| 31. |
- Bratt, Ola
(författare)
-
Familial and Hereditary Prostate Cancer
- 1999
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- This thesis is based on research concerning epidemiological, clinical, and psychological aspects of familial and hereditary prostate cancer. Epidemiology: Male first-degree relatives of prostate cancer patients had a three-fold increased prostate cancer risk. The risk was higher for relatives of younger patients than for relatives of older patients, most likely due to the effect of the higher prevalence of hereditary prostate cancer found among the former. For first-degree relatives of men with early onset prostate cancer, the risk of developing prostate cancer before the age of 70 years was increased 3.4 times, but their total cancer risk was not increased. Short CAG repeats in the androgen receptor gene correlated with early age at diagnosis of non-hereditary prostate cancer, but not with the risk of developing the disease per se. Clinical aspects: Patients with hereditary prostate cancer were diagnosed, on an average, 7 years earlier than those with sporadic prostate cancer. Family history of prostate cancer was not significantly associated with survival for patients with early onset disease. Psychological aspects: Most men with a family history of prostate cancer worried about the possibility of inheriting the disease. Almost all of them (90-94%) had positive attitudes towards genetic investigations, including genetic testing, and screening. Forty percent of unaffected men in families with hereditary prostate cancer substantially overestimated their lifetime risk of the disease. Perception of high risk was associated with symptoms of depression and cancer worries that affected daily living. High levels of cancerspecific stress may have counteracted participation in screening for some men.
|
|
| 32. |
- Bratt, Ola, et al.
(författare)
-
Family History and Probability of Prostate Cancer, Differentiated by Risk Category : A Nationwide Population-Based Study
- 2016
-
Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 108:10
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Familial prostate cancer risk estimates are inflated by clinically insignificant low-risk cancer, diagnosed after prostate-specific antigen testing. We provide age-specific probabilities of non-low-and high-risk prostate cancer. Methods: Fifty-one thousand, eight hundred ninety-seven brothers of 32 807 men with prostate cancer were identified in Prostate Cancer data Base Sweden (PCBaSe). Nelson-Aalen estimates with 95% confidence intervals (CIs) were calculated for cumulative, family history-stratified probabilities of any, non-low-(any of Gleason score >= 7, prostate-specific antigen [PSA] >= 10 ng/mL, T3-4, N1, and/or M1) and high-risk prostate cancer (Gleason score >= 8 and/or T3-4 and/or PSA >= 20 ng/mL and/or N1 and/or M1). Results: The population probability of any prostate cancer was 4.8% (95% CI = 4.8% to 4.9%) at age 65 years and 12.9% (95% CI = 12.8% to 12.9%) at age 75 years, of non-low-risk prostate cancer 2.8% (95% CI = 2.7% to 2.8%) at age 65 years and 8.9% (95% CI = 8.8% to 8.9%) at age 75 years, and of high-risk prostate cancer 1.4% (95% CI = 1.3% to 1.4%) at age 65 years and 5.2% (95% CI = 5.1% to 5.2%) at age 75 years. For men with one affected brother, probabilities of any prostate cancer were 14.9% (95% CI = 14.1% to 15.8%) at age 65 years and 30.3% (95% CI = 29.3% to 31.3%) at age 75 years, of non-low-risk prostate cancer 7.3% (95% CI = 6.7% to 7.9%) at age 65 years and 18.8% (95% CI = 17.9% to 19.6%) at age 75 years, and of high-risk prostate cancer 3.0% (95% CI = 2.6% to 3.4%) at age 65 years and 8.9% (95% CI = 8.2% to 9.5%) at age 75 years. Probabilities were higher for men with a stronger family history. For example, men with two affected brothers had a 13.6% (95% CI = 9.9% to 17.6 %) probability of high-risk cancer at age 75 years. Conclusions: The age-specific probabilities of non-low-and high-risk cancer presented here are more informative than relative risks of any prostate cancer and more suitable to use for counseling men with a family history of prostate cancer.
|
|
| 33. |
|
|
| 34. |
|
|
| 35. |
|
|
| 36. |
|
|
| 37. |
|
|
| 38. |
|
|
| 39. |
- Bratt, Ola, et al.
(författare)
-
Metaphase cytogenetics and DNA flow cytometry with analysis of S-phase fraction in prostate cancer: influence on prognosis
- 1996
-
Ingår i: Urology. - 1527-9995. ; 47:2, s. 218-224
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To compare the prognostic significance of chromosome aberrations, DNA ploidy, and S-phase fraction (SPF) in prostate adenocarcinomas and to compare the sensitivity of metaphase cytogenetics with flow cytometry (FCM) in detecting abnormal tumor clones. METHODS: Prostate adenocarcinomas from 57 men were previously successfully analyzed with metaphase cytogenetics. Archival material from these tumors were further analyzed with FCM for DNA content and SPF. RESULTS: The patients were followed for 4.5 to 7.7 years. DNA ploidy was analyzed in 51, and SPF in 45 of the 57 tumors. Clonal chromosomal aberrations, DNA aneuploidy, and high SPF were all significantly associated with poor survival. Of these three variables, SPF was the best predictor of survival, but compared with tumor stage and grade in multivariate analysis, SPF was not an independent prognostic factor. Patients with locally advanced tumors or metastatic disease with SPF less than 8% had a median survival of 5.9 years, compared with only 1.3 years for those with SPF more than 8%. Twenty-eight abnormal clones were detected with FCM and 20 with cytogenetic analysis, but only for two of these clones could the results from the two different methods be regarded as concordant. CONCLUSIONS: SPF was superior to karyotype and ploidy in predicting death in prostate cancer, but it remains to be shown whether SPF analysis adds prognostic information to tumor stage and grade. The cytogenetic analyses correlated poorly with results of FCM, indicating low sensitivity of both methods.
|
|
| 40. |
|
|
