| 21. |
- Sjövall, Katarina, et al.
(författare)
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Influence on the health of the partner affected by tumor disease in the wife or husband based on a population-based register study of cancer in Sweden
- 2009
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Ingår i: Journal of Clinical Oncology. - : American Society of Clinical Oncology. - 0732-183X .- 1527-7755. ; 27:28, s. 4781-4786
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Tidskriftsartikel (refereegranskat)abstract
- Purpose To examine health care use and health care costs among partners of persons with cancer.Patients and Methods Partners of patients with colon, rectal, lung, breast, and prostate cancer (N = 11,076) were identified via linked data from the Tumor Registry of Southern Sweden and Census Registry of Sweden. Health care use, total costs of health care, and diagnosis of the partner were studied before and after diagnosis of the cancer patient.Results Health care use for partners increased in terms of in-patient care after the cancer diagnosis. A significant increase was seen the second year for partners of patients with colon cancer (risk ratio [RR], 1.55; 95% CI, 1.28 to 1.87) and lung cancer (RR, 1.50; 95% CI, 1.26 to 1.79). Psychiatric diagnoses increased after the cancer diagnosis in the total sample, with a significant increase for partners of colon (RR, 2.66; 95% CI, 1.71 to 4.22), lung (RR, 3.16; 95% CI, 2.23 to 4.57), and prostate cancer patients (RR, 1.68; 95% CI, 1.32 to 2.15). Costs of care increased more than the consumer price index the two years after the cancer diagnosis. Costs of care increased most formale partners and especially for younger male partners (age 25 to 64 years) of patients with colon, rectal, and lung cancers.Conclusion The results showed increased health care costs and an increase in psychiatric diagnoses after the cancer diagnosis among partners of cancer patients. Further research is needed to learn more about the situation of the partner and to identify persons at risk of psychiatric morbidity. Knowledge is also needed on how to support the partner in the most efficient way.
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| 22. |
- Setlur, Sunita R., et al.
(författare)
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Estrogen-dependent signaling in a molecularly distinct subclass of aggressive prostate cancer
- 2008
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Ingår i: Journal of the National Cancer Institute. - Oxford : Oxford University Press. - 0027-8874 .- 1460-2105. ; 100:11, s. 815-825
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The majority of prostate cancers harbor gene fusions of the 5'-untranslated region of the androgen-regulated transmembrane protease serine 2 (TMPRSS2) promoter with erythroblast transformation-specific transcription factor family members. The common fusion between TMPRESS2 and v-ets erythroblastosis virus E26 oncogene homolog (avian) (ERG) is associated with a more aggressive clinical phenotype, implying the existence of a distinct subclass of prostate cancer defined by this fusion. METHODS: We used complementary DNA-mediated annealing, selection, ligation, and extension to determine the expression profiles of 6144 transcriptionally informative genes in archived biopsy samples from 455 prostate cancer patients in the Swedish Watchful Waiting cohort (1987-1999) and the United States-based Physicians(') Health Study cohort (1983-2003). A gene expression signature for prostate cancers with the TMPRSS2-ERG fusion was determined using partitioning and classification models and used in computational functional analysis. Cell proliferation and TMPRSS2-ERG expression in androgen receptor-negative (NCI-H660) prostate cancer cells after treatment with vehicle or estrogenic compounds were assessed by viability assays and quantitative polymerase chain reaction, respectively. All statistical tests were two-sided. RESULTS: We identified an 87-gene expression signature that distinguishes TMPRSS2-ERG fusion prostate cancer as a discrete molecular entity (area under the curve = 0.80, 95% confidence interval [CI] = 0.792 to 0.81; P < .001). Computational analysis suggested that this fusion signature was associated with estrogen receptor (ER) signaling. Viability of NCI-H660 cells decreased after treatment with estrogen (viability normalized to day 0, estrogen vs vehicle at day 8, mean = 2.04 vs 3.40, difference = 1.36, 95% CI = 1.12 to 1.62) or ERbeta agonist (ERbeta agonist vs vehicle at day 8, mean = 1.86 vs 3.40, difference = 1.54, 95% CI = 1.39 to 1.69) but increased after ERalpha agonist treatment (ERalpha agonist vs vehicle at day 8, mean = 4.36 vs 3.40, difference = 0.96, 95% CI = 0.68 to 1.23). Similarly, expression of TMPRSS2-ERG decreased after ERbeta agonist treatment (fold change over internal control, ERbeta agonist vs vehicle at 24 hours, NCI-H660, mean = 0.57- vs 1.0-fold, difference = 0.43-fold, 95% CI = 0.29- to 0.57-fold) and increased after ERalpha agonist treatment (ERalpha agonist vs vehicle at 24 hours, mean = 5.63- vs 1.0-fold, difference = 4.63-fold, 95% CI = 4.34- to 4.92-fold). CONCLUSIONS: TMPRSS2-ERG fusion prostate cancer is a distinct molecular subclass. TMPRSS2-ERG expression is regulated by a novel ER-dependent mechanism.
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| 23. |
- Tomlins, Scott A., et al.
(författare)
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The role of SPINK1 in ETS rearrangement-negative prostate cancers
- 2008
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Ingår i: Cancer Cell. - Amsterdam : Elsevier. - 1535-6108 .- 1878-3686. ; 13:6, s. 519-28
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Tidskriftsartikel (refereegranskat)abstract
- ETS gene fusions have been characterized in a majority of prostate cancers; however, the key molecular alterations in ETS-negative cancers are unclear. Here we used an outlier meta-analysis (meta-COPA) to identify SPINK1 outlier expression exclusively in a subset of ETS rearrangement-negative cancers ( approximately 10% of total cases). We validated the mutual exclusivity of SPINK1 expression and ETS fusion status, demonstrated that SPINK1 outlier expression can be detected noninvasively in urine, and observed that SPINK1 outlier expression is an independent predictor of biochemical recurrence after resection. We identified the aggressive 22RV1 cell line as a SPINK1 outlier expression model and demonstrate that SPINK1 knockdown in 22RV1 attenuates invasion, suggesting a functional role in ETS rearrangement-negative prostate cancers.
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| 24. |
- Larsson, Susanna C., et al.
(författare)
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Cultured milk, yogurt, and dairy intake in relation to bladder cancer risk in a prospective study of Swedish women and men
- 2008
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Ingår i: American Journal of Clinical Nutrition. - Bethseda, Md. : American Society for Nutrition. - 0002-9165 .- 1938-3207. ; 88:4, s. 1083-1087
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Tidskriftsartikel (refereegranskat)abstract
- Background:Findings from epidemiologic studies of the effect of dairy foods (mainly milk) on the risk of bladder cancer have been inconsistent. Objective:We aimed to examine the association between the intake of cultured milk and other dairy foods and the incidence of bladder cancer in a prospective, population-based cohort. Design:We prospectively followed 82 002 Swedish women and men who were cancer-free and who completed a 96-item food-frequency questionnaire in 1997. Incident cases of bladder cancer were identified in the Swedish cancer registries. Results:During a mean follow-up of 9.4 y, 485 participants (76 women and 409 men) were diagnosed with bladder cancer. Total dairy intake was not significantly associated with risk of bladder cancer [7.0 servings/d compared with < 3.5 servings/d: multivariate rate ratio (RR) = 0.87; 95% CI: 0.66, 1.15; P for trend = 0.33]. However, a statistically significant inverse association was observed for the intake of cultured milk (sour milk and yogurt). The multivariate RRs for the highest category of cultured milk intake (2 servings/d) compared with the lowest category (0 serving/d) were 0.62 (95% CI: 0.46, 0.85; P for trend = 0.006) in women and men combined, 0.55 (95% CI: 0.25, 1.22; P for trend = 0.06) in women, and 0.64 (95% CI: 0.46, 0.89; P for trend = 0.03) in men. The intake of milk or cheese was not associated with bladder cancer risk.
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| 25. |
- Augsten, Martin, et al.
(författare)
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CXCL14 is an autocrine growth factor for fibroblasts and acts as a multi-modal stimulator of prostate tumor growth
- 2009
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 106:9, s. 3414-3419
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Tidskriftsartikel (refereegranskat)abstract
- This study explored the role of secreted fibroblast-derived factors in prostate cancer growth. Analyses of matched normal and tumor tissue revealed up-regulation of CXCL14 in cancer-associated fibroblasts of a majority of prostate cancer. Fibroblasts over-expressing CXCL14 promoted the growth of prostate cancer xenografts, and increased tumor angiogenesis and macrophage infiltration. Mechanistic studies demonstrated that autocrine CXCL14-stimulation of fibroblasts stimulate migration and ERK-dependent proliferation of fibroblasts. CXCL14-stimulation of monocyte migration was also demonstrated. Furthermore, CXCL14-producing fibroblasts, but not recombinant CXCL14, enhanced in vitro proliferation and migration of prostate cancer cells and in vivo angiogenesis. These studies thus identify CXCL14 as a novel autocrine stimulator of fibroblast growth and migration, with multi-modal tumor-stimulatory activities. In more general terms, our findings suggest autocrine stimulation of fibroblasts as a previously unrecognized mechanism for chemokine-mediated stimulation of tumor growth, and suggest a novel mechanism whereby cancer-associated fibroblasts achieve their pro-tumorigenic phenotype.
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| 26. |
- Dreifaldt, Ann Charlotte, 1964-
(författare)
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Epidemiological aspects on malignant diseases in childhood
- 2006
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The trends of malignant diseases in children aged 0 to 14 years, reported to the Swedish Cancer Registry 1960–1998 (n=9 298) were analyzed. The most common diagnoses were leukemia, 29.7%, tumors of the central nervous system (CNS), 27.6%, and lymphomas, 10.2%. The average annual incidence rate of childhood malignant diseases 1990–1998 was 16.19/100 000 person-years. Average annual change in incidence rate of all childhood cancer was +1.01% (95% confidence interval (CI)=0.80-1.22). Statistically significant increase was seen for leukemia +0.85% (95% CI=0.42–1.28), lymphomas +1.87% (95% CI=1.17–2.58), CNS tumors +1.45% (95% CI=1.02–1.88), sympathetic nervous system tumors +1.61% (95% CI=0.79–2.44), hepatic tumors +2.62% (95% CI=2.02–3.21), and germ cell and gonadal tumors +1.21% (95% CI=0.23–2.19). Children are exposed to persistent organic pollutants (POPs) during fetal life and breast-feeding. In a case-control study including cases of childhood cancer reported to the Cancer Registry 1988–1991 (n=962) we used breastfeeding duration as a surrogate for exposure to POPs. One matched control per case was used. Information on breast-feeding, vaccinations and chronic illness was collected from copies of the children’s Child Health Center records. Overall, breast-feeding did not affect the risk of childhood cancer, OR=1.0 (95% CI=0.7–1.3) using breast-feeding up to one month as reference. For non-Hodgkin lymphoma (NHL) OR for breast-feeding for >1 month yielded OR=5.0 (95% CI=1.1–23). No association was seen between preschool vaccinations and childhood cancer except for lymphomas and measles/measles-mumps-rubella vaccination, OR=0.2 (95% CI=0.1–0.6). Increased risk of all cancer was found for congenital malformations, OR=1.7 (95% CI=0.97–2.9), especially of leukemia, OR=3.0 (95% CI=1.5–5.8). Children with disorders of brain function had an increased risk of all cancer, OR=6.0 (95% CI=1.3–27), especially of brain tumors, OR=10 (95% CI=1.3–78). A childhood population expected to be more exposed to POPs is children of fishermen. In a register-based study, the cancer incidence rates in a cohort of fishermen children (at age 0-19 years) were compared to the rates of referent children. A modestly increased incidence rate ratio (IRR) of childhood cancer was found, IRR=1.38 (95% CI=0.96–2.00) and an increased IRR for acute lymphoid leukemia, IRR=2.65 (95% CI=1.005–6.97). In west coast fishermen children, an increased IRR was observed for NHL, IRR=3.19 (95% CI=0.98–10.4).
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| 27. |
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| 28. |
- Carlsson, Christina, et al.
(författare)
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Benefits from membership in cancer patient associations: relations to gender and involvement.
- 2006
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Ingår i: Acta oncologica. - : Informa UK Limited. - 0284-186X .- 1651-226X. ; 45:5, s. 559-563
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Tidskriftsartikel (refereegranskat)abstract
- Cancer patient associations report a growing number of members and increasing possibilities to influence health care, but knowledge about the members' views on the benefit of involvement is scarce. We therefore investigated how members (n = 1742) of Swedish patient associations for breast cancer and prostate cancer rate the benefit of membership for their physical and psychological well-being and social adjustment to cancer. Using a scoring scale, 2/3 of the members reported that membership had benefit for psychological well-being, whereas half of the members reported benefit for physical well-being and social adjustment. Individuals who had been actively involved in board work and/or contact person activities within the associations reported significantly more benefit for all three parameters. Gender differences were observed with men, represented by individuals affected by prostate cancer, reporting greater benefit for all three parameters, although especially evident for psychological well-being. Individuals who obtained membership within two years of diagnosis reported greater benefit for psychological well-being and social adjustment compared to those who became members later. In conclusion, members in patient associations for cancer report benefit particularly for their psychological well-being and actively involved members and men affected by prostate cancer perceive the greatest benefit from membership.
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| 29. |
- Krzemieniecki, Krzysztof, et al.
(författare)
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Targeting of solid tumors and blood malignancies by antibody-based therapies - EGFR-pathway as an example
- 2006
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Ingår i: Central European Journal of Biology. - : Versita. - 1895-104X .- 1644-3632. ; 1:2, s. 167-182
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Tidskriftsartikel (refereegranskat)abstract
- A well-coordinated interaction between extracellular signals and intracellular response forms the basis of life within multicellular organisms, with growth factors playing a crucial role in these interactions. Discoveries in recent years have shown that components of the Epidermal Growth Factor (EGF) signaling system have frequently been used by cancer cells to autonomously provide survival and proliferation signals. The main focus of this review is the ErbB epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases including ErbB1/EGFR, ErbB2/HER2/neu, ErbB3/HER3, and ErbB4/HER4 as therapeutic targets. Since the ErbB receptor family regulates cell proliferation through the Ras-mitogen-activated protein kinase (RAS/MAPK) pathway, and cell survival and transformation through the phosphatidylinositol 3-kinase (PI3K/AKT) pathway, pharmacological targeting of these pathways is also discussed. We will also address the clinical studies that have been conducted to evaluate antibody-based therapies mostly on solid tumors and hematologic malignancies. (c) Versita Warsaw and Springer-Verlag Berlin Heidelberg. All rights reserved.
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| 30. |
- Bergman, Annika, et al.
(författare)
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A high frequency of germline BRCA1/2 mutations in western Sweden detected with complementary screening techniques
- 2005
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Ingår i: Familial Cancer. - : Springer. - 1389-9600 .- 1573-7292. ; 4:2, s. 89-96
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Tidskriftsartikel (refereegranskat)abstract
- Dominant inheritance is presumed in 6-10% of breast and ovarian cancers. Mutations in BRCA1 and BRCA2 genes are the most commonly identified causative genes in such families. The frequency of mutation carriers with breast/ovarian cancer depends on the population studied, and display considerable variation that coincides with ethnic and geographical diversity. Mutation analyses were performed in 143 families registered at the Cancer Genetic Counseling Clinic of western Sweden. In a thorough mutation screening procedure, the entire BRCA1 and BRCA2 genes were analyzed using a combination of complementary mutation detection techniques. Mutations in either BRCA1 or BRCA2 were detected in 36% (52 out of 143) of all screened families. All families were clinically evaluated regarding age at diagnosis, type of cancer and number of cancer cases in the family. Among high-risk families, the mutation detection rate was 39% (46 out of 117). The detection rate observed among families with cases of ovarian cancer (42 out of 62, 68%), was substantially higher than in families with only breast cancer (10 out of 81, 12%). Age at ovarian cancer did not seem to have an effect on the detection rate. The analyses revealed 11 frameshift mutations, 4 nonsense mutations and 2 large deletions. Notably, the BRCA1 c.3171ins5 mutation accounted for 34 of 52 (65%) identified mutations. Seven mutations are novel: BRCA1c.409_410del; c.1912T>G; c.2228_2229del; c.3029delA; c.3433delA, a large deletion covering exons 1-3 of BRCA1and one BRCA2 mutation; BRCA2c.6287_6290del. We have shown that the founder mutation BRCA1 c.3171ins5 has a great influence on western Swedish breast/ovarian cancer families along with a high number of mutations unique for the region. In order to achieve a high mutation detection rate we suggest a combination of several detection techniques.
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