SwePub
Tyck till om SwePub Sök här!
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Adami Hans Olov) srt2:(1995-1999);srt2:(1997);pers:(Adami Hans Olov)"

Sökning: WFRF:(Adami Hans Olov) > (1995-1999) > (1997) > Adami Hans Olov

  • Resultat 1-6 av 6
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Adami, Hans-Olov, et al. (författare)
  • Pregnancy and risk of non-Hodgkin´s lymphoma : a prospective study
  • 1997
  • Ingår i: International Journal of Cancer. - 0020-7136 .- 1097-0215. ; 70:2, s. 155-158
  • Tidskriftsartikel (refereegranskat)abstract
    • The etiology of non-Hodgkin's lymphomas (NHL), including chronic lymphocytic leukemia (CLL), is likely to be related to immune function. In the light of the established immunologic effects of a pregnancy, we decided to examine the risk of NHL and CLL in relationship to full-term pregnancies. Within a nationwide cohort we identified 1,546 women with NHL and 198 women with CLL, all 15 years or older, born 1925-1972. Five age-matched controls were selected for each case patient. Conditional logistic regression was used to estimate the odds ratios after mutual adjustment for number of births and age at first birth. We found a weak, negative association between parity and risk of NHL (p for trend 0.11) and a transient, 10-40% decrease in risk within 5-14 years after the last birth among women with various parity status. The risk of CLL decreased more markedly, and orderly with increasing parity, but the trend was not significant (p = 0.18). Small numbers of cases with CLL prevented more detailed analyses of temporal relationships. Age at first birth appeared unrelated to the risk of both NHL and CLL. We conclude that the immunologic alterations associated with a pregnancy have limited, if any, relevance to the etiology of NHL and CLL; changing reproductive pattern is an unlikely contributor to the marked increase in incidence of NHL seen in many populations.
  •  
2.
  •  
3.
  • Frisch, Morten, et al. (författare)
  • Sexually transmitted infection as a cause of anal cancer
  • 1997
  • Ingår i: New England Journal of Medicine. - 0028-4793 .- 1533-4406. ; 337:19, s. 1350-1358
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The incidence of anal cancer has increased in recent decades, particularly among women. To identify underlying risk factors, we conducted a population-based case-control study in Denmark and Sweden. METHODS: We conducted telephone interviews with 324 women and 93 men in whom invasive or in situ anal cancer was diagnosed between 1991 and 1994, 534 controls with adenocarcinoma of the rectum, and 554 population controls. The interviews covered a wide spectrum of possible risk factors for anal cancer. Odds ratios were calculated by logistic regression. Specimens of anal-cancer tissue and samples of rectal adenocarcinomas were tested for human papillomavirus (HPV) DNA with the polymerase chain reaction. RESULTS: Multivariate analysis revealed consistent and statistically significant associations between measures of sexual promiscuity and the risk of anal cancer in both men and women. There was a significant trend toward an association between higher numbers of partners of the opposite sex in women (P<0.001) and men (P<0.05) and strong associations with a variety of venereal diseases. In women, receptive anal intercourse, particularly before the age of 30 years, and venereal infections in the partner were also associated with an increased risk (odds ratios, 3.4 and 2.4, respectively). Fifteen percent of the men with anal cancer reported having had homosexual contact, as compared with none of the controls (P<0.001). High-risk types of HPV, notably HPV-16, were detected in 84 percent of the anal-cancer specimens examined, whereas all rectal-adenocarcinoma specimens tested were negative for HPV. CONCLUSIONS: Our study provides strong evidence that a sexually transmitted infection causes anal cancer. The presence of high-risk types of HPV, notably HPV-16 (which is known to cause cancer of the cervix), in the majority of anal-cancer tissue specimens suggests that most anal cancers are potentially preventable.
  •  
4.
  • Gustafsson, Leif, et al. (författare)
  • International incidence rates of invasive cervical cancer after introduction of cytological screening
  • 1997
  • Ingår i: Cancer Causes and Control. - 0957-5243 .- 1573-7225. ; 8:5, s. 755-763
  • Tidskriftsartikel (refereegranskat)abstract
    • Because Pap-smear screening can detect pre-invasive cervical cancer, such screening can markedly reduce the occurrence of invasive cancer. However, its impact in different populations is uncertain. This study compares the changes in cervical cancer incidence at different ages after the introduction of screening in different populations, and addresses the impact of organized and opportunistic smear taking. We identified 17 cancer registries large enough and existing long enough to analyze screening effects. For each registry, we calculated the relative reduction in age-specific incidence rates and in incidence rates age-standardized to the world population after the introduction of cytologic screening. In 11 of the 17 populations, age-standardized incidence rates declined markedly from 27 percent in Norway and to 77 percent in Finland. Age-specific declines were confined to women aged 30 to 70 years old with a nadir around ages 40 to 55. In six other populations, age-standardized incidence rates declined less than 25 percent, an amount too small to provide unambiguous evidence of a screening effect. In several populations, cytologic screening had a more pronounced effect than is generally recognized. Because age-specific declines in cervical cancer incidence rates were strikingly similar in populations with widely different screening practices, organized screening may not be markedly superior to opportunistic screening. The reduction in reported cancer incidence because of screening is smaller in younger and older women.
  •  
5.
  • Gustafsson, Leif, et al. (författare)
  • International incidence rates of invasive cervical cancer before cytological screening
  • 1997
  • Ingår i: International Journal of Cancer. - 0020-7136 .- 1097-0215. ; 71:2, s. 159-165
  • Tidskriftsartikel (refereegranskat)abstract
    • Huge differences in incidence rates of invasive cervical cancer occur among populations. These differences reflect the influences of both etiological environmental factors and removal of precursor lesions detected upon screening. The purposes of this article are (i) to describe similarities and differences in the shapes and magnitudes of age-specific incidence rates of invasive cervical cancer before screening had an effect, (ii) to provide baseline data for further global study of screening effects, and (iii) to provide baseline incidence data for the design of optimal screening programs. To eliminate the impact of screening effects, we have selected age-specific incidence rates from times when and from populations in which screening was insignificant. The selected rates were suitably scaled and compared regarding age at onset of increase in incidence, age at peak incidence, and rate of subsequent decline. Despite a 16-fold difference in incidence rates, all curves had the same basic structure, with an increase to a peak followed by a decline or a plateau. Although all populations but one had an onset around age 25, 7 European countries showed an earlier peak age (mean = 46 vs. 59) and a more rapid decline after the peak than most other populations. The common basic shape of the age-specific incidence curve, overall, suggests a relatively similar development of invasive cervical cancer in different populations. These results illustrate the underlying similarities in the markedly different age-specific incidence rates of invasive cervical cancer. They also provide a basis for studying screening effects and for optimizing screening programs in specific geographic areas.
  •  
6.
  • Johansson, Jan-Erik, et al. (författare)
  • Fifteen-year survival in prostate cancer : a prospective, population-based study in Sweden
  • 1997
  • Ingår i: Journal of the American Medical Association (JAMA). - : American Medical Association (AMA). - 0098-7484 .- 1538-3598. ; 277:6, s. 467-471
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To describe the natural history of initially untreated early-stage prostate cancer. A key secondary objective was to calculate long-term survival rates by stage, grade, and age at diagnosis. DESIGN: Prospective cohort study. SETTING: Population-based in 1 county of Sweden, without screening for prostate cancer. PATIENTS: A group of 642 patients with prostate cancer of any stage, consecutively diagnosed between 1977 and 1984 at a mean age of 72 years with complete follow-up to 1994. MAIN OUTCOME MEASURES: Proportion of patients who died from prostate cancer, and 15-year survival (with 95% confidence interval [CI]), corrected for causes of death other than prostate cancer. RESULTS: In the entire cohort, prostate cancer accounted for 201 (37%) of all 541 deaths. Among 300 patients with a diagnosis of localized disease (T0-T2), 33 (11%) died of prostate cancer. In this group, the corrected 15-year survival rate was similar in 223 patients with deferred treatment (81%; 95% CI, 72%-89%) and in 77 who received initial treatment (81%; 95% CI, 67%-95%). The corrected 15-year survival was 57% (95% CI, 45%-68%) in 183 patients with locally advanced cancer (T3-T4) and 6% (95% CI, 0%-12%) in those 159 who had distant metastases at the time of diagnosis. CONCLUSION: Patients with localized prostate cancer have a favorable outlook following watchful waiting, and the number of deaths potentially avoidable by radical initial treatment is limited. Without reliable prognostic indicators, an aggressive approach to all patients with early disease would entail substantial overtreatment. In contrast, patients with locally advanced or metastatic disease need trials of aggressive therapy to improve their poor prognosis.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-6 av 6

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy