SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Heim Sverre) "

Sökning: WFRF:(Heim Sverre)

  • Resultat 1-10 av 64
  • [1]234567Nästa
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Heim, Sverre, et al. (författare)
  • Cytogenetic nomenclature
  • 2015. - 4th
  • Ingår i: Cancer Cytogenetics : Chromosomal and Molecular Genetic Aberrations of Tumor Cells, - Chromosomal and Molecular Genetic Aberrations of Tumor Cells. - : Wiley-Blackwell. - 9781118795569 - 9781118795538 ; , s. 19-25
  • Bokkapitel (refereegranskat)abstract
    • This chapter elaborates on human chromosome nomenclature. It provides a brief summary of the most essential cytogenetic terminology related to the description of chromosome aberrations in neoplastic cells. The chapter outlines criteria for designation of regions and bands for chromosome nomenclature. Regions and bands are numbered consecutively from the centromere outward along each chromosome arm. This chapter outlines guidelines and conventions foy karyotypic nomenclature. It provides a detailed account on nomenclature of tumor cell populations. The introduction of various in situ hybridization technologies into the cytogenetic analysis of interphase and metaphase cells has led the International Standing Committee on Human Cytogenetic Nomenclature to propose an in situ hybridization (ish) nomenclature system that may be used to describe abnormalities at the molecular level by indicating, for example, the presence, absence, amplification, or separation of specific probe signals.
  •  
2.
  • Heim, Sverre, et al. (författare)
  • Nonrandom chromosome abnormalities in cancer : An overview
  • 2015. - 4th
  • Ingår i: Cancer Cytogenetics : Chromosomal and Molecular Genetic Aberrations of Tumor Cells - Chromosomal and Molecular Genetic Aberrations of Tumor Cells. - : Wiley-Blackwell. - 9781118795569 - 9781118795538 ; , s. 26-41
  • Bokkapitel (refereegranskat)abstract
    • This chapter discusses neoplastic karyotypes. It emphasizes the difference between primary and secondary changes and address the questions of why, how, when, and where chromosome abnormalities arise; compare numerical and structural aberrations in terms of how they contribute to tumor development; and also touch upon the issues of what causes cancer-associated chromosome abnormalities and whether they are necessary and/or sufficient to transform a normal cell into a cancer cell. It discusses some of the more principal differences between the cytogenetic and molecular genetic approaches to the study of acquired somatic cell mutations. Numerous specific chromosomal abnormalities have been detected in almost all tumor types that have been examined. This chapter explores when do chromosome aberrations arise and in which cells do chromosome aberrations arise. It also discusses whether acquired chromosome aberrations are sufficient for neoplastic proliferation. The chapter discusses the general effects of structural and numerical chromosome abnormalities.
  •  
3.
  • Heim, Sverre, et al. (författare)
  • Preface to the Fourth Edition
  • 2015. - 4th
  • Ingår i: Cancer Cytogenetics : Chromosomal and Molecular Genetic Aberrations of Tumor Cells - Chromosomal and Molecular Genetic Aberrations of Tumor Cells. - : Wiley-Blackwell. - 9781118795569 - 9781118795538
  • Bokkapitel (övrigt vetenskapligt)
  •  
4.
  • Mertens, Fredrik, et al. (författare)
  • Tumors of the skin
  • 2015. - 4th
  • Ingår i: Cancer Cytogenetics : Chromosomal and Molecular Genetic Aberrations of Tumor Cells - Chromosomal and Molecular Genetic Aberrations of Tumor Cells. - : Wiley-Blackwell. - 9781118795569 - 9781118795538 ; , s. 555-565
  • Bokkapitel (refereegranskat)abstract
    • Skin cancer is the most common malignancy in humans. Clonal chromosome abnormalities have been reported in approximately 100 basal cell epitheliomas (BCC). In contrast to BCC, which has no recognized precursor lesion, squamous cell carcinoma (SCC) of the skin is known to develop through histologic stages, the most important of which are actinic keratosis (squamous cell dysplasia) and carcinoma in situ (severe dysplasia). A wide range of clinically and pathologically different benign and malignant melanocytic tumors are recognized. Appendageal tumors are subdivided into more than 30 benign and malignant subtypes showing apocrine and eccrine differentiation or follicular and sebaceous differentiation. Merkel cell carcinomas have near-diploid karyotypes, often showing rearrangements of chromosome 1. Dermal cylindromas may show similar genetic features to adenoid cystic carcinomas with the occurrence of a t (6; 9) (q22-23; p23-24) leading to a MYB-NFIB fusion gene.
  •  
5.
  • Mitelman, Felix, et al. (författare)
  • How it all began : Cancer cytogenetics before sequencing
  • 2015. - 4th
  • Ingår i: Cancer Cytogenetics : Chromosomal and Molecular Genetic Aberrations of Tumor Cells - Chromosomal and Molecular Genetic Aberrations of Tumor Cells. - : Wiley-Blackwell. - 9781118795569 - 9781118795538 ; , s. 1-10
  • Bokkapitel (refereegranskat)abstract
    • According to Boveri's hypothesis, chromosome abnormalities were the cellular changes causing the transition from normal to malignant proliferation. Technical difficulties prevented reliable visualization of mammalian chromosomes, in both normal and neoplastic cells, throughout the entire first half of the 20th century. Nowell and Hungerford's discovery greatly stimulated interest in cancer cytogenetics in the early 1960s, but for several reasons, the Ph chromosome long remained an exceptional finding. The advent of molecular genetics in the 1980s and the development of a range of powerful molecular cytogenetic technologies, such as fluorescence in situ hybridization (FISH), multicolor FISH, comparative genomic hybridization (CGH), various array-based genotyping technologies, and DNA and RNA sequencing, have widened one's knowledge and understanding of the molecular mechanisms that are operative in neoplastic initiation and progression. In the 100 years since Boveri first postulated that chromosome change may initiate the carcinogenic process, cancer cytogenetics has come of age.
  •  
6.
  • Andersen, Mette K, et al. (författare)
  • Paediatric B-cell precursor acute lymphoblastic leukaemia with t(1;19)(q23;p13): clinical and cytogenetic characteristics of 47 cases from the Nordic countries treated according to NOPHO protocols.
  • 2011
  • Ingår i: British journal of haematology. - Oxford : Blackwell Scientific. - 1365-2141 .- 0007-1048. ; 155:2
  • Tidskriftsartikel (refereegranskat)abstract
    • The translocation t(1;19)(q23;p13)/der(19)t(1;19) is a risk stratifying aberration in childhood B-cell precursor acute lymphoblastic leukaemia (BCP ALL) in the Nordic countries. We have identified 47 children/adolescents with t(1;19)/der(19)t(1;19)-positive BCP ALL treated on two successive Nordic Society of Paediatric Haematology and Oncology (NOPHO) protocols between 1992 and 2007 and have reviewed the clinical and cytogenetic characteristics of these cases, comprising 1·8% of all cases. The translocation was balanced in 15 cases (32%) and unbalanced in 29 cases (62%). The most common additional chromosome abnormalities were del(9p), i(9q), del(6q), and del(13q). The median age was 7 years, the median white blood cell (WBC) count was 16 × 10(9) /l, and the female/male ratio was 1·2. The predicted event-free survival (EFS) at 5 and 10 years was 0·79, whereas the predicted overall survival (OS) at 5 and 10 years was 0·85 and 0·82, respectively. Nine patients had a bone marrow relapse after a median of 23 months; no patient had a central nervous system relapse. Additional cytogenetic abnormalities, age, gender, WBC count or whether the t(1;19) was balanced or unbalanced did not influence EFS or OS. Compared to cases with t(12,21) and high hyperdiploidy, EFS was similar, but overall survival was worse in patients with t(1;19)/der(19)t(1;19) (P = 0·004).
  •  
7.
  •  
8.
  • Elmula, Imad, et al. (författare)
  • Chromosomal aberrations in benign and malignant Bilharzia-associated bladder lesions analyzed by comparative genomic hybridization.
  • 2002
  • Ingår i: BMC Cancer. - : BioMed Central (BMC). - 1471-2407. ; 2:5
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Bilharzia-associated bladder cancer (BAC) is a major health problem in countries where urinary schistosomiasis is endemic. Characterization of the genetic alterations in this cancer might enhance our understanding of the pathogenic mechanisms of the disease but, in contrast to nonbilharzia bladder cancer, BAC has rarely been the object of such scrutiny. In the present study, we aimed to characterize chromosomal imbalances in benign and malignant post-bilharzial lesions, and to determine whether their unique etiology yields a distinct cytogenetic profile as compared to chemically induced bladder tumors. METHODS: DNAs from 20 archival paraffin-embedded post-bilharzial bladder lesions (6 benign and 14 malignant) obtained from Sudanese patients (12 males and 8 females) with a history of urinary bilharziasis were investigated for chromosomal imbalances using comparative genomic hybridization (CGH). Subsequent FISH analysis with pericentromeric probes was performed on paraffin sections of the same cases to confirm the CGH results. RESULTS: Seven of the 20 lesions (6 carcinomas and one granuloma) showed chromosomal imbalances varying from 1 to 6 changes. The most common chromosomal imbalances detected were losses of 1p21-31, 8p21-pter, and 9p and gain of 19p material, seen in three cases each, including the benign lesion. CONCLUSION: Most of the detected imbalances have been repeatedly reported in non-bilharzial bladder carcinomas, suggesting that the cytogenetic profiles of chemical- and bilharzia-induced carcinomas are largely similar. However, loss of 9p seems to be more ubiquitous in BAC than in bladder cancer in industrialized countries.
  •  
9.
  • Fadl-Elmula, Imad, et al. (författare)
  • Characterization of chromosomal abnormalities in uroepithelial carcinomas by G-banding, spectral karyotyping and fish analysis
  • 2001
  • Ingår i: International Journal of Cancer. - : John Wiley and Sons. - 0020-7136. ; 92:6, s. 824-831
  • Tidskriftsartikel (refereegranskat)abstract
    • Chromosome analysis by G-banding, spectral karyotyping (SKY) and fluorescence in situ hybridization (FISH) was per formed on 24 short-term cultured transitional cell bladder carcinomas and 5 cell lines established from bladder carcinomas. Except for one tumor with an apparently normal chromosomal constitution, clonal chromosome abnormalities were detected in all examined cases by the combined approach. The application of SKY and FISH techniques improved the karyotypic descriptions, originally based on C-banding only, by identifying 32 additional numerical changes, by establishing the chromosomal origin of 27 markers and 2 ring chromosomes, by redefining 53 aberrations and by detecting 15 hidden chromosomal rearrangements. No recurrent translocation, however, was detected. The most prominent: karyotypic feature was thus the occurrence of deletions and losses of whole chromosome copies indicating the importance of tumor suppressor genes in transitional cell carcinoma pathogenesis. Invasive carcinomas were karyotypically more complex than were low grade superficial tumors. Specific leases of material from chromosome 9 and from chromosome arms I Ip and 8p, and gains of 8q and Iq seem to be early changes appearing in superficial tumors, whereas losses from 4p and 17p and the formation of an isochromosome for 5p were associated with more aggressive tumor phenotypes.
  •  
10.
  • Forestier, Erik, et al. (författare)
  • Clinical and cytogenetic features of pediatric dic(9;20)(p13.2;q11.2)-positive B-Cell precursor acute lymphoblastic leukemias: A nordic series of 24 cases and review of the literature
  • 2008
  • Ingår i: Genes, Chromosomes and Cancer. - : John Wiley and Sons. - 1045-2257 .- 1098-2264. ; 47:2, s. 149-158
  • Forskningsöversikt (refereegranskat)abstract
    • Although dic(9;20)(p13.2;q11.2) is a characteristic abnormality in childhood B-cell precursor acute lymphoblastic leukemias (BCP ALL), little is known about its clinical impact or the type and frequency of additional aberrations it may occur together with. We here review the clinical and cytogenetic features of a Nordic pediatric series of 24 patients with dic(9;20)-positive BCP ALL diagnosed 1996-2006, constituting 1.3% of the BCP ALL, as well as 47 childhood cases from the literature. Consistent immunophenotypic features of the Nordic cases included positivity for HLA-DR, CID 10, CID19, CD20, and CD22 and negativity for T-cell and myeloid markers; no detailed immunophenotypes were reported for the previously published cases. In the entire cohort of 71 cases, the modal chromosome distribution was 45 (62%), 46 (21%), 47 (7%), 48 (4%), 49 (3%), 44 (1%), and 50 (1%). Additional changes were present in 63%, the most frequent of which were homozygous loss of CDKN2A (33%) and gains of chromosomes 21 (28%) and x (10%). The median patient age was 3 years, the female/male ratio was 2.0, the median white blood cell count was 24 x 10(9)/1, 11% had central nervous system involvement, and 5% had a mediastinal mass at diagnosis. Risk group stratification was nonstandard risk in 79%. The event-free survival and overall survival at 5 years for the 24 Nordic cases was 0.62 and 0.82, respectively. Thus, although relapses are quite common, postrelapse treatment of many patients is successful. This article contains Supplementary Material available at http://www.interscience.wiley.com/ jpages/1045-2257/suppmat.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 64
  • [1]234567Nästa

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