Multi-step testing might enhance performance of the prostate cancer diagnostic pipeline. Using PSA >1 ng/ml for first-line risk stratification and the Stockholm 3 Model (S3M) blood-test >10% risk of Gleason Score > 7 prostate cancer to inform biopsy decisions has been suggested. We aimed to determine the effects of changing the PSA cutoff to perform reflex testing with S3M and the subsequent S3M cutoff to recommend prostate biopsy while maintaining the sensitivity to detect Gleason Score ≥ 7 prostate cancer.We used data from the prospective, population-based, paired, diagnostic Stockholm 3 (STHLM3) study with participants invited by date of birth from the Swedish Population Register during 2012-2014. All participants underwent testing with PSA and S3M (a combination of plasma protein biomarkers [PSA, free PSA, intact PSA, hK2, MSMB, MIC1], genetic polymorphisms, and clinical variables [age, family, history, previous prostate biopsy, prostate exam]). Of 47,688 men in the STHLM3 main study, we used data from 3133 men with S3M >10% and prostate biopsy data. Logistic regression models were used to calculate prostate cancer detection rates and proportion saved biopsies.44.2%, 62.5% and 67.9% of the participants had PSA <1, <1.5 and <1.7 ng/ml, respectively. Increasing the PSA cut-off for additional work-up from 1 ng/ml to 1.5 ng/ml would thus save 18.3% of the performed tests, 4.9% of the biopsies and 1.3% (10/765) of Gleason Grade ≥ 7 cancers would be un-detected. By lowering the S3M cutoff to recommend biopsy, sensitivity to high-grade prostate cancer can be restored, to the cost of increasing the number of performed biopsies modestly.The sensitivity to detect prostate cancer can be maintained when using different PSA cutoffs to perform additional testing. Biomarker cut-offs have implications on number of tests and prostate biopsies performed. A PSA cutoff of 1.5 ng/ml to perform additional testing such as the S3M test might be considered.ISRCTN84445406 .
Cellular proliferation was studied by incorporation of 3H-thymidine in the hearts of young, adult and old swimming-exercised rats. The proliferative activity was measured by scintillation counting. The swimming exercise induced a significant proliferation of capillary wall cells in the younger age groups, suggesting a neoformation of myocardial capillaries in these rats, whereas no cell proliferation was recorded in the old rats.
An attempt was made to see if new forms of treatment of fungal and bacterial septicemia, or new cytostatic combinations have changed the causes of death in leukemia and lymphoma. Autopsies were studied of 16 cases with acute leukemia, 2 with chronic granulocytic leukemia and 24 with lymphoma. 10 of the 18 patients with leukemia and 10/24 lymphoma patients died although they had no, or only slight, tumor infiltration in the bone marrow and parenchymatous organs; only 1/18 leukemias had extensive infiltration. There was a statistically significant correlation between the extent of marrow andorgan infiltration. Cardiac failure (5/18 patients) was almost as common as the main cause of death as septicemia (7/18) in leukemia. The corresponding figures in lymphoma were5/24 and 9/24, respectively. The present findings contrast with earlier ones, where more septicemia and tumor infiltration were found at autopsy, and less cardiac failure was observed. 15 of 16 cases with septicemia at autopsy had terminal fever. Bacteriological and histological signs of septicemia at autopsy agreed satisfactorily. There was a suprising absence of agreement between terminal granulocytopenia and septicemia; 13 of 16 patients with septicemia had over 0.1 × 109 and 10 over 0.5 × 109 granulocytes/liter blood.
Tumour size and nodal involvement are the two main prognostic factors in breast cancer (BC). Their impact on the natural history of BC is not fully captured by analyses that ignore their quantitative nature.Data pertaining to 18 159 patients treated with primary surgery: 3661 at the Institut Gustave-Roussy (IGR, France) between 1954 and 1983, and 14 498 in the breast cancer registry in the Stockholm-Gotland Health Care region (SG, Sweden) between 1976 and 1999, were collected. The risks of distant metastases (DMs) and of nodal involvement were analysed according to tumour size with parametric models.Using SG 1976-1990 as the reference group, relative risks (RRs) for DM were equal to 1.42 (95% CI: 1.29-1.56; P<10(-10)) in IGR and 0.61 (95% CI: 0.55-0.67; P<10(-10)) in SG 1991-1999. Differences in tumour size explained the increased risk in IGR (RR adjusted for tumour size 1.09; 95% CI: 0.99-1.20; P=0.07), but not the decreased risk in SG 1991-1999 (adjusted RR: 0.63; 95% CI: 0.57-0.69; P<10(-10)). The relationship between tumour size and DM risk changed significantly during the 1990s.Early diagnosis is sufficient to explain differences in the prognosis before 1990. After 1990, the use of adjuvant systemic therapies is the main reason for the reduction in DM.
The long term survival of patients with prostate carcinoma is not well understood. The objective of the current study was to investigate the temporal trend of prostate carcinoma mortality in patients who survived > or = 10 years after diagnosis.Men with prostate carcinoma diagnosed from 1958 through 1983 in the Stockholm/Gotland region in Sweden and who survived > or = 10 years after the diagnosis were investigated regarding survival beyond 10 years. The expected survival was calculated from an annually selected age and time-matched cohort of men from the general population in the same geographic region. The relative survival was expressed as the annual quotient of the observed survival over the expected survival.The authors identified 1896 patients who had survived > or = 10 years. The relative survival decreased up to approximately 18 years after the diagnosis, whereupon it reached a plateau that was constant up to 30 years after diagnosis.Men with prostate carcinoma surviving > or = 10 years have an excess mortality compared with age-matched controls. This excess mortality ceases 20 to 23 years after diagnosis and the observed and the expected survival are similar, indicating few, if any, deaths from prostate carcinoma from there on.
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