly indicate a single reason for the observed differences in incidence or mortality, and it seems likely that the source of this difference is multifactorial.
    • For 2008, the American Cancer Society estimated 186,320 new cases of prostate cancer in the United States.

    Mortality - United States:

    • Estimated new cases and deaths from prostate cancer in the United States in 2012:

      New cases: 241,740
      Deaths: 28,170

    • In 2008, the American Cancer Society estimated 28,660 prostate cancer–related deaths in the United States, for an approximate annual rate of 23.3 per 100,000 population, representing a 41% decrease from the peak in 1991.
    Incidence and Mortality - Worldwide:
    • Incidence rates show that prostate cancer is the fifth most common malignancy worldwide and the second most common in men.
    • Prostate cancer makes up 11.7% of new cancer cases overall, 19% in developed countries, and 5.3% in developing countries. Its incidence varies widely between countries and ethnic populations, with disease rates differing by more than 100-fold.
    • The lowest yearly incidence rates occur in Asia (1.9 cases per 100,000 in China) and the highest in North America and Scandinavia, especially in African-Americans (249 cases per 100,000).  
    • As in the United States, prostate cancer incidence has increased in many countries since the early 1990s, with the largest increases in high-risk countries.  
    • Mortality also varies widely among countries, being highest in the Caribbean (28 per 100,000 per year) and lowest in Southeast Asia, China, and North Africa (<5 per 100,000 per year).  
    • The CONCORD study, a worldwide population-based analysis of cancer survival in five continents, recently analyzed international differences in survival for breast, colorectal, and prostate cancer.  
    • Using data from cancer registries, age-standardized 5-year survival rates were found to vary greatly, ranging from 80% or higher in the United States (92%), Australia, and Canada, to less than 40% in Denmark, Poland, and Algeria.
    • Whether these racial differences in incidence and mortality are due to socioeconomic or biological factors remains controversial. Differences in screening rates between whites and African-Americans may play a role in explaining the differences in mortality, although the 2005 National Health Interview Survey demonstrated that among men ages 40 to 49 years, African-American men were more likely to have had a PSA test than white men, and there were no significant differences in PSA screening rates by race/ethnicity in men ages 50 to 79 years.  
    • Data from autopsy studies have shown, however, a higher incidence of prostate intraepithelial neoplasia in African American men when compared with Caucasian men, suggesting that biological differences in tumorigenesis may exist. 
    • Data from radical prostatectomy specimens demonstrates a higher incidence of tumors in both the peripheral and transition zones of African American men compared with Caucasian men. 
    • Even among those treated with “watchful waiting,” African- American men may receive less intensive follow-up.
    • Thus far, a number of racial differences at the molecular level have been described and include variation in the androgen signaling and steroid biosynthesis pathways. 
    • Studies have consistently shown that African-American men are more likely to receive androgen-deprivation therapy, expectant management or external beam radiation therapy, and are less likely to undergo radical prostatectomy compared with white men.  
    • Autopsy incidence. Incidental prostate cancer is noted in 30% of men in the 6th decade of life and increases significantly through the ninth decade. These data have been reproduced in populations for several areas in the world. 
    • Recent studies also suggest that this significant sub-clinical level of prostate cancer is present in men as early as the fourth decade of life.
    References
    • Albertson PC, Hanley JA, Gleason DR, Barry MJ: Competing risk analysis of men aged 55 to 74 years at diagnosis managed conservatively for clinically localized prostate cancer. JAMA 280:975-980, 1998.
    • American Cancer Society. American Cancer Society : Cancer facts and figures 2008.  http://www.cancer.org/acs/groups/content/@nho/documents/document/2008cafffinalsecuredpdf.pdf
    • Andriole GL, Grubb 3rd RL, Buys SS, et al: Mortality results from a randomized prostate-cancer screening trial. N Engl J Med  2009; 360:1310-1319.
    • Coleman MP, Quaresma M, Berrino F, et al: Cancer survival in five continents: a worldwide population-based study (CONCORD). Lancet Oncol  2008; 9:730-756.
    • Cooney, K. A., J. D. McCarthy, et al. (1997). "Prostate cancer susceptibility locus on chromosome 1q: a confirmatory study." J Natl Cancer Inst 89(13): 955-9.
    • Devgan, S. A., B. E. Henderson, et al. (1997). "Genetic variation of 3 beta-hydroxysteroid dehydrogenase type II in three racial/ethnic groups: implications for prostate cancer risk." Prostate 33(1): 9-12.
    • Greenlee, R. T., T. Murray, et al. (2000). "Cancer statistics, 2000." CA Cancer J Clin 50(1): 7-33.
    • Jemal, A., T. Murray, et al. (2003). "Cancer statistics, 2003." CA Cancer J Clin 53(1): 5-26.
    • Kalapurakal, J. A., A. N. Jacob, et al. (1999). "Racial differences in prostate cancer related to loss of heterozygosity on chromosome 8p12-23." Int J Radiat Oncol Biol Phys 45(4): 835-40.
    • Makridakis, N., R. K. Ross, et al. (1997). "A prevalent missense substitution that modulates activity of prostatic steroid 5alpha-reductase." Cancer Res 57(6): 1020-2.
    • Makridakis, N. M., R. K. Ross, et al. (1999). "Association of mis-sense substitution in SRD5A2 gene with prostate cancer in African-American and Hispanic men in Los Angeles, USA." Lancet 354(9183): 975-8.
    • Nationl Cancer Institute (accessed April 2, 2012) http://www.cancer.gov/cancertopics/types/prostate
    • Parkin DM, Bray F, Ferlay J, Pisani P: Global cancer statistics, 2002. CA Cancer J Clin  2005; 55:74-108.
    • Polascik TJ, Oesterling JE, Parting AW: Prostate specific antigen: A decade of discovery-What we have learned and where we are going. J Urol 162:293-306, 1999.
    • Pettaway, C. A., P. Troncoso, et al. (1998). "Prostate specific antigen and pathological features of prostate cancer in black and white patients: a comparative study based on radical prostatectomy specimens." J Urol 160(2): 437-42.
    • Platz, E. A., M. N. Pollak, et al. (1999). "Racial variation in insulin-like growth factor-1 and binding protein-3 concentrations in middle-aged men." Cancer Epidemiol Biomarkers Prev 8(12): 1107-10.
    • Ross, R. K., L. Bernstein, et al. (1992). "5-alpha-reductase activity and risk of prostate cancer among Japanese and US white and black males." Lancet 339(8798): 887-9.
    • Sakr, W. A., D. J. Grignon, et al. (1995). "Epidemiology of high grade prostatic intraepithelial neoplasia." Pathol Res Pract 191(9): 838-41.
    • Smith, J. R., D. Freije, et al. (1996). "Major susceptibility locus for prostate cancer on chromosome 1 suggested by a genome-wide search." Science 274(5291): 1371-4.
    • Shavers VL, Brown M, Klabunde CN, et al: Race/ethnicity and the intensity of medical monitoring under “watchful waiting” for prostate cancer. Med Care  2004; 42:239-250.
    • Thompson IM, Pauler DK, Goodman PJ, Tangen CM, Lucia MS, Parnes HL, Minasian LM, Ford LG, Lippman SM, Crawford ED, Crowley JJ, Coltman CA Jr. Prevalence of prostate cancer among men with a prostate-specific antigen level < or =4.0 ng per milliliter. N Engl J Med. 2004 May 27;350(22):2239-46.
    • Tricoli, J. V., D. L. Winter, et al. (1999). "Racial differences in insulin-like growth factor binding protein-3 in men at increased risk of prostate cancer." Urology 54(1): 178-82.
    • Underwood 3rd W, Jackson J, Wei JT, et al: Racial treatment trends in localized/regional prostate carcinoma: 1992-1999. Cancer  2005; 103:538-545.
    • Winter, D. L., A. L. Hanlon, et al. (2001). "Plasma levels of IGF-1, IGF-2, and IGFBP-3 in white and African-American men at increased risk of prostate cancer." Urology 58(4): 614-8.
    • Xu, J., D. Meyers, et al. (1998). "Evidence for a prostate cancer susceptibility locus on the X chromosome." Nat Genet 20(2): 175-9.
    Published April 2, 2012
  • Prostate Specific Antigen Doubling Time as a Surrogate End Point for Prostate Cancer Specific Mortality Following Radical Prostatectomy or Radiation Therapy

    PURPOSE:

    A short post treatment prostate specific antigen (PSA)-doubling time (DT) following radical prostatectomy or radiation therapy was evaluated as a surrogate end point for prostate cancer specific mortality (PCSM).

    MATERIALS AND METHODS:

    Baseline, treatment and followup information was compiled on a cohort of 8,669 patients with prostate cancer treated with surgery (5,918) or radiation (2,751) from January 1, 1988 to January 1, 2002 for clinical stage T1c-4NxMo prostate cancer, forming the study cohort. Cox regression analysis was used to test whether Prentice criteria were violated in this cohort.

    RESULTS:

    After PSA defined recurrence PSA-DT less than 3 months and the specific value of PSA-DT at 3 months or greater were statistically significantly associated with time to PCSM and with time to all cause mortality after PSA defined recurrence (each Cox p <0.001). Treatment received was not statistically significant associated with time to PCSM following PSA defined recurrence in patients with PSA-DT less than 3 months (Cox p = 0.90) and in patients with PSA-DT 3 months or greater (Cox p = 0.28). Furthermore, after PSA defined recurrence PSA-DT less than 3 months was statistically significantly associated with PCSM (HR 19.6, 95% CI 12.5 to 30.9).

    CONCLUSIONS:

    Post treatment PSA-DT appears to be a surrogate end point for PCSM following surgery or radiation therapy. We recommend that consideration should be given to enrollment onto a clinical trial and/or initiating androgen suppression therapy at the time of PSA defined recurrence when PSA-DT is less than 3 months to delay the imminent sequelae of metastatic bone disease.


    J Urol. 2004 Nov;172(5 Pt 2):S42-6; discussion S46-7.

    Author Information:

    D'Amico AV1, Moul J, Carroll PR, Sun L, Lubeck D, Chen MH.

    1 Department of Radiation Oncology, Brigham and Women's Hospital and Dana Farber Cancer Institute, Boston, Massachusetts 02215, USA.

    Pub Med: https://www.ncbi.nlm.nih.gov/pubmed/15535442
    Published October 17, 2017
  • Self-reported sleep disturbances and prostate cancer morbidity and mortality in Swedish men: A longitudinal study over 40 years.

    The present study, with an observational period of about 40 years, examined the association between self-reported sleep disturbances (i.e. problems with falling and staying asleep; use of hypnotics) and prostate cancer morbidity and mortality in initially 2322 men (all 50 years old at baseline).

    Published May 18, 2018
  • Should Everyone with Prostate Cancer be on a Statin?

    I am regularly asked about whether men undergoing active treatment for prostate cancer should add a statin to their daily medication routine to reduce the risk of prostate cancer recurrence, mortality, and complications.  Nearly as often I hear questions about whether statins may be of use in prostate cancer survivors or men at risk of prostate cancer, raising the general idea that everyone and anyone may benefit from treatment with these commonly used medications. 
    Published October 26, 2017
  • Vascular morphology differentiates prostate cancer mortality risk among men with higher Gleason grade.

    Higher Gleason grade is associated with prostate cancer mortality; however, there is significant heterogeneity in this association. We evaluated whether vessel morphology, a biomarker of angiogenesis, aided in distinguishing mortality risks among men with high Gleason grading.

    Published July 8, 2016
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