| 1. |
- Bill-Axelson, Anna, et al.
(författare)
-
Radical prostatectomy versus watchful waiting in localized prostate cancer : the Scandinavian prostate cancer group-4 randomized trial
- 2008
-
Ingår i: Journal of the National Cancer Institute. - : Oxford University Press. - 0027-8874 .- 1460-2105. ; 100:16, s. 1144-1154
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The benefit of radical prostatectomy in patients with early prostate cancer has been assessed in only one randomized trial. In 2005, we reported that radical prostatectomy improved prostate cancer survival compared with watchful waiting after a median of 8.2 years of follow-up. We now report results after 3 more years of follow-up.METHODS: From October 1, 1989, through February 28, 1999, 695 men with clinically localized prostate cancer were randomly assigned to radical prostatectomy (n = 347) or watchful waiting (n = 348). Follow-up was complete through December 31, 2006, with histopathologic review and blinded evaluation of causes of death. Relative risks (RRs) were estimated using the Cox proportional hazards model. Statistical tests were two-sided.RESULTS: During a median of 10.8 years of follow-up (range = 3 weeks to 17.2 years), 137 men in the surgery group and 156 in the watchful waiting group died (P = .09). For 47 of the 347 men (13.5%) who were randomly assigned to surgery and 68 of the 348 men (19.5%) who were not, death was due to prostate cancer. The difference in cumulative incidence of death due to prostate cancer remained stable after about 10 years of follow-up. At 12 years, 12.5% of the surgery group and 17.9% of the watchful waiting group had died of prostate cancer (difference = 5.4%, 95% confidence interval [CI] = 0.2 to 11.1%), for a relative risk of 0.65 (95% CI = 0.45 to 0.94; P = .03). The difference in cumulative incidence of distant metastases did not increase beyond 10 years of follow-up. At 12 years, 19.3% of men in the surgery group and 26% of men in the watchful waiting group had been diagnosed with distant metastases (difference = 6.7%, 95% CI = 0.2 to 13.2%), for a relative risk of 0.65 (95% CI = 0.47 to 0.88; P = .006). Among men who underwent radical prostatectomy, those with extracapsular tumor growth had 14 times the risk of prostate cancer death as those without it (RR = 14.2, 95% CI = 3.3 to 61.8; P < .001).CONCLUSION: Radical prostatectomy reduces prostate cancer mortality and risk of metastases with little or no further increase in benefit 10 or more years after surgery.
|
|
| 2. |
- Chang, Ellen T., et al.
(författare)
-
Body mass index and risk of malignant lymphoma in Scandinavian men and women
- 2005
-
Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 97:3, s. 210-218
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The incidence of non-Hodgkin lymphoma and prevalence of obesity are increasing globally. A suggested positive association between obesity and risk of non-Hodgkin lymphoma has prompted us to investigate the relationship between body mass index (BMI) and risk of malignant lymphoma subtypes in a population-based case-control study. METHODS: Telephone interviews were conducted with 3055 case patients with non-Hodgkin lymphoma and 618 case patients with Hodgkin lymphoma diagnosed between October 1, 1999, and August 30, 2002, and 3187 population-based control subjects. The interviews assessed current height, normal adult weight, and other possible risk factors. Multivariable odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for risk of lymphoma were estimated by unconditional logistic regression. All statistical tests were two-sided. RESULTS: BMI was not associated with risk of overall non-Hodgkin lymphoma or of Hodgkin lymphoma (for example, comparing the highly obese group [BMI > or =35.0 kg/m2] with the normal-weight group [BMI = 18.5-24.9 kg/m2], OR for risk of non-Hodgkin lymphoma = 0.9, 95% CI = 0.6 to 1.3; P(trend) across all categories of BMI = .27). BMI was also not associated with risk of any non-Hodgkin lymphoma subtype evaluated, although there was some evidence of a positive association with risk of diffuse large B-cell lymphoma (for example, comparing the highly obese group with the normal-weight group, OR for diffuse large B-cell lymphoma = 1.5, 95% CI = 0.9 to 2.4; P(trend) =.05). CONCLUSIONS: Excess weight does not appear to be associated with an increased risk of malignant lymphoma in general, or with a risk of most major lymphoma subtypes. Hence, the growing incidence of obesity is unlikely to be an important contributor to the increasing incidence of non-Hodgkin lymphoma worldwide.
|
|
| 3. |
- Chang, Ellen T., et al.
(författare)
-
Family history of hematopoietic malignancy and risk of lymphoma
- 2005
-
Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 97:19, s. 1466-1474
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- BACKGROUND: A family history of hematopoietic malignancy is associated with an increased risk of non-Hodgkin lymphoma (NHL) and Hodgkin lymphoma (HL), although the magnitude of the relative risk is unclear. We estimated the association between familial hematopoietic cancer and risk of lymphoma using validated, registry-based family data, and we also investigated whether associations between some environmental exposures and risk of lymphoma vary between individuals with and without such a family history. METHODS: In a population-based case-control study of malignant lymphoma, 1506 case patients and 1229 control subjects were linked to the Swedish Multi-Generation Register and then to the Swedish Cancer Register to ascertain history of cancer in first-degree relatives of patients with malignant lymphoma. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for associations with the risk of lymphoma. RESULTS: A history of hematopoietic malignancy in any first-degree relative was associated with an increased risk of all NHL (OR = 1.8, 95% CI = 1.2 to 2.5), common B-cell NHL subtypes, and HL. Relative risks were generally stronger in association with sibling hematopoietic cancer (OR for all NHL = 3.2, 95% CI = 1.3 to 7.6) than with parental hematopoietic cancer (OR = 1.6, 95% CI = 1.1 to 2.3). A family history of NHL or chronic lymphocytic leukemia (CLL) was associated with an increased risk of several NHL subtypes and HL, whereas familial multiple myeloma was associated with a higher risk of follicular lymphoma. There was no statistically significant heterogeneity in NHL risk associations with environmental factors between individuals with and without familial hematopoietic malignancy. CONCLUSIONS: The increased risk of NHL and HL among individuals with a family history of hematopoietic malignancy was approximately twofold for both lymphoma types. There was no evidence that etiologic associations varied between familial NHL and nonfamilial NHL.
|
|
| 4. |
- Chang, Ellen T., et al.
(författare)
-
Reliability of self-reported family history of cancer in a large case-control study of lymphoma
- 2006
-
Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 98:1, s. 61-68
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Case-control studies of familial cancer risk traditionally rely on self-reported family history of cancer, which may bias results due to differential recall between case patients and control subjects. To evaluate the reliability of self-reported data, we analyzed questionnaire and registry-based data on familial cancer from a population-based case-control study of malignant lymphoma. METHODS: All 1508 lymphoma case patients and 1229 control subjects completed a telephone interview assessing cancer in family members. Participants were linked to the Swedish Multi-Generation Register and Cancer Register to identify confirmed cancer diagnoses in first-degree relatives. The sensitivity and specificity of self-reported familial cancer were calculated among case patients and control subjects and were compared using logistic regression. All statistical tests were two-sided. RESULTS: Lymphoma case patients reported a family history of any cancer with statistically significantly higher sensitivity than control subjects (0.85, 95% confidence interval [CI] = 0.83 to 0.87 and 0.80, 95% CI = 0.77 to 0.82, respectively) but with marginally lower specificity (0.89, 95% CI = 0.87 to 0.91 and 0.92, 95% CI = 0.90 to 0.94, respectively). The sensitivity of self-reporting familial cancers by site ranged from less than 0.20 for rare malignancies to nearly 0.75 for more common types, whereas specificity was generally 0.98 or greater. For most sites, the reliability of self-report was similar in patients and control subjects. However, patients reported familial hematopoietic cancer with statistically significantly higher sensitivity (0.60, 95% CI = 0.57 to 0.62) than control subjects (0.38, 95% CI = 0.35 to 0.40). Odds ratios for the association between familial cancer and risk of non-Hodgkin lymphoma were consistently higher when based on self-reported, compared with registry data-based, family history of any cancer or of hematopoietic cancer. CONCLUSIONS: Reliability of self-reported family history of cancer varies between case patients and control subjects. Recall bias may thus produce biased results in case-control studies of familial cancer risk.
|
|
| 5. |
- Cnattingius, Sven, et al.
(författare)
-
Prenatal and neonatal risk factors for childhood lymphatic leukemia
- 1995
-
Ingår i: Journal of the National Cancer Institute. - 0027-8874 .- 1460-2105. ; 87:12, s. 908-914
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Because the incidence of childhood acute lymphatic leukemia peaks between 2 and 4 years of age, the risk factors may exert their influence during the prenatal and/or the neonatal periods. Results of previous studies of perinatal risk factors have been contradictory, perhaps because most studies either have been hospital based or have been restricted to limited geographical areas. PURPOSE: A nationwide case-control study was carried out to identify maternal and perinatal risk factors for this disease. METHODS: The case-control study was nested in cohorts defined by all live births in Sweden recorded in the nationwide Medical Birth Register. Since 1973, this register has routinely collected information on all hospital births in regard to maternal demographic data, reproductive history, pregnancy, delivery, and the neonatal period. From the Swedish National Cancer Register, 613 case subjects were identified in successive birth cohorts from 1973 through 1989. Five control subjects per case subject were randomly selected from the pool of children matched by sex and month and year of birth. Conditional logistic regression was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) for potential risk factors and to estimate their effects after adjustment for possible confounders. RESULTS: Risk of childhood lymphatic leukemia at all ages increased with Down's syndrome (OR = 20.0; 95% CI = 4.2-94.2), maternal renal disease (OR = 4.4; 95% CI = 1.6-12.1), use of supplementary oxygen (OR = 2.3; 95% CI = 1.5-3.6), postpartum asphyxia (OR = 1.8; 95% CI = 1.2-2.6), birth weight of more than 4500 g (OR = 1.7; 95% CI = 1.1-2.7), and hypertensive disease during pregnancy (OR = 1.4; 95% CI = 1.0-1.9). Down's syndrome affected risk mostly in children younger than 5 years, whereas other factors affected those children 5 years old or older. Being one of a multiple birth also increased risk among older children (OR = 2.5; 95% CI = 1.0-6.0). Use of supplementary oxygen may act as a causal intermediate (surrogate) for postpartum asphyxia and its causes, as would high birth weight for its causes. CONCLUSIONS: Several maternal and perinatal risk factors were found to be associated with childhood lymphatic leukemia, but they showed age-specific differences. Overall, only a few risk factors were identified, and these accounted for a small proportion of cases. We concluded that most risk factors for childhood lymphatic leukemia remain unidentified in very young children.
|
|
| 6. |
- Fall, Katja, et al.
(författare)
-
Prostate-specific antigen levels as a predictor of lethal prostate cancer
- 2007
-
Ingår i: Journal of the National Cancer Institute. - Oxford : Oxford Univ. Press. - 0027-8874 .- 1460-2105. ; 99:7, s. 526-532
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Rates of long-term survival among patients with untreated localized prostate cancer are high. To avoid unnecessary treatment, tools are needed to identify the small proportion of patients who are destined to develop lethal prostate cancer. Methods: To evaluate the accuracy of early changes in prostate-specific antigen (PSA) levels as predictors of prostate cancer outcome, we assessed serial measurements of PSA level among 267 men with localized prostate cancer in a Scandinavian cohort of men who were diagnosed between 1989 and 1999 and who were managed by watchful waiting. We then 1) fitted individual regression lines to the PSA values assessed for each patient during the first 2 years of follow-up by using three different models, 2) evaluated early PSA curve characteristics as determinants of the cumulative incidence of lethal prostate cancer and calculated hazard ratios for baseline PSA value and rate of change in PSA level to prostate cancer outcome, and 3) plotted time-dependent receiver operating characteristic (ROC) curves. All P values are two-sided. Results: During complete follow-up for a mean of 8.5 years, 34 patients (13%) died from prostate cancer, and 18 (7%) developed metastases but were still alive at end of follow-up. In a log-linear model, both PSA value at baseline (P = .05) and the rate of PSA change (P<.001) were associated with the development of lethal prostate cancer. In the ROC analysis, however, the accuracy of classifying the disease as either indolent or destined to progress was low, regardless of the cut point chosen for initial PSA level or rate of change in PSA level. Conclusions: Although baseline PSA value and rate of PSA change are prognostic factors for lethal prostate cancer, they are poor predictors of lethal prostate cancer among patients with localized prostate cancer who are managed by watchful waiting.
|
|
| 7. |
- Fang, Fang, et al.
(författare)
-
Immediate risk of suicide and cardiovascular death after a prostate cancer diagnosis : cohort study in the United States
- 2010
-
Ingår i: Journal of the National Cancer Institute. - New York, USA : Elsevier. - 0027-8874 .- 1460-2105. ; 102:5, s. 307-14
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Receiving a cancer diagnosis is a stressful event that may increase risks of suicide and cardiovascular death, especially soon after diagnosis.Methods: We conducted a cohort study of 342,497 patients diagnosed with prostate cancer from January 1, 1979, through December 31, 2004, in the Surveillance, Epidemiology, and End Results Program. Follow-up started from the date of prostate cancer diagnosis to the end of first 12 calendar months after diagnosis. The relative risks of suicide and cardiovascular death were calculated as standardized mortality ratios (SMRs) comparing corresponding incidences among prostate cancer patients with those of the general US male population, with adjustment for age, calendar period, and state of residence. We compared risks in the first year and months after a prostate cancer diagnosis. The analyses were further stratified by calendar period at diagnosis, tumor characteristics, and other variables.Results: During follow-up, 148 men died of suicide (mortality rate = 0.5 per 1000 person-years) and 6845 died of cardiovascular diseases (mortality rate = 21.8 per 1000 person-years). Patients with prostate cancer were at increased risk of suicide during the first year (SMR = 1.4, 95% confidence interval [CI] = 1.2 to 1.6), especially during the first 3 months (SMR = 1.9, 95% CI = 1.4 to 2.6), after diagnosis. The elevated risk was apparent in pre-prostate-specific antigen (PSA) (1979-1986) and peri-PSA (1987-1992) eras but not since PSA testing has been widespread (1993-2004). The risk of cardiovascular death was slightly elevated during the first year (SMR = 1.09, 95% CI = 1.06 to 1.12), with the highest risk in the first month (SMR = 2.05, 95% CI = 1.89 to 2.22), after diagnosis. The first-month risk was statistically significantly elevated during the entire study period, and the risk was higher for patients with metastatic tumors (SMR = 3.22, 95% CI = 2.68 to 3.84) than for those with local or regional tumors (SMR = 1.57, 95% CI = 1.42 to 1.74).Conclusion: A diagnosis of prostate cancer may increase the immediate risks of suicide and cardiovascular death.
|
|
| 8. |
- Frisch, Morten, et al.
(författare)
-
Tobacco smoking as a risk factor in anal carcinoma : an antiestrogenic mechanism?
- 1999
-
Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 91:8, s. 708-715
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Human papillomavirus-associated anogenital carcinogenesis depends on poorly defined cofactors. Smoking was recently suggested to increase the risk of anal cancer more in premenopausal women than in postmenopausal women. Thus, we used our population-based anal cancer case-control study in Denmark and Sweden to test this hypothesis. METHODS: Our study included 417 patients (324 women and 93 men) who were diagnosed with anal cancer (84% invasive cancer) from 1991 through 1994; it also included five patients diagnosed in 1995. Two control groups were used: 1) 554 population control subjects (349 women and 205 men) and 2) 534 patients with rectal adenocarcinoma (343 women and 191 men). Odds ratios (ORs), calculated from logistic regression analyses, were used as measures of relative risk. All P values are two-sided. RESULTS: Compared with the risk for lifelong nonsmokers, the risk of anal cancer was high among premenopausal women who currently smoked tobacco (multivariate OR = 5.6; 95% confidence interval [CI] = 2.4-12.7) and increased linearly by 6.7% per pack-year smoked (one pack-year is equivalent to one pack of cigarettes smoked per day for 1 year) (P for trend <.001). Smoking was not statistically significantly associated with anal cancer risk in postmenopausal women or men. Women whose menstrual periods started late were at high risk (multivariate OR = 3.6; 95% CI = 1.8-7.3, for > or = 17 years of age versus < or = 12 years of age; P for trend <.001), and body mass index (weight in kg/[height in m]2) was inversely associated with risk among women (P<.001). CONCLUSIONS: Because the risk of anal cancer associated with smoking was restricted to premenopausal women and because higher risk was associated with late menarche and lean body composition, female sex hormones may be a factor in anal cancer development in women. Since the anal mucosa is an estrogen-sensitive area, we hypothesize an antiestrogenic mechanism of action for smoking in anal carcinogenesis.
|
|
| 9. |
- Helgesen, Fred, et al.
(författare)
-
Trends in prostate cancer survival in Sweden, 1960 through 1988 : Evidence of increasing diagnosis of nonlethal tumors
- 1996
-
Ingår i: Journal of the National Cancer Institute. - 0027-8874 .- 1460-2105. ; 88:17, s. 1216-1221
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The incidence of prostate cancer has increased during the past 30 years but has been paralleled by increases in survival rates from this disease, despite the absence of documented major improvement in curative treatment. Since a high prevalence of microscopic prostate cancer has been observed in autopsied men and because many prostate cancers may never surface clinically, increased diagnostic activities might have led to increased detection of less aggressive tumors. PURPOSE: This study was conducted to elucidate whether the trends in prostate cancer incidence and patient survival may be due to increasing diagnoses of nonlethal tumors. METHODS: We analyzed a population-based cohort comprising all cases of prostate cancer (n = 80,901) detected in Sweden during the period of 1960 through 1988. Five hundred eighteen patients (0.64% of the total number) who could not be followed because of emigration or an incomplete national registration number were excluded. Observed and relative survival rates were calculated for the entire cohort of 80,383 assessable patients per 5-year age group in 5-year periods of diagnosis and according to diagnostic method and were compared between geographic areas with differences in incidence rates. To estimate the independent effects of these determinants, multivariate analyses were performed. RESULTS: For the 80,383 patients with complete follow-up, the 10- and 20-year observed survival rates were 17.5% (95% confidence interval [CI] = 17.2%-17.9%) and 3.5% (95% CI = 3.2%-3.7%), and the relative survival rates were 41.1% (95% CI = 40.3%-41.9%) and 28.6% (95% CI = 26.5%-30.1%), respectively. Relative survival rates improved markedly over time; 10-year relative survival rates increased from 29% (95% CI = 27%-31%) among case patients diagnosed in 1960 through 1964 to 45% (95% CI = 43%-46%) among those diagnosed in 1975 through 1979. Relative survival rates leveled off after about 18 years at 18% (95% CI = 15%-20%) among patients diagnosed in 1960 through 1964 and at 31% (95% CI = 28%-34%) among those diagnosed in 1970 through 1974. An even more favorable outlook was observed in those case patients diagnosed later. In areas with a high or low incidence of prostate cancer, the 10-year relative survival rates were 45% (95% CI = 44%-47%) and 36% (95% CI = 34%-38%), respectively. In the early 1960s, the calculated loss of life expectancy after diagnosis varied from about 68% (95% CI = 61%-75%) of the expected length of life in the youngest age group to about 48% (95% CI = 46%-50%) in the oldest age group. From 1960 through 1964 to 1985 through 1988, the loss of life expectancy decreased by more than 50% in all age groups. The differences in relative survival rates between age groups were small, with a gradual decrease in age groups more than 60-64 years of age. CONCLUSIONS: Most of the great temporal improvement and geographic variation in survival rates are quantitatively consistent, with likely increases in the rate of detection of nonlethal tumors. IMPLICATIONS: The increase in relative survival rates must be taken into consideration when evaluating the outcome of treatment of prostate cancer, since nonrandomized comparisons may be confounded by time trends. Diagnosis of nonlethal tumors raises concerns because the individual would suffer from the psychologic burden of a cancer diagnosis without any therapeutic benefit.
|
|
| 10. |
- Lee, Jung Eun, et al.
(författare)
-
Alcohol intake and renal cell cancer in a pooled analysis of 12 prospective studies
- 2007
-
Ingår i: Journal of the National Cancer Institute. - Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA. Karolinska Inst, Dept Med Epidemiol & Biostat, Div Nutr Epidemiol, Natl Inst Environm Med, Stockholm, Sweden. NCI, Div Canc Epidemiol & Genet, Dept Hlth & Hlth Serv, NIH, Bethesda, MD USA. Univ So Calif, Dept Prevent Med, Los Angeles, CA USA. Univ So Calif, Norriss Comprehens Canc Ctr, Los Angeles, CA USA. Maastricht Univ, Dept Epidemiol, Nutr & Toxicol Res Inst, Maastricht, Netherlands. Univ Minnesota, Sch Publ Hlth, Dept Epidemiol & Community Hlth, Minneapolis, MN USA. SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA. No Calif Canc Ctr, Fremont, CA USA. Amer Canc Soc, Epidemiol & Surveillance Res, Atlanta, GA USA. Univ Toronto, Dept Publ Hlth Sci, Toronto, ON, Canada. Mayo Clin, Coll Med, Dept Urol, Jacksonville, FL USA. Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA. Natl Publ Hlth Inst, Dept Hlth Promot & Chron Dis Prevent, Helsinki, Finland. : OXFORD UNIV PRESS INC. - 0027-8874 .- 1460-2105. ; 99:10, s. 801-810
-
Tidskriftsartikel (refereegranskat)abstract
- Background The association between alcohol intake and risk of renal cell cancer has been inconsistent in case-control studies. An inverse association between alcohol intake and risk of renal cell cancer has been suggested in a few prospective studies, but each of these studies included a small number of cases. Methods We performed a pooled analysis of 12 prospective studies that included 530469 women and 229575 men with maximum follow-up times of 7-20 years. All participants had completed a validated food-frequency questionnaire at baseline. Using the primary data from each study, the study-specific relative risks (RRs) for renal cell cancer were calculated using Cox proportional hazards models and then pooled using a random-effects model. All statistical tests were two-sided. Results A total of 1430 (711 women and 719 men) cases of incident renal cell cancer were identified. The study-standardized incidence rates of renal cell cancer were 23 per 100000 person-years among nondrinkers and 15 per 100000 person-years among those who drank 15 g/day or more of alcohol. Compared with non-drinking, alcohol consumption (>= 15 g/day, equivalent to slightly more than one alcoholic drink per day) was associated with a decreased risk of renal cell cancer (pooled multivariable RR = 0.72, 95% confidence interval = 0.60 to 0.86; P-trend <.001); statistically significant inverse trends with increasing intake were seen in both women and men. No difference by sex was observed (P-heterogeneity = .89). Associations between alcohol intake and renal cell cancer were not statistically different across alcoholic beverage type (beer versus wine versus liquor) (P = .40). Conclusion Moderate alcohol consumption was associated with a lower risk of renal cell cancer among both women and men in this pooled analysis.
|
|
