Association Between Lead Time and Prostate Cancer Grade: Evidence of Grade Progression from Long-term Follow-up of Large Population-based Cohorts Not Subject to Prostate-specific Antigen Screening
Lead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for prostate cancer (PCa) using archived blood samples from cohorts followed for many years without screening. To determine the association between LT and PCa g...
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| Published in | European urology Vol. 73; no. 6; pp. 961 - 967 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
Elsevier B.V
01.06.2018
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| Online Access | Get full text |
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| Abstract | Lead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for prostate cancer (PCa) using archived blood samples from cohorts followed for many years without screening.
To determine the association between LT and PCa grade at diagnosis to provide an insight into whether grade progresses or is stable over time.
The setting was three long-term epidemiologic studies in Sweden including men not subject to prostate-specific antigen (PSA) screening. The cohort included 1041 men with PSA of 3–10 ng/ml at blood draw and subsequently diagnosed with PCa with grade data available.
Multivariable logistic regression was used to predict high-grade (Gleason grade group ≥2 or World Health Organization grade 3) versus low-grade PCa at diagnosis in terms of LT, defined as the time between the date of elevated PSA and the date of PCa diagnosis with adjustment for cohort and age.
The probability that PCa would be high grade at diagnosis increased with LT. Among all men combined, the risk of high-grade disease increased with LT (odds ratio 1.13, 95% confidence interval [CI] 1.10–1.16; p<0.0001), with no evidence of differences in effect by age group or cohort. Higher PSA predicted shorter LT by 0.46 yr (95% CI 0.28–0.64; p<0.0001) per 1 ng/ml increase in PSA. However, there was no interaction between PSA and grade, suggesting that the longer LT for high-grade tumors is not simply related to age. Limitations include the assumption that men with elevated PSA and subsequently diagnosed with PCa would have had biopsy-detectable PCa at the time of PSA elevation.
Our data support grade progression, whereby following a prostate over time would reveal transitions from benign to low-grade and then high-grade PCa.
Men with a longer lead time between elevated prostate-specific antigen and subsequent prostate cancer diagnosis were more likely to have high-grade cancers at diagnosis.
The probability that a cancer will be of high grade at diagnosis increases with the lead time. Our findings provide evidence of grade progression, whereby a prostate followed over time would exhibit transitions from benign to low-grade to high-grade prostate cancer. |
|---|---|
| AbstractList | Lead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for prostate cancer (PCa) using archived blood samples from cohorts followed for many years without screening.
To determine the association between LT and PCa grade at diagnosis to provide an insight into whether grade progresses or is stable over time.
The setting was three long-term epidemiologic studies in Sweden including men not subject to prostate-specific antigen (PSA) screening. The cohort included 1041 men with PSA of 3–10 ng/ml at blood draw and subsequently diagnosed with PCa with grade data available.
Multivariable logistic regression was used to predict high-grade (Gleason grade group ≥2 or World Health Organization grade 3) versus low-grade PCa at diagnosis in terms of LT, defined as the time between the date of elevated PSA and the date of PCa diagnosis with adjustment for cohort and age.
The probability that PCa would be high grade at diagnosis increased with LT. Among all men combined, the risk of high-grade disease increased with LT (odds ratio 1.13, 95% confidence interval [CI] 1.10–1.16; p<0.0001), with no evidence of differences in effect by age group or cohort. Higher PSA predicted shorter LT by 0.46 yr (95% CI 0.28–0.64; p<0.0001) per 1 ng/ml increase in PSA. However, there was no interaction between PSA and grade, suggesting that the longer LT for high-grade tumors is not simply related to age. Limitations include the assumption that men with elevated PSA and subsequently diagnosed with PCa would have had biopsy-detectable PCa at the time of PSA elevation.
Our data support grade progression, whereby following a prostate over time would reveal transitions from benign to low-grade and then high-grade PCa.
Men with a longer lead time between elevated prostate-specific antigen and subsequent prostate cancer diagnosis were more likely to have high-grade cancers at diagnosis.
The probability that a cancer will be of high grade at diagnosis increases with the lead time. Our findings provide evidence of grade progression, whereby a prostate followed over time would exhibit transitions from benign to low-grade to high-grade prostate cancer. BACKGROUND: Lead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for prostate cancer (PCa) using archived blood samples from cohorts followed for many years without screening. OBJECTIVE: To determine the association between LT and PCa grade at diagnosis to provide an insight into whether grade progresses or is stable over time. DESIGN, SETTING, AND PARTICIPANTS: The setting was three long-term epidemiologic studies in Sweden including men not subject to prostate-specific antigen (PSA) screening. The cohort included 1041 men with PSA of 3-10 ng/ml at blood draw and subsequently diagnosed with PCa with grade data available. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Multivariable logistic regression was used to predict high-grade (Gleason grade group ≥2 or World Health Organization grade 3) versus low-grade PCa at diagnosis in terms of LT, defined as the time between the date of elevated PSA and the date of PCa diagnosis with adjustment for cohort and age. RESULTS AND LIMITATIONS: The probability that PCa would be high grade at diagnosis increased with LT. Among all men combined, the risk of high-grade disease increased with LT (odds ratio 1.13, 95% confidence interval [CI] 1.10-1.16; p<0.0001), with no evidence of differences in effect by age group or cohort. Higher PSA predicted shorter LT by 0.46 yr (95% CI 0.28-0.64; p<0.0001) per 1 ng/ml increase in PSA. However, there was no interaction between PSA and grade, suggesting that the longer LT for high-grade tumors is not simply related to age. Limitations include the assumption that men with elevated PSA and subsequently diagnosed with PCa would have had biopsy-detectable PCa at the time of PSA elevation. CONCLUSIONS: Our data support grade progression, whereby following a prostate over time would reveal transitions from benign to low-grade and then high-grade PCa. PATIENT SUMMARY: Men with a longer lead time between elevated prostate-specific antigen and subsequent prostate cancer diagnosis were more likely to have high-grade cancers at diagnosis. Background: Lead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for prostate cancer (PCa) using archived blood samples from cohorts followed for many years without screening. Objective: To determine the association between LT and PCa grade at diagnosis to provide an insight into whether grade progresses or is stable over time. Design, setting, and participants: The setting was three long-term epidemiologic studies in Sweden including men not subject to prostate-specific antigen (PSA) screening. The cohort included 1041 men with PSA of 3-10 ng/ml at blood draw and subsequently diagnosed with PCa with grade data available. Outcome measurements and statistical analysis: Multivariable logistic regression was used to predict high-grade (Gleason grade group >= 2 or World Health Organization grade 3) versus low-grade PCa at diagnosis in terms of LT, defined as the time between the date of elevated PSA and the date of PCa diagnosis with adjustment for cohort and age. Results and limitations: The probability that PCa would be high grade at diagnosis increased with LT. Among all men combined, the risk of high-grade disease increased with LT (odds ratio 1.13, 95% confidence interval [CI] 1.10-1.16; p < 0.0001), with no evidence of differences in effect by age group or cohort. Higher PSA predicted shorter LT by 0.46 yr (95% CI 0.28-0.64; p < 0.0001) per 1 ng/ml increase in PSA. However, there was no interaction between PSA and grade, suggesting that the longer LT for high-grade tumors is not simply related to age. Limitations include the assumption that men with elevated PSA and subsequently diagnosed with PCa would have had biopsy-detectable PCa at the time of PSA elevation. Conclusions: Our data support grade progression, whereby following a prostate over time would reveal transitions from benign to low-grade and then high-grade PCa. Patient summary: Men with a longer lead time between elevated prostate-specific antigen and subsequent prostate cancer diagnosis were more likely to have high-grade cancers at diagnosis. Background: Lead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for prostate cancer (PCa) using archived blood samples from cohorts followed for many years without screening. Objective: To determine the association between LT and PCa grade at diagnosis to provide an insight into whether grade progresses or is stable over time. Design, setting, and participants: The setting was three long-term epidemiologic studies in Sweden including men not subject to prostate-specific antigen (PSA) screening. The cohort included 1041 men with PSA of 3–10 ng/ml at blood draw and subsequently diagnosed with PCa with grade data available. Outcome measurements and statistical analysis: Multivariable logistic regression was used to predict high-grade (Gleason grade group ≥2 or World Health Organization grade 3) versus low-grade PCa at diagnosis in terms of LT, defined as the time between the date of elevated PSA and the date of PCa diagnosis with adjustment for cohort and age. Results and limitations: The probability that PCa would be high grade at diagnosis increased with LT. Among all men combined, the risk of high-grade disease increased with LT (odds ratio 1.13, 95% confidence interval [CI] 1.10–1.16; p < 0.0001), with no evidence of differences in effect by age group or cohort. Higher PSA predicted shorter LT by 0.46 yr (95% CI 0.28–0.64; p < 0.0001) per 1 ng/ml increase in PSA. However, there was no interaction between PSA and grade, suggesting that the longer LT for high-grade tumors is not simply related to age. Limitations include the assumption that men with elevated PSA and subsequently diagnosed with PCa would have had biopsy-detectable PCa at the time of PSA elevation. Conclusions: Our data support grade progression, whereby following a prostate over time would reveal transitions from benign to low-grade and then high-grade PCa. Patient summary: Men with a longer lead time between elevated prostate-specific antigen and subsequent prostate cancer diagnosis were more likely to have high-grade cancers at diagnosis. The probability that a cancer will be of high grade at diagnosis increases with the lead time. Our findings provide evidence of grade progression, whereby a prostate followed over time would exhibit transitions from benign to low-grade to high-grade prostate cancer. Lead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for prostate cancer (PCa) using archived blood samples from cohorts followed for many years without screening.BACKGROUNDLead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for prostate cancer (PCa) using archived blood samples from cohorts followed for many years without screening.To determine the association between LT and PCa grade at diagnosis to provide an insight into whether grade progresses or is stable over time.OBJECTIVETo determine the association between LT and PCa grade at diagnosis to provide an insight into whether grade progresses or is stable over time.The setting was three long-term epidemiologic studies in Sweden including men not subject to prostate-specific antigen (PSA) screening. The cohort included 1041 men with PSA of 3-10 ng/ml at blood draw and subsequently diagnosed with PCa with grade data available.DESIGN, SETTING, AND PARTICIPANTSThe setting was three long-term epidemiologic studies in Sweden including men not subject to prostate-specific antigen (PSA) screening. The cohort included 1041 men with PSA of 3-10 ng/ml at blood draw and subsequently diagnosed with PCa with grade data available.Multivariable logistic regression was used to predict high-grade (Gleason grade group ≥2 or World Health Organization grade 3) versus low-grade PCa at diagnosis in terms of LT, defined as the time between the date of elevated PSA and the date of PCa diagnosis with adjustment for cohort and age.OUTCOME MEASUREMENTS AND STATISTICAL ANALYSISMultivariable logistic regression was used to predict high-grade (Gleason grade group ≥2 or World Health Organization grade 3) versus low-grade PCa at diagnosis in terms of LT, defined as the time between the date of elevated PSA and the date of PCa diagnosis with adjustment for cohort and age.The probability that PCa would be high grade at diagnosis increased with LT. Among all men combined, the risk of high-grade disease increased with LT (odds ratio 1.13, 95% confidence interval [CI] 1.10-1.16; p<0.0001), with no evidence of differences in effect by age group or cohort. Higher PSA predicted shorter LT by 0.46 yr (95% CI 0.28-0.64; p<0.0001) per 1 ng/ml increase in PSA. However, there was no interaction between PSA and grade, suggesting that the longer LT for high-grade tumors is not simply related to age. Limitations include the assumption that men with elevated PSA and subsequently diagnosed with PCa would have had biopsy-detectable PCa at the time of PSA elevation.RESULTS AND LIMITATIONSThe probability that PCa would be high grade at diagnosis increased with LT. Among all men combined, the risk of high-grade disease increased with LT (odds ratio 1.13, 95% confidence interval [CI] 1.10-1.16; p<0.0001), with no evidence of differences in effect by age group or cohort. Higher PSA predicted shorter LT by 0.46 yr (95% CI 0.28-0.64; p<0.0001) per 1 ng/ml increase in PSA. However, there was no interaction between PSA and grade, suggesting that the longer LT for high-grade tumors is not simply related to age. Limitations include the assumption that men with elevated PSA and subsequently diagnosed with PCa would have had biopsy-detectable PCa at the time of PSA elevation.Our data support grade progression, whereby following a prostate over time would reveal transitions from benign to low-grade and then high-grade PCa.CONCLUSIONSOur data support grade progression, whereby following a prostate over time would reveal transitions from benign to low-grade and then high-grade PCa.Men with a longer lead time between elevated prostate-specific antigen and subsequent prostate cancer diagnosis were more likely to have high-grade cancers at diagnosis.PATIENT SUMMARYMen with a longer lead time between elevated prostate-specific antigen and subsequent prostate cancer diagnosis were more likely to have high-grade cancers at diagnosis. Lead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for prostate cancer (PCa) using archived blood samples from cohorts followed for many years without screening. To determine the association between LT and PCa grade at diagnosis to provide an insight into whether grade progresses or is stable over time. The setting was three long-term epidemiologic studies in Sweden including men not subject to prostate-specific antigen (PSA) screening. The cohort included 1041 men with PSA of 3-10 ng/ml at blood draw and subsequently diagnosed with PCa with grade data available. Multivariable logistic regression was used to predict high-grade (Gleason grade group ≥2 or World Health Organization grade 3) versus low-grade PCa at diagnosis in terms of LT, defined as the time between the date of elevated PSA and the date of PCa diagnosis with adjustment for cohort and age. The probability that PCa would be high grade at diagnosis increased with LT. Among all men combined, the risk of high-grade disease increased with LT (odds ratio 1.13, 95% confidence interval [CI] 1.10-1.16; p<0.0001), with no evidence of differences in effect by age group or cohort. Higher PSA predicted shorter LT by 0.46 yr (95% CI 0.28-0.64; p<0.0001) per 1 ng/ml increase in PSA. However, there was no interaction between PSA and grade, suggesting that the longer LT for high-grade tumors is not simply related to age. Limitations include the assumption that men with elevated PSA and subsequently diagnosed with PCa would have had biopsy-detectable PCa at the time of PSA elevation. Our data support grade progression, whereby following a prostate over time would reveal transitions from benign to low-grade and then high-grade PCa. Men with a longer lead time between elevated prostate-specific antigen and subsequent prostate cancer diagnosis were more likely to have high-grade cancers at diagnosis. |
| Author | Bergh, Anders Stattin, Pär Assel, Melissa Dahlin, Anders Vickers, Andrew J. Ulmert, David Lilja, Hans |
| AuthorAffiliation | c Department of Clinical Sciences, Lund University, Skåne University Hospital, Malmö, Sweden b Department of Clinical Microbiology, Lund University, Skåne University Hospital, Malmö, Sweden a Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA h Urology Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA e Department of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden g Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University Hospital, Umeå, Sweden j Department of Translational Medicine, Lund University, Malmö, Sweden d Molecular Pharmacology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA i Departments of Laboratory Medicine and Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA k Nuffield Department of Surgical Sciences, University of Oxford, Oxford, UK f Department of Surgical Sciences, Uppsala Un |
| AuthorAffiliation_xml | – name: e Department of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden – name: h Urology Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA – name: i Departments of Laboratory Medicine and Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA – name: k Nuffield Department of Surgical Sciences, University of Oxford, Oxford, UK – name: d Molecular Pharmacology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA – name: c Department of Clinical Sciences, Lund University, Skåne University Hospital, Malmö, Sweden – name: f Department of Surgical Sciences, Uppsala University Hospital, Uppsala, Sweden – name: g Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University Hospital, Umeå, Sweden – name: b Department of Clinical Microbiology, Lund University, Skåne University Hospital, Malmö, Sweden – name: j Department of Translational Medicine, Lund University, Malmö, Sweden – name: a Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA |
| Author_xml | – sequence: 1 givenname: Melissa surname: Assel fullname: Assel, Melissa organization: Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA – sequence: 2 givenname: Anders surname: Dahlin fullname: Dahlin, Anders organization: Department of Clinical Microbiology, Lund University, Skåne University Hospital, Malmö, Sweden – sequence: 3 givenname: David surname: Ulmert fullname: Ulmert, David organization: Department of Clinical Sciences, Lund University, Skåne University Hospital, Malmö, Sweden – sequence: 4 givenname: Anders surname: Bergh fullname: Bergh, Anders organization: Department of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden – sequence: 5 givenname: Pär surname: Stattin fullname: Stattin, Pär organization: Department of Surgical Sciences, Uppsala University Hospital, Uppsala, Sweden – sequence: 6 givenname: Hans surname: Lilja fullname: Lilja, Hans email: liljah@mskcc.org organization: Urology Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA – sequence: 7 givenname: Andrew J. surname: Vickers fullname: Vickers, Andrew J. email: vickersa@mskcc.org organization: Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA |
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| CitedBy_id | crossref_primary_10_1016_j_eururo_2018_10_003 crossref_primary_10_1038_s41585_020_0287_y crossref_primary_10_1002_pros_23790 crossref_primary_10_1007_s00120_021_01505_9 crossref_primary_10_1136_bmjsit_2019_000015 crossref_primary_10_1002_path_5604 crossref_primary_10_1002_ijc_33940 crossref_primary_10_3390_cancers14174149 crossref_primary_10_1016_j_eururo_2022_01_018 crossref_primary_10_1056_NEJMoa2209454 crossref_primary_10_1111_bju_14580 crossref_primary_10_1016_j_eururo_2018_10_004 |
| Cites_doi | 10.1093/jnci/94.13.981 10.1373/clinchem.2005.050641 10.1093/jnci/djp001 10.1046/j.1365-2796.2000.00568.x 10.1080/02841860802247664 10.1111/j.1365-2796.1993.tb00647.x 10.1158/1055-9965.EPI-09-1251 10.1016/j.ejca.2010.09.034 10.1002/ijc.11554 10.1016/j.urology.2014.02.035 10.1016/j.eururo.2015.01.009 |
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| Copyright | 2017 European Association of Urology Copyright © 2017 European Association of Urology. Published by Elsevier B.V. All rights reserved. |
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| CorporateAuthor | Tumor microenvironment Institutionen för kliniska vetenskaper, Lund Institutionen för translationell medicin Department of Translational Medicine Lunds universitet Profile areas and other strong research environments Department of Clinical Sciences, Malmö Clinical Chemistry, Malmö Lund University Tumörmikromiljö Department of Clinical Sciences, Lund Strategiska forskningsområden (SFO) Section I EpiHealth: Epidemiology for Health Faculty of Medicine Internmedicin - epidemiologi Strategic research areas (SRA) Sektion I Medicinska fakulteten Profilområden och andra starka forskningsmiljöer Klinisk kemi, Malmö Internal Medicine - Epidemiology Institutionen för kliniska vetenskaper, Malmö |
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| Keywords | Screening Prostate cancer Lead-time PSA |
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| References_xml | – volume: 46 start-page: 3102 year: 2010 end-page: 3108 ident: bib0070 article-title: Lead-time in the European Randomised Study of Screening for Prostate Cancer publication-title: Eur J Cancer – volume: 247 start-page: 19 year: 2000 end-page: 29 ident: bib0090 article-title: Long-term outcome of the Malmo preventive project: mortality and cardiovascular morbidity publication-title: J Intern Med – volume: 19 start-page: 1201 year: 2010 end-page: 1207 ident: bib0080 article-title: Empirical estimates of the lead time distribution for prostate cancer based on two independent representative cohorts of men not subject to prostate-specific antigen screening publication-title: Cancer Epidemiol Biomarkers Prev – volume: 52 start-page: 235 year: 2006 end-page: 239 ident: bib0110 article-title: Reproducibility and accuracy of measurements of free and total prostate-specific antigen in serum vs plasma after long-term storage at −20 degrees C publication-title: Clin Chem – volume: 233 start-page: 45 year: 1993 end-page: 51 ident: bib0095 article-title: The Malmo Diet and Cancer Study. 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| Snippet | Lead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for prostate cancer... Background: Lead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for... BACKGROUND: Lead time (LT) is of key importance in early detection of cancer, but cannot be directly measured. We have previously provided LT estimates for... |
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| SubjectTerms | Adult Aged Cancer and Oncology Cancer och onkologi Clinical Medicine Disease Progression Early Detection of Cancer Follow-Up Studies Humans Klinisk medicin Lead-time Male Medical and Health Sciences Medicin och hälsovetenskap Middle Aged Neoplasm Grading Prostate cancer Prostate-Specific Antigen - blood Prostatic Neoplasms - blood Prostatic Neoplasms - diagnosis Prostatic Neoplasms - pathology PSA Screening Time Factors |
| Title | Association Between Lead Time and Prostate Cancer Grade: Evidence of Grade Progression from Long-term Follow-up of Large Population-based Cohorts Not Subject to Prostate-specific Antigen Screening |
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