| 1. |
- Braian, Michael, et al.
(författare)
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Tolerance Measurements on Internal- and External-Hexagon Implants
- 2014
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Ingår i: International Journal of Oral & Maxillofacial Implants. - : Quintessence. - 0882-2786 .- 1942-4434. ; 29:4, s. 846-852
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: To measure the horizontal machining tolerances of the interface between internal-and external-hexagon implants and analogs with corresponding components after delivery from the manufacturer. These values may be a valuable tool for evaluating increasing misfit caused by fabrication, processing, and wear. Materials and Methods: Seven implants and seven analogs with external-and internal-hexagon connections (Biomet 3i) with corresponding prefabricated gold cylinders and gold screws, prefabricated cylindric plastic cylinders, and laboratory screws were studied. One set of components from the external and internal groups was measured manually and digitally. Measurements from the test subjects were compared with identical measurements from the virtual model to obtain threshold values. The virtual model was then used to obtain optimally oriented cuts. Results: The horizontal machining tolerances for castable plastic abutments on external implants were 12 +/- 89 mu m, and for internal implants they were 86 +/- 47 mu m. Tolerance measurements on prefabricated gold abutments for external implants were 44 +/- 9 mu m, and for internal implants they were 58 +/- 28 mu m. Conclusion: The groups with metallic components showed the smallest tolerance at < 50 mu m for the external group and < 90 mu m for the internal group. The prefabricated plastic cylinder groups ranged from < 100 mu m for external and < 130 mu m for internal connection.
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| 2. |
- Diogo Löfgren, Christina, et al.
(författare)
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A systematic review of methods to diagnose oral dryness and salivary gland function
- 2012
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Ingår i: BMC Oral Health. - : BioMed Central. - 1472-6831 .- 1472-6831. ; 12:29
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Tidskriftsartikel (refereegranskat)abstract
- Background The most advocated clinical method for diagnosing salivary dysfunction is to quantitate unstimulated and stimulated whole saliva (sialometry). Since there is an expected and wide variation in salivary flow rates among individuals, the assessment of dysfunction can be difficult. The aim of this systematic review is to evaluate the quality of the evidence for the efficacy of diagnostic methods used to identify oral dryness. Methods A literature search, with specific indexing terms and a hand search, was conducted for publications that described a method to diagnose oral dryness. The electronic databases of PubMed, Cochrane Library, and Web of Science were used as data sources. Four reviewers selected publications on the basis of predetermined inclusion and exclusion criteria. Data were extracted from the selected publications using a protocol. Original studies were interpreted with the aid of Quality Assessment of Diagnostic Accuracy Studies (QUADAS) tool. Results The database searches resulted in 224 titles and abstracts. Of these abstracts, 80 publications were judged to meet the inclusion criteria and read in full. A total of 18 original studies were judged relevant and interpreted for this review. In all studies, the results of the test method were compared to those of a reference method. Based on the interpretation (with the aid of the QUADAS tool) it can be reported that the patient selection criteria were not clearly described and the test or reference methods were not described in sufficient detail for it to be reproduced. None of the included studies reported information on uninterpretable/intermediate results nor data on observer or instrument variation. Seven of the studies presented their results as a percentage of correct diagnoses. Conclusions The evidence for the efficacy of clinical methods to assess oral dryness is sparse and it can be stated that improved standards for the reporting of diagnostic accuracy are needed in order to assure the methodological quality of studies. There is need for effective diagnostic criteria and functional tests in order to detect those individuals with oral dryness who may require oral treatment, such as alleviation of discomfort and/or prevention of diseases.
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| 3. |
- Diogo Löfgren, Christina, et al.
(författare)
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Screening for Oral Dryness in Relation to Salivary Flow Rate Addresses the Need for Functional Tests of Saliva
- 2010
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Ingår i: Oral health & preventive dentistry. - : Quintessence. - 1757-9996 .- 1602-1622. ; 8:3, s. 243-252
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: The aim of the present study was to assess the occurrence of reported subjective oral dryness in relation to objective sialometric values in a randomly selected group and a dental care-seeking group. Materials and Methods: A questionnaire assessing subjective oral dryness was sent out to a randomly selected sample of 200 individuals. The dental care-seeking group was recruited from among patients attending the Department of Oral Diagnostics, Malmo University. A total of 200 patients were asked to participate in the present study. In total, 312 individuals (78%) completed the survey and 157 individuals agreed to participate in the complementary clinical examination that included measures of salivary flow rate. Results: The reported subjective oral dryness was 20% and 28.6% for the randomly selected group and the dental care-seeking group, respectively. No statistically significant differences were found between the two study populations with regard to percentage of reported subjective oral dryness, and stimulated and unstimulated salivary flow rates (P > 0.05). In the dental care-seeking group, individuals reporting subjective oral dryness presented 'a small degree of abrasion in the dentine in the incisor region' to a greater extent (P < 0.05). No statistically significant association between subjective oral dryness and unstimulated and stimulated salivary flow rates was found in either of the studied populations (P > 0.05). Individuals identified with subjective or objective oral dryness presented to a greater extent a history of oral rehabilitation compared to individuals who showed no indication of oral dryness. Conclusions: No association between sialometric measures and subjective report of oral dryness was found in the present study.
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| 4. |
- Holm, Karolina, et al.
(författare)
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Characterisation of amplification patterns and target genes at chromosome 11q13 in CCND1-amplified sporadic and familial breast tumours.
- 2012
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Ingår i: Breast Cancer Research and Treatment. - : Springer Science and Business Media LLC. - 1573-7217 .- 0167-6806. ; 133:2, s. 583-594
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Tidskriftsartikel (refereegranskat)abstract
- Amplification of chromosomal region 11q13, containing the cell cycle regulatory gene CCND1, is frequently found in breast cancer and other malignancies. It is associated with the favourable oestrogen receptor (ER)-positive breast tumour phenotype, but also with poor prognosis and treatment failure. 11q13 spans almost 14 Mb and contains more than 200 genes and is affected by various patterns of copy number gains, suggesting complex mechanisms and selective pressure during tumour progression. In this study, we used 32 k tiling BAC array CGH to analyse 94 CCND1-amplified breast tumours from sporadic, hereditary, and familial breast cancers to fine map chromosome 11q13. A set containing 281 CCND1-non-amplified breast tumours was used for comparisons. We used gene expression data to further validate the functional effect of gene amplification. We identified six core regions covering 11q13.1-q14.1 that were amplified in different combinations. The major core contained CCND1, whereas two cores were found proximal of CCND1 and three distal. The majority of the CCND1-amplified tumours were ER-positive and classified as luminal B. Furthermore, we found that CCND1 amplification is associated with a more aggressive phenotype within histological grade 2 tumours and luminal A subtype tumours. Amplification was equally prevalent in familial and sporadic tumours, but strikingly rare in BRCA1- and BRCA2-mutated tumours. We conclude that 11q13 includes many potential target genes in addition to CCND1.
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| 5. |
- Holm, Karolina, et al.
(författare)
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Molecular subtypes of breast cancer are associated with characteristic DNA methylation patterns
- 2010
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Ingår i: Breast Cancer Research. - : Springer Science and Business Media LLC. - 1465-5411 .- 1465-542X. ; 12:3
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Five different molecular subtypes of breast cancer have been identified through gene expression profiling. Each subtype has a characteristic expression pattern suggested to partly depend on cellular origin. We aimed to investigate whether the molecular subtypes also display distinct methylation profiles. Methods: We analysed methylation status of 807 cancer-related genes in 189 fresh frozen primary breast tumours and four normal breast tissue samples using an array-based methylation assay. Results: Unsupervised analysis revealed three groups of breast cancer with characteristic methylation patterns. The three groups were associated with the luminal A, luminal B and basal-like molecular subtypes of breast cancer, respectively, whereas cancers of the HER2-enriched and normal-like subtypes were distributed among the three groups. The methylation frequencies were significantly different between subtypes, with luminal B and basal-like tumours being most and least frequently methylated, respectively. Moreover, targets of the polycomb repressor complex in breast cancer and embryonic stem cells were more methylated in luminal B tumours than in other tumours. BRCA2-mutated tumours had a particularly high degree of methylation. Finally, by utilizing gene expression data, we observed that a large fraction of genes reported as having subtype-specific expression patterns might be regulated through methylation. Conclusions: We have found that breast cancers of the basal-like, luminal A and luminal B molecular subtypes harbour specific methylation profiles. Our results suggest that methylation may play an important role in the development of breast cancers.
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| 6. |
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| 7. |
- Jönsson, Göran B, et al.
(författare)
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Genomic subtypes of breast cancer identified by array-comparative genomic hybridization display distinct molecular and clinical characteristics
- 2010
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Ingår i: Breast Cancer Research. - : Springer Science and Business Media LLC. - 1465-5411 .- 1465-542X. ; 12:3
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Breast cancer is a profoundly heterogeneous disease with respect to biologic and clinical behavior. Gene-expression profiling has been used to dissect this complexity and to stratify tumors into intrinsic gene-expression subtypes, associated with distinct biology, patient outcome, and genomic alterations. Additionally, breast tumors occurring in individuals with germline BRCA1 or BRCA2 mutations typically fall into distinct subtypes. Methods: We applied global DNA copy number and gene-expression profiling in 359 breast tumors. All tumors were classified according to intrinsic gene-expression subtypes and included cases from genetically predisposed women. The Genomic Identification of Significant Targets in Cancer (GISTIC) algorithm was used to identify significant DNA copy-number aberrations and genomic subgroups of breast cancer. Results: We identified 31 genomic regions that were highly amplified in > 1% of the 359 breast tumors. Several amplicons were found to co-occur, the 8p12 and 11q13.3 regions being the most frequent combination besides amplicons on the same chromosomal arm. Unsupervised hierarchical clustering with 133 significant GISTIC regions revealed six genomic subtypes, termed 17q12, basal-complex, luminal-simple, luminal-complex, amplifier, and mixed subtypes. Four of them had striking similarity to intrinsic gene-expression subtypes and showed associations to conventional tumor biomarkers and clinical outcome. However, luminal A-classified tumors were distributed in two main genomic subtypes, luminal-simple and luminal-complex, the former group having a better prognosis, whereas the latter group included also luminal B and the majority of BRCA2-mutated tumors. The basal-complex subtype displayed extensive genomic homogeneity and harbored the majority of BRCA1-mutated tumors. The 17q12 subtype comprised mostly HER2-amplified and HER2-enriched subtype tumors and had the worst prognosis. The amplifier and mixed subtypes contained tumors from all gene-expression subtypes, the former being enriched for 8p12-amplified cases, whereas the mixed subtype included many tumors with predominantly DNA copy-number losses and poor prognosis. Conclusions: Global DNA copy-number analysis integrated with gene-expression data can be used to dissect the complexity of breast cancer. This revealed six genomic subtypes with different clinical behavior and a striking concordance to the intrinsic subtypes. These genomic subtypes may prove useful for understanding the mechanisms of tumor development and for prognostic and treatment prediction purposes.
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| 8. |
- Jönsson, Göran B, et al.
(författare)
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The retinoblastoma gene undergoes rearrangements in BRCA1-deficient basal-like breast cancer.
- 2012
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Ingår i: Cancer Research. - 1538-7445. ; 72:16, s. 4028-4036
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Tidskriftsartikel (refereegranskat)abstract
- Breast tumors from BRCA1 germ line mutation carriers typically exhibit features of the basal-like molecular subtype. However, the specific genes recurrently mutated as a consequence of BRCA1 dysfunction have not been fully elucidated. In this study, we utilized gene expression profiling to molecularly subtype 577 breast tumors, including 72 breast tumors from BRCA1/2 mutation carriers. Focusing on the RB1 locus, we analyzed 33 BRCA1-mutated, 36 BRCA2-mutated and 48 non-BRCA1/2-mutated breast tumors using a custom-designed high-density oligomicroarray covering the RB1 gene. We found a strong association between the basal-like subtype and BRCA1-mutated breast tumors and the luminal B subtype and BRCA2-mutated breast tumors. RB1 was identified as a major target for genomic disruption in tumors arising in BRCA1 mutation carriers and in sporadic tumors with BRCA1 promoter-methylation, but rarely in other breast cancers. Homozygous deletions, intragenic breaks, or microdeletions were found in 33% of BRCA1-mutant tumors, 36% of BRCA1 promoter-methylated basal-like tumors, 13% of non-BRCA1 deficient basal-like tumors, and 3% of BRCA2-mutated tumors. In conclusion, RB1 was frequently inactivated by gross gene disruption in BRCA1-related hereditary breast cancer and BRCA1-methylated sporadic basal-like breast cancer, but rarely in BRCA2-hereditary breast cancer and non-BRCA1-deficient sporadic breast cancers. Together, our findings demonstrate the existence of genetic heterogeneity within the basal-like breast cancer subtype that is based upon BRCA1-status.
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| 9. |
- Manogue, Michael, et al.
(författare)
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Curriculum structure, content, learning and assessment in European undergraduate dental education - update 2010
- 2011
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Ingår i: European journal of dental education. - : John Wiley & Sons. - 1396-5883 .- 1600-0579. ; 15:3, s. 133-141
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Tidskriftsartikel (refereegranskat)abstract
- Abstract This paper presents an updated statement on behalf of the Association for Dental Education in Europe (ADEE) in relation to proposals for undergraduate Curriculum Structure, Content, Learning, Assessment and Student / Staff Exchange for dental education in Europe. A task force was constituted to consider these issues and the two previous, related publications produced by the Association (Plasschaert et al 2006 and 2007) were revised. The broad European dental community was circulated and contributed to the revisions. The paper was approved at the General Assembly of ADEE, held in Amsterdam in August 2010 and will be updated again in 2015.
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| 10. |
- Olsson, Eleonor, et al.
(författare)
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CD44 isoforms are heterogeneously expressed in breast cancer and correlate with tumor subtypes and cancer stem cell markers.
- 2011
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Ingår i: BMC Cancer. - : Springer Science and Business Media LLC. - 1471-2407. ; 11
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The CD44 cell adhesion molecule is aberrantly expressed in many breast tumors and has been implicated in the metastatic process as well as in the putative cancer stem cell (CSC) compartment. We aimed to investigate potential associations between alternatively spliced isoforms of CD44 and CSCs as well as to various breast cancer biomarkers and molecular subtypes. METHODS: We used q-RT-PCR and exon-exon spanning assays to analyze the expression of four alternatively spliced CD44 isoforms as well as the total expression of CD44 in 187 breast tumors and 13 cell lines. ALDH1 protein expression was determined by IHC on TMA. RESULTS: Breast cancer cell lines showed a heterogeneous expression pattern of the CD44 isoforms, which shifted considerably when cells were grown as mammospheres. Tumors characterized as positive for the CD44+/CD24- phenotype by immunohistochemistry were associated to all isoforms except the CD44 standard (CD44S) isoform, which lacks all variant exons. Conversely, tumors with strong expression of the CSC marker ALDH1 had elevated expression of CD44S. A high expression of the CD44v2-v10 isoform, which retain all variant exons, was correlated to positive steroid receptor status, low proliferation and luminal A subtype. The CD44v3-v10 isoform showed similar correlations, while high expression of CD44v8-v10 was correlated to positive EGFR, negative/low HER2 status and basal-like subtype. High expression of CD44S was associated with strong HER2 staining and also a subgroup of basal-like tumors. Unsupervised hierarchical cluster analysis of CD44 isoform expression data divided tumors into four main clusters, which showed significant correlations to molecular subtypes and differences in 10-year overall survival. CONCLUSIONS: We demonstrate that individual CD44 isoforms can be associated to different breast cancer subtypes and clinical markers such as HER2, ER and PgR, which suggests involvement of CD44 splice variants in specific oncogenic signaling pathways. Efforts to link CD44 to CSCs and tumor progression should consider the expression of various CD44 isoforms.
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