Pauliina Kronqvist

University of Turku, Turku, Province of Western Finland, Finland

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Publications (54)185.12 Total impact

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    ABSTRACT: Background:Cdc20 is an essential component of cell division and responsible for anaphase initiation regulated by securin degradation. Cdc20 function is strongly regulated by the spindle assembly checkpoint to ensure the timely separation of sister chromatids and integrity of the genome. We present the first results on Cdc20 in a large clinical breast cancer material.Methods:The study was based on 445 breast cancer patients with up to 20 years of follow-up (mean 10.0 years). DNA content was determined by image cytometry on cell imprints, and Cdc20 and securin immunohistochemistry on tissue microarrays of breast cancer tissue.Results:In our results, high Cdc20 and securin expression was associated with aneuploid DNA content. In prognostic analyses, high Cdc20 immunoexpression alone and in combination with high securin immunoexpression indicated aggressive course of disease and up to 6.8-fold (P<0.001) risk of breast cancer death. Particularly, high Cdc20 and securin immunoexpression identified a patient subgroup with extremely short, on average 2.4 years, breast cancer survival and triple-negative breast cancer (TNBC) subtype.Conclusions:We report for the first time the association of high Cdc20 and securin immunoexpression with extremely poor outcome of breast cancer patients. Our experience indicates that Cdc20 and securin are promising candidates for clinical applications in breast cancer prognostication, especially in the challenging prognostic decisions of TNBC.British Journal of Cancer advance online publication, 22 May 2014; doi:10.1038/bjc.2014.252 www.bjcancer.com.
    British journal of cancer. 05/2014;
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    ABSTRACT: Cell cycle regulators cdc27 and securin participate in control of the mitotic checkpoint and survey the mitotic spindle to maintain chromosomal integrity. This is achieved by their functions in metaphase-anaphase transition, DNA damage repair, enhancement of mitotic arrest and apoptosis. We report on the roles of cdc27 and securin in aneuploidy and prognosis of breast cancer. The study comprises 429 breast cancer patients with up to 22 years of follow-up. DNA content was determined by image cytometry, and immunopositivity for cdc27 and securin was based on tissue microarrays. An inverse association between cdc27 and securin expression was observed in both image cytometric and immunohistochemical analyses. Low cdc27 and high securin expression identified patients with significant difference in disease outcome. Cdc27 and securin immunoexpression identified patients at risk of early cancer death within five years from diagnosis. In multivariate analysis, the combination of cdc27 and securin immunohistochemistry was the strongest predictor of cancer death after lymph node status. We demonstrate, for the first time in human breast cancer, the prognostic value of cdc27 and securin immunohistochemistry. Cdc27 and securin appear promising biomarkers for applications in predicting disease progression, prognostication of individual patients and potential in anti-mitotic drug development.
    Apmis 06/2013; · 2.07 Impact Factor
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    ABSTRACT: Over the years, the role and extent of the basic sciences in medical curricula have been challenged by research on clinical expertise, clinical teachers, and medical students, as well as by the development and diversification of the medical curricula themselves. The aim of this study was to examine how prior knowledge of basic histology and histopathology among students predicts early learning of diagnostic pathology. Participants (N=118, representing 91% of the full student cohort) were medical students at the University of Turku, Finland. Data were collected during two preclinical courses that students attended in their first and second years of medical school. The measurements included tests on biomedical and clinical knowledge and a performance test in diagnostic pathology. Second-year performance on the diagnostic pathology examinations was predicted by the students' prior knowledge of histology, but not by the students' prior knowledge of histopathology. Although earlier research has demonstrated similar results in studies with shorter longitudinal designs, the present study demonstrates that the effect remains even if there is a considerably long time delay (a year) between the measurements, thus confirming the long-term value of basic science studies in the preclinical phase. Anat Sci Educ. © 2013 American Association of Anatomists.
    Anatomical Sciences Education 03/2013;
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    ABSTRACT: ADAM12 is a metalloprotease implicated in cancer progression. ADAM12 can activate membrane-anchored proteins, such as sonic hedgehog, Delta-like 1, and certain epidermal growth factor receptor ligands, through a process called ectodomain shedding. We screened several membrane-anchored proteins to further dissect the substrate profile of ADAM12-mediated ectodomain shedding, and found shedding of five previously unreported substrates (Kitl1, VE-cadherin, Flk-1, Tie-2, and VCAM-1), of which the latter four are specifically expressed by endothelial cells. We also observed that ADAM12 expression was increased in the tumour vasculature of infiltrating ductal carcinoma of the human breast as compared with little to no expression in normal breast-tissue vasculature, suggesting a role for ADAM12 in tumour vessels. These data prompted us to further evaluate ADAM12-mediated shedding of two endothelial cell proteins, VE-cadherin and Tie-2. Endogenous ADAM 12 expression was very low in cultured endothelial cells, but was significantly increased by cytokine stimulation. In parallel, the shed form of VE-cadherin was elevated in such cytokine-stimulated endothelial cells, and ADAM12 siRNA knockdown reduced cytokine-induced shedding of VE-cadherin. In conclusion, our data demonstrate a role for ADAM12 in ectodomain shedding of several membrane-anchored endothelial proteins. We speculate that this process may have importance in tumour neovascularization or/and tumour-cell extravasation.
    Biochemical Journal 03/2013; · 4.65 Impact Factor
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    ABSTRACT: Notch signaling is frequently hyperactivated in breast cancer, but how the enhanced signaling contributes to the tumor process is less well understood. In this report, we identify the proinflammatory cytokine interleukin-6 (IL-6) as a novel Notch target in breast tumor cells. Enhanced Notch signaling upregulated IL-6 expression, leading to activation of autocrine and paracrine Janus kinase/signal transducers and activators of transcription signaling. IL-6 upregulation was mediated by non-canonical Notch signaling, as it could be effectuated by a cytoplasmically localized Notch intracellular domain and was independent of the DNA-binding protein CSL. Instead, Notch-mediated IL-6 upregulation was controlled by two proteins in the nuclear factor (NF)-κB signaling cascade, IKKα and IKKβ (inhibitor of nuclear factor kappa-B kinase subunit alpha and beta, respectively), as well as by p53. Activation of IL-6 by Notch required IKKα/IKKβ function, but interestingly, did not engage canonical NF-κB signaling, in contrast to IL-6 activation by inflammatory agents such as lipopolysaccharide. With regard to p53 status, IL-6 expression was upregulated by Notch when p53 was mutated or lost, and restoring wild-type p53 into p53-mutated or -deficient cells abrogated the IL-6 upregulation. Furthermore, Notch-induced transcriptomes from p53 wild-type and -mutated breast tumor cell lines differed extensively, and for a subset of genes upregulated by Notch in a p53-mutant cell line, this upregulation was reduced by wild-type p53. In conclusion, we identify IL-6 as a novel non-canonical Notch target gene, and reveal roles for p53 and IKKα/IKKβ in non-canonical Notch signaling in breast cancer and in the generation of cell context-dependent diversity in the Notch signaling output.Oncogene advance online publication, 26 November 2012; doi:10.1038/onc.2012.517.
    Oncogene 11/2012; · 8.56 Impact Factor
  • Oncogene 11/2012; · 8.56 Impact Factor
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    Laura Helle, Markus Nivala, Pauliina Kronqvist
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    ABSTRACT: The adoption of virtual microscopy at the University of Turku, Finland, created a unique real-world laboratory for exploring ways of reforming the learning environment. The purpose of this study was to evaluate the students' reactions and the impact of a set of measures designed to boost an experimental group's understanding of abnormal histology through an emphasis on knowledge of normal cells and tissues. The set of measures included (1) digital resources to review normal structures and an entrance examination for enforcement, (2) digital course slides highlighting normal and abnormal tissues, and (3) self-diagnostic quizzes. The performance of historical controls was used as a baseline, as previous students had never been exposed to the above-mentioned measures. The students' understanding of normal histology was assessed in the beginning of the module to determine the impact of the first set of measures, whereas that of abnormal histology was assessed at the end of the module to determine the impact of the whole set of measures. The students' reactions to the instructional measures were assessed by course evaluation data. Additionally, four students were interviewed. Results confirmed that the experimental group significantly outperformed the historical controls in understanding normal histology. The students held favorable opinions on the idea of emphasizing normal structures. However, with regards to abnormal histology, the historical controls outperformed the experimental group. In conclusion, allowing students access to high-quality digitized materials and boosting prerequisite skills are clearly not sufficient to boost final competence. Instead, the solution may lie in making students externally accountable for their learning throughout their training. Anat Sci Educ. © 2012 American Association of Anatomists.
    Anatomical Sciences Education 08/2012;
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    ABSTRACT: Securin is known to participate in maintaining chromosomal integrity during the cell cycle through regulation of metaphase-anaphase transition, DNA damage repair, and apoptosis. The aim of this study was to investigate the role of securin in aneuploidy and prognosis in human breast cancer. The study was based on 603 breast cancer patients with up to 20 years of follow-up. DNA content was determined by image cytometry on cell imprints, and securin immunohistochemistry was performed on tissue microarrays of breast cancer tissue. We show, for the first time in human breast cancer, that high-level securin expression predicts abnormal DNA content, with up to 9.8-fold odds for aneuploid DNA content (P = 0.0007). Securin also shows strong independent prognostic value for disease-specific survival, with a significant difference in survival time between patients with low-level and high-level securin expression. The main result of the present study is the association of aneuploidy and securin expression. According to our results, securin immunohistochemistry is also a potential new prognosticator for treatment decisions concerning breast cancer patients.
    Histopathology 03/2012; 60(4):586-96. · 2.86 Impact Factor
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    ABSTRACT: Notch signaling is frequently hyperactivated in breast cancer, but how the enhanced signaling contributes to the tumor process is less well understood. In this report, we identify the proinflammatory cytokine interleukin-6 (IL-6) as a novel Notch target in breast tumor cells. Enhanced Notch signaling upregulated IL-6 expression, leading to activation of autocrine and paracrine Janus kinase/signal transducers and activators of transcription signaling. IL-6 upregulation was mediated by non-canonical Notch signaling, as it could be effectuated by a cytoplasmically localized Notch intracellular domain and was independent of the DNA-binding protein CSL. Instead, Notch-mediated IL-6 upregulation was controlled by two proteins in the nuclear factor (NF)-kB signaling cascade, IKKa and IKKb (inhibitor of nuclear factor kappa-B kinase subunit alpha and beta, respectively), as well as by p53. Activation of IL-6 by Notch required IKKa/IKKb function, but interestingly, did not engage canonical NF-kB signaling, in contrast to IL-6 activation by inflammatory agents such as lipopolysaccharide. With regard to p53 status, IL-6 expression was upregulated by Notch when p53 was mutated or lost, and restoring wild-type p53 into p53-mutated or -deficient cells abrogated the IL-6 upregulation. Furthermore, Notch-induced transcriptomes from p53 wild-type and -mutated breast tumor cell lines differed extensively, and for a subset of genes upregulated by Notch in a p53-mutant cell line, this upregulation was reduced by wild-type p53. In conclusion, we identify IL-6 as a novel non-canonical Notch target gene, and reveal roles for p53 and IKKa/IKKb in non-canonical Notch signaling in breast cancer and in the generation of cell context-dependent diversity in the Notch signaling output.
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    ABSTRACT: A switch from oxidative phosphorylation to glycolysis is frequently observed in cancer cells and is linked to tumor growth and invasion, but the underpinning molecular mechanisms controlling the switch are poorly understood. In this report we show that Notch signaling is a key regulator of cellular metabolism. Both hyper- and hypoactivated Notch induce a glycolytic phenotype in breast tumor cells, although by distinct mechanisms: hyperactivated Notch signaling leads to increased glycolysis through activation of the phosphatidylinositol 3-kinase/AKT serine/threonine kinase pathway, whereas hypoactivated Notch signaling attenuates mitochondrial activity and induces glycolysis in a p53-dependent manner. Despite the fact that cells with both hyper- and hypoactivated Notch signaling showed enhanced glycolysis, only cells with hyperactivated Notch promoted aggressive tumor growth in a xenograft mouse model. This phenomenon may be explained by that only Notch-hyperactivated, but not -hypoactivated, cells retained the capacity to switch back to oxidative phosphorylation. In conclusion, our data reveal a role for Notch in cellular energy homeostasis, and show that Notch signaling is required for metabolic flexibility.
    Proceedings of the National Academy of Sciences 11/2011; 108(46):18814-9. · 9.81 Impact Factor
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    ABSTRACT: Expression of ADAM12 is low in most normal tissues but is markedly increased in numerous human cancers, including breast carcinomas. We have previously shown that overexpression of ADAM12 accelerates tumor progression in a mouse model of breast cancer (PyMT). In this study, we found that ADAM12 deficiency reduces breast tumor progression in the PyMT model. However, the catalytic activity of ADAM12 seems to be dispensable for its tumor-promoting effect. Interestingly, we show that ADAM12 endogenously expressed in tumor-associated stroma in the PyMT model does not influence tumor progression, but that ADAM12 expression by tumor cells is necessary for tumor progression in these mice. This finding is consistent with our observation that in human breast carcinoma, ADAM12 is almost exclusively located in tumor cells and, only rarely, seen in the tumor-associated stroma. We hypothesized, however, that the tumor-associated stroma may stimulate ADAM12 expression in tumor cells, on the basis of the fact that TGF-β1 stimulates ADAM12 expression and is a well-known growth factor released from tumor-associated stroma. TGF-β1 stimulation of ADAM12-negative Lewis lung tumor cells induced ADAM12 synthesis, and growth of these cells in vivo induced more than 200-fold increase in ADAM12 expression. Our observation that ADAM12 expression is significantly higher in the terminal duct lobular units (TDLU) adjacent to human breast carcinoma compared with TDLUs found in normal breast tissue supports our hypothesis that tumor-associated stroma triggers ADAM12 expression.
    Molecular Cancer Research 08/2011; 9(11):1449-61. · 4.35 Impact Factor
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    ABSTRACT: Syndecan proteoglycans may be key regulators of tumor invasion and metastasis because this four-member family of transmembrane receptors regulates cell adhesion, proliferation, and differentiation. Their expression can also serve as prognostic markers. In breast carcinomas, syndecan-1 overexpression correlates with poor prognosis and aggressive phenotype. Syndecan-4 is expressed in most breast carcinoma cell lines, but its role in malignancy is unclear. A possible relationship between syndecan-1 and syndecan-4 expression and established prognostic factors in breast carcinomas was examined. Duplicate samples of 114 benign and malignant breast disease cases were stained for the two syndecans. Clinicopathological information was available for all cases. Syndecan-1 was detected in 72.8% of cases, with significant association between its expression and histological tumor type (p<0.05) and high grade tumors (p<0.05). Syndecan-4 was expressed in 66.7% of cases; expression correlated significantly with positive estrogen (p<0.01) and progesterone (p<0.01) receptor status. Independent expression of the two syndecans was noted from an analysis of single and double positive cases. There was a statistical relationship between syndecan-1 presence in high-grade tumors and absence of syndecan-4, whereas syndecan-4 presence in cases positive for estrogen and progesterone receptor associated with syndecan-1 absence. These syndecans may, therefore, have distinct roles in regulating breast carcinoma cell behavior.
    Journal of Histochemistry and Cytochemistry 03/2011; 59(6):615-29. · 2.26 Impact Factor
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    ABSTRACT: Virtual microscopy is being introduced in medical education as an approach for learning how to interpret information in microscopic specimens. It is, however, far from evident how to incorporate its use into existing teaching practice. The aim of the study was to explore the consequences of introducing virtual microscopy tasks into an undergraduate pathology course in an attempt to render the instruction more process-oriented. The research questions were: 1) How is virtual microscopy perceived by students? 2) Does work on virtual microscopy tasks contribute to improvement in performance in microscopic pathology in comparison with attending assistant-led demonstrations only? During a one-week period, an experimental group completed three sets of virtual microscopy homework assignments in addition to attending demonstrations. A control group attended the demonstrations only. Performance in microscopic pathology was measured by a pre-test and a post-test. Student perceptions of regular instruction and virtual microscopy were collected one month later by administering the Inventory of Intrinsic Motivation and open-ended questions. The students voiced an appreciation for virtual microscopy for the purposes of the course and for self-study. As for learning gains, the results indicated that learning was speeded up in a subgroup of students consisting of conscientious high achievers. The enriched instruction model may be suited as such for elective courses following the basic course. However, the instructional model needs further development to be suited for basic courses.
    Diagnostic Pathology 01/2011; 6 Suppl 1:S8. · 1.85 Impact Factor
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    ABSTRACT: OBJECTIVES There has been long-standing controversy regarding aptitude testing and selection for medical education. Visual perception is considered particularly important for detecting signs of disease as part of diagnostic procedures in, for example, microscopic pathology, radiology and dermatology and as a component of perceptual motor skills in medical procedures such as surgery. In 1968 the Perceptual Ability Test (PAT) was introduced in dental education. The aim of the present pilot study was to explore possible predictors of performance in diagnostic classification based on microscopic observation in the context of an undergraduate pathology course. METHODS A pre- and post-test of diagnostic classification performance, test of visual perceptual skill (Test of Visual Perceptual Skills, 3rd edition [TVPS-3]) and a self-report instrument of personality (Big Five Personality Inventory) were administered. In addition, data on academic performance (performance in histology and cell biology, a compulsory course taken the previous year, in addition to performance on the microscopy examination and final examination) were collected. RESULTS The results indicated that one personality factor (Conscientiousness) and one element of visual perceptual ability (spatial relationship awareness) predicted performance on the pre-test. The only factor to predict performance on the post-test was performance on the pre-test. Similarly, the microscopy examination score was predicted by the pre-test score, in addition to the histology and cell biology grade. The course examination score was predicted by two personality factors (Conscientiousness and lack of Openness) and the histology and cell biology grade. CONCLUSIONS Visual spatial ability may be related to performance in the initial phase of training in microscopic pathology. However, from a practical point of view, medical students are able to learn basic microscopic pathology using worked-out examples, independently of measures of personality or visual perceptual ability. This finding should reassure students about their abilities to improve with training independently of their scores on tests on basic abilities and personality.
    Medical Education 06/2010; 44(6):621-9. · 3.55 Impact Factor
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    ABSTRACT: The study focuses on p120catenin, a regulator of cell adhesion, which has previously been described in many malignancies and suggested with a role in invasion and metastatic behaviour. In this study, we investigate the role of altered immunoexpression of p120catenin isoforms in the prognosis of invasive breast cancer (n = 351). We used cDNA microarrays to screen differences in gene expression in invasive breast cancer in general, and between local and metastasized disease particularly. On this basis, we performed p120catenin immunohistochemistry in order to confirm the prognostic value of p120catenin isoforms on tissue microarrays comprising 341 patients from the era of mammographic screening, directed to modern surgical and oncological treatments, and followed-up for maximum of 20 years. In cDNA microarray analysis, p120catenin was discovered down-regulated along with E-cadherin and alpha-catenin. In addition, p120catenin distinguished metastasized breast cancer from local disease. Immunohistochemistry confirmed the value of p120catenin as an independent prognosticator of breast cancer survival. In our results, p120catenin was associated with 3.7-fold risk of breast cancer death in multivariate Cox's regression analyses adjusted for the established prognosticators of breast cancer (p = 0.039). Particularly, the long isoform of p120catenin predicted metastatic disease (p = 0.029). The present paper is the first report on p120catenin in invasive breast cancer based on a well-characterized patient material with long-term follow-up. We observed altered expression of p120catenin isoforms in invasive breast cancer and, in our material, the decrease in p120 immunoexpression was significantly associated with poor outcome of disease.
    Journal of Cancer Research and Clinical Oncology 02/2010; 136(9):1377-87. · 2.91 Impact Factor
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    ABSTRACT: Securin is a recently recognised oncogene with multiple known functions in initiation, progression and cell cycle regulation in several malignant diseases, including breast carcinoma. In this paper, the prognostic value of securin is evaluated by immunohistochemistry in 310 patients diagnosed with invasive breast cancer during a mammographic screening programme in Central Finland. All patients were directed to modern surgical and oncological treatments and were followed up for a maximum of 20 years. Our results suggest that securin immunopositivity is an independent prognosticator of invasive breast cancer. In our study, securin predicted breast cancer-specific survival among all cases of invasive breast cancer and subgroups divided according to histological type, Ki-67 proliferation status and tumour size. Especially in a multivariate analysis standardised for axillary lymph node status, patient's age and tumour size at the time of diagnosis, securin immunopositivity indicated a 13.1-fold risk of breast cancer death (P=0.024) among invasive ductal breast carcinomas with low Ki-67 positivity. Our present and previous results suggest that securin could be useful in clinical pathology to intensify the power of the established prognosticators of invasive breast cancer and, especially, to assist in identifying patients with a more favourable outcome than that indicated by Ki-67 alone.
    British Journal of Cancer 09/2009; 101(6):1005-10. · 5.08 Impact Factor
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    ABSTRACT: Prolyl hydroxylase domain proteins constitute a family of oxygen sensors that regulate the expression of hypoxia-inducible factor-1 alpha (HIF-1alpha), which mediates transcription of many genes under low oxygen concentration. PHD2 (Prolyl hydroxylase domain protein 2) isoform is the main regulator of HIF-1alpha degradation in normoxia and mild hypoxia. The aim of our study was to evaluate the relationship between expression of PHD2 and radiosensitivity in squamous cell cancer of the head and neck (HNSCC). Paraffin embedded sections from untreated primary tumours were obtained for immunohistochemistry in 48 HNSCC patients scheduled for preoperative radiotherapy (RT). Nuclear expression of PHD2 was evaluated as a percentage of tumour cells showing positively stained nucleus. RT was a split-course accelerated hyperfractionated regimen (1.6 Gy twice a day) in 15 patients and standard in 33 patients. Viability of cancer cells was routinely evaluated histologically from resected tumours at planned surgery 3-4 weeks after RT. The follow-up time after multimodality treatment was five years or until death. PHD2 expression was low in normal tissues and well differentiated tumours. The expression was increased and predominantly nuclear in poorly differentiated tumours. In tumours later found to be sterilised by RT, nuclear PHD2 expression was markedly lower as compared to tumours showing viable cells at surgery (p = 0.04). A low nuclear staining of PHD2 (<10% of PHD2-positive nuclei) in the primary tumour was found to associate with good radiation response (p = 0.005). We found low PHD2 expression and in particular low nuclear expression to predict a favourable response to RT. Therefore, nuclear PHD2 expression may act as a surrogate marker for radiation resistance in HNSCC.
    International Journal of Radiation Biology 07/2009; 85(10):900-8. · 1.84 Impact Factor
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    ABSTRACT: Mammographic screening is associated with a reduced risk of breast cancer recurrence. The objective of the study was to evaluate treatment costs due to breast cancer recurrence in relation to patients' use of mammographic screening, consecutively collected in a defined population. The study included 418 women exposed to screening and 109 women unexposed to screening diagnosed with stage I-III breast cancer. During the first eight years after primary diagnosis, 19% (N=80) of the exposed women and 33% (N=36) of the unexposed women developed recurrent disease, P=0.002. In the exposed group, 41% of the 8-year treatment costs were for the treatment of patients who developed recurrent disease, compared with 52% in the unexposed group, P=0.039. Among the relapsed patients, the mean post-recurrence costs were EUR14,950, accounting for 65% of their total 8-year costs. The mean post-recurrence costs were comparable for both exposure groups irrespective of the detection method.
    Breast (Edinburgh, Scotland) 11/2008; 17(6):550-4. · 2.09 Impact Factor
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    ABSTRACT: We introduce a new proliferation marker, securin (pituitary tumour-transforming 1 (PTTG1)), analysed in invasive ductal breast carcinomas by cDNA microarrays and immunohistochemistry. In cDNA microarray of a total of 4000 probes of genes, securin was revealed with a significant change in expression among the several proliferation-related genes studied. The value of securin as a proliferation marker was verified immunohistochemically (n=44) in invasive ductal breast cancer. In follow-up analyses of the sample of patients, the prognostic value of securin was compared with the established markers of breast cancer proliferation, Ki-67 and mitotic activity index (MAI). Our results of a small sample of patients suggest that low securin expression identifies a distinct subgroup of more favourable outcome among patients with high Ki-67 immunoexpression or high MAI. In univariate analysis of Cox's regression, 10-unit increment of securin immunopositivity was associated with a 2.3-fold overall risk of death due to breast cancer and a 7.1-fold risk of death due to breast cancer in the sample of patients stratified according to the cutoff points of 10 and 20% of securin immunopositivity. We suggest that securin immunostaining is a promising and clinically applicable proliferation marker. The finding urges further prognostic studies with a large sample of patients.
    British Journal of Cancer 08/2008; 99(2):335-40. · 5.08 Impact Factor
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    ABSTRACT: In order to meet the changing needs of health care, the University of Turku has introduced a graduate entry programme aimed at students with previous education and experience in health care professions. In this study, we look at the study performance of students with different educational backgrounds with special emphasis on graduate entry students. We surveyed the study orientations of 145 first-year medical students with different educational backgrounds in the Medical Faculty of the University of Turku, Finland. Special emphasis was placed on graduate entry students (n = 25) with previous education and work experience in health care professions. The students were characterized based on student records and the questionnaire Inventory of General Study Orientation (IGSO). Our results revealed that after the first year of medical studies the graduate entry students showed exceptionally strong theoretical and practical commitment to their studies with a strong work-life orientation which makes them a distinct group among medical students.
    Medical Teacher 11/2007; 29(8):836-8. · 1.82 Impact Factor

Publication Stats

646 Citations
185.12 Total Impact Points

Institutions

  • 1995–2014
    • University of Turku
      • • Department of Pathology
      • • Department of Internal Medicine
      Turku, Province of Western Finland, Finland
  • 2013
    • Turku University Hospital
      Turku, Province of Western Finland, Finland
  • 2002–2005
    • University of Copenhagen
      • Eye Pathology Institute
      Copenhagen, Capital Region, Denmark