| 21. |
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| 22. |
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| 23. |
- Erlinge, Sam, et al.
(författare)
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Can vertebrate predators regulate their prey?
- 1984
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Ingår i: The American Naturalist. ; 123:1, s. 125-133
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Tidskriftsartikel (refereegranskat)abstract
- Whether vertebrate predators can regulate their prey or not has long been a controversial question. At the one extreme it has been claimed that predators have no impact on prey numbers but consume only a doomed surplus (Errington 1946), and at the other that predators strongly interact with their prey causing either stable equilibria or cycles (Tanner 1975; Keith et al. 1977). However,.there are no field studies showing a regulatory effect of predation among vertebrates. Here we report on such a study.
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| 24. |
- Erlinge, S, et al.
(författare)
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Predation on brown hare and ring-necked pheasant populations on southern Sweden
- 1984
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Ingår i: Holarctic Ecology. ; 7:3, s. 300-304
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Tidskriftsartikel (refereegranskat)abstract
- in an open field area in southern Sweden. Biomass and numbers of hares and pheasants eaten by the predators were calculated from data on food habits, food requirements, and numbers of the mammalian and avian predators present (11 species). At the same time estimates of numbers and production of hares and pheasants were obtained. At least 40% of the estimated annual production of hares and almost 60% of subadult-adultp heasants in autumn were consumed by the predators. Estimated numbers of hares and pheasants taken by the predators greatly exceeded shootinga nd road mortality.F oxes and cats were the predominantp reda-tors on hares( about9 0%o f total harec onsumption). Foxesa ccountedf or aboutt wo-thirds of predation on pheasants; cats and goshawks were of secondary importance. Pheasant nests were preyed upon by hooded crows and also by badgers. Hares and pheasantsc ontributedo nly about 3 and 1%, respectively,o f the food of the predators.
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| 25. |
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| 26. |
- Gulis, K., et al.
(författare)
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A prospective cohort study identifying radiologic and tumor related factors of importance for breast conserving surgery after neoadjuvant chemotherapy
- 2023
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Ingår i: European Journal of Surgical Oncology. - : Elsevier BV. - 0748-7983. ; 49:7, s. 1189-1195
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Neoadjuvant chemotherapy (NAC) is an established treatment option for early breast cancer, potentially downstaging the tumor and increasing the eligibility for breast-conserving surgery (BCS). The primary aim of this study was to assess the rate of BCS after NAC, and the secondary aim was to identify predictors of application of BCS after NAC. Materials and methods: This was an observational prospective cohort study of 226 patients in the SCAN-B (Clinical Trials NCT02306096) neoadjuvant cohort during 2014–2019. Eligibility for BCS was assessed at baseline and after NAC. Uni- and multivariable logistic regression analyses were performed using covariates with clinical relevance and/or those associated with outcome (BCS versus mastectomy), including tumor subtype, by gene expression analysis. Results: The overall BCS rate was 52%, and this rate increased during the study period (from 37% to 52%). Pathological complete response was achieved in 69 patients (30%). Predictors for BCS were smaller tumor size on mammography, visibility on ultrasound, histological subtype other than lobular, benign axillary status, and a diagnosis of triple-negative or HER2-positive subtype, with a similar trend for gene expression subtypes. Mammographic density was negatively related to BCS in a dose-response pattern. In the multivariable logistic regression model, tumor stage at diagnosis and mammographic density showed the strongest association with BCS. Conclusion: The rate of BCS after NAC increased during the study period to 52%. With modern treatment options for NAC the potential for tumor response and BCS eligibility might further increase.
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| 27. |
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| 28. |
- Hamdi, Yosr, et al.
(författare)
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Association of breast cancer risk in BRCA1 and BRCA2 mutation carriers with genetic variants showing differential allelic expression : identification of a modifier of breast cancer risk at locus 11q22.3
- 2017
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Ingår i: Breast Cancer Research and Treatment. - : Springer Science and Business Media LLC. - 0167-6806 .- 1573-7217. ; 161:1, s. 117-134
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: Cis-acting regulatory SNPs resulting in differential allelic expression (DAE) may, in part, explain the underlying phenotypic variation associated with many complex diseases. To investigate whether common variants associated with DAE were involved in breast cancer susceptibility among BRCA1 and BRCA2 mutation carriers, a list of 175 genes was developed based of their involvement in cancer-related pathways. Methods: Using data from a genome-wide map of SNPs associated with allelic expression, we assessed the association of ~320 SNPs located in the vicinity of these genes with breast and ovarian cancer risks in 15,252 BRCA1 and 8211 BRCA2 mutation carriers ascertained from 54 studies participating in the Consortium of Investigators of Modifiers of BRCA1/2. Results: We identified a region on 11q22.3 that is significantly associated with breast cancer risk in BRCA1 mutation carriers (most significant SNP rs228595 p = 7 × 10−6). This association was absent in BRCA2 carriers (p = 0.57). The 11q22.3 region notably encompasses genes such as ACAT1, NPAT, and ATM. Expression quantitative trait loci associations were observed in both normal breast and tumors across this region, namely for ACAT1, ATM, and other genes. In silico analysis revealed some overlap between top risk-associated SNPs and relevant biological features in mammary cell data, which suggests potential functional significance. Conclusion: We identified 11q22.3 as a new modifier locus in BRCA1 carriers. Replication in larger studies using estrogen receptor (ER)-negative or triple-negative (i.e., ER-, progesterone receptor-, and HER2-negative) cases could therefore be helpful to confirm the association of this locus with breast cancer risk.
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| 29. |
- Haraldsson, K, et al.
(författare)
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BRCA2 germ-line mutations are frequent in male breast cancer patients without a family history of the disease
- 1998
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Ingår i: Cancer Research. - 1538-7445. ; 58:7, s. 71-1367
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Tidskriftsartikel (refereegranskat)abstract
- Breast cancer is a rare disease in men, affecting less than 0.1% of the male population. Two heritable gene defects have been associated with a predisposition to male breast cancer development, ie., germ-line mutations in the breast cancer susceptibility gene BRCA2 and the androgen receptor (AR) gene. In this study, the entire coding regions of BRCA2 and AR were screened for mutations in 34 consecutive male breast cancer patients. Five different truncating BRCA2 mutations were identified in 7 (21%) of the 34 cases, with all mutations being of germ-line origin. Three of the mutated cases carried the same mutation (4186delG), which has been found earlier in two Swedish families with multiple female breast cancer cases. Haplotype analysis supported a common ancestry of 4186delG. One mutation, 6503delTT, was found in a male carrying also a previously identified COOH-terminal polymorphic stop codon (Lys3326ter). No differences were seen between mutation carriers and noncarriers with respect to clinical stage and estrogen or progesterone receptor status. Mutation carriers tended to be younger at diagnosis. No germ-line AR mutations were found in the present material, but the number of AR polyglutamine repeats tended to be lower among mutation carriers. Most surprisingly, only one of the seven BRCA2 mutation carriers had a positive family history of breast cancer, suggesting a lower penetrance of some BRCA2 mutations or an influence of modifying factors for disease development in males and females. The present study implies that approximately one-fifth of all male breast cancer cases in the Swedish population are due to germ-line BRCA2 mutations.
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| 30. |
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