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  • CHROMOSOMAL INSTABILITY  (2)
  • 1
    Keywords: EXPRESSION ; tumor ; carcinoma ; CELL ; Germany ; human ; INFORMATION ; HEPATOCELLULAR-CARCINOMA ; HISTORY ; GENE ; GENES ; HYBRIDIZATION ; DIFFERENTIATION ; TUMORS ; RESOLUTION ; DNA ; MECHANISM ; mechanisms ; ADENOMAS ; hepatocellular carcinoma ; PROGRESSION ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY NUMBER ; NUMBER ; CHROMOSOMAL-ABERRATIONS ; ABERRATIONS ; IN-SITU HYBRIDIZATION ; TUMOR-SUPPRESSOR GENE ; REGION ; INSTABILITY ; REGIONS ; ONCOGENE ; TRANSFORMATION ; ORAL-CONTRACEPTIVES ; CARCINOMAS ; IMBALANCES ; CLUSTER ; MOLECULAR-MECHANISM ; TUMOR-SUPPRESSOR ; INCREASE ; CLUSTER-ANALYSIS ; CHROMOSOMAL INSTABILITY ; CHIP ; tumor suppressor gene ; cluster analysis ; LOSSES ; GLYCOGEN-STORAGE-DISEASE ; genomic ; HUMAN HEPATOCELLULAR-CARCINOMA ; ARRAY CGH ; CHROMOSOMAL-ABNORMALITIES ; TUMOR-SUPPRESSOR GENES ; ARRAY-CGH ; LIVER-CELL ADENOMAS
    Abstract: Background & Alms: To gain more information about the molecular mechanisms leading to dedifferentiation of hepatocellular adenoma (HCA) and hepatocellular carcinoma (HCC), high-resolution array-based comparative genomic hybridization (array-CGH) was performed on 24 cases of HCC and 10 cases of HCA. Methods: DNA chips containing 6251 individual bacterial artificial chromosome/plasmid artificial chromosome clones were used. They allowed for a genome-wide resolution of 1 Mb and an even higher resolution of up to 100 kb for chromosome regions recurrently involved in human tumors and for regions containing known tumor-suppressor genes and oncogenes. Results: Copy number changes on the genomic scale were found by array-based comparative genomic hybridization in all cases. In HCC, gains of chromosomal regions 1q (91.6%), and 8q (58.3%), and losses of 8p (54%) were found most frequently. Hierarchic cluster analysis branched all HCA from HCC. However, in 2 adenomas with a known history of glycogenosis type I and adenomatosis hepatis gains of 1q were found, too. The critically gained region was narrowed down to bands 1q22-23. Although no significant differences in the mean number of chromosomal aberrations were seen between adenomas and well-differentiated carcinomas (2.7 vs 4.6), a significant increase accompanied the dedifferentiation of HCC (14.1 in HCC-G2 and 16.3 in HCC-G2/3; P 〈 .02). Dedifferentiation of HCC also was correlated closely to losses of 4q and 13q (P 〈 .001 and 〈 .005, respectively). Conclusions: The increased chromosomal instability during dedifferentiation of HCC leads to an accumulation of structural chromosomal aberrations and losses and gains of defined chromosome regions
    Type of Publication: Journal article published
    PubMed ID: 16979954
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  • 2
    Keywords: Germany ; THERAPY ; FOLLOW-UP ; NETWORK ; DISEASE ; DISEASES ; NEW-YORK ; GENE ; HYBRIDIZATION ; SAMPLE ; SAMPLES ; TIME ; PATIENT ; COMPLEX ; COMPLEXES ; MARKER ; chromosome ; bone marrow ; BONE-MARROW ; early detection ; IN-SITU ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; CHROMOSOMAL-ABERRATIONS ; leukemia ; ABERRATIONS ; ACUTE LYMPHOBLASTIC-LEUKEMIA ; IN-SITU HYBRIDIZATION ; INSTABILITY ; FAILURE ; FLUORESCENCE ; fluorescence in situ hybridization ; MANAGEMENT ; ACUTE MYELOGENOUS LEUKEMIA ; in situ hybridization ; SINGLE ; DISORDERS ; TRANSITION ; CHROMOSOMAL INSTABILITY ; USA ; genomic ; FANCONI-ANEMIA ; congenital ; aberration ; chromosomal aberration ; AML1 ; congenital neutropenia ; inherited bone marrow failure syndromes ; leukemogenesis ; NEUTROPENIA ; SHWACHMAN-DIAMOND-SYNDROME
    Abstract: As chromosomal instability may contribute to leukemogenesis in patients with congenital bone marrow failure (CBMF) disorders, it was the aim of this study to characterize chromosomally aberrant clones that arise during the clinical course of disease by means of R-banding and fluorescence in situ hybridization (FISH) analyses. In addition, multicolor-FISH and array-comparative genomic hybridization (CGH) were applied to characterize clonal chromosome aberrations in more detail. Between January 2004 and December 2005, we prospectively analyzed 90 samples of 73 patients with proven or suspected CBMF disorders enrolled in a German Study Network of CBMF diseases. Clonal aberrations could be identified in four of 73 patients examined. In one child with congenital thrombocytopenia, Jacobsen syndrome [del(11)(q24)c] was diagnosed, and thus a CBMF could be excluded. In a girl with Shwachman-Diamond syndrome, two independent clones, one with an isochromosome i(7)(q10), another with a complex aberrant karyotype, were identified. Simultaneously, transition into a myelodysplastic syndrome (MDS) occurred. The brother, who was also afflicted with Shwachman-Diamond syndrome, showed an isochromosome i(7q) as a single aberration. In the fourth patient with severe congenital neutropenia, an add(21)(q22) marker containing a low-level amplification of the AML1 gene was identified at the time point of transition into acute myelogenous leukemia (AML). In summary, we suggest that follow-up of patients with CBMF using chromosome and FISH analyses will be helpful for the early detection of transition into MDS or AML and thus should be an integral part of the clinical management of these patients
    Type of Publication: Journal article published
    PubMed ID: 17653548
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