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See detailFamilial adenomatous polyposis: clinical presentation, detection and surveillance.
Laurent, S.; Franchimont, D.; Vander Auwera, Jacqueline ULg et al

in Acta Gastro-Enterologica Belgica (2011), 74(3), 415-20

Colorectal cancer (CRC) is a leading cause of cancer related death in the western countries. It remains an important health problem, often under-diagnosed. The symptoms can appear very late and about 25 ... [more ▼]

Colorectal cancer (CRC) is a leading cause of cancer related death in the western countries. It remains an important health problem, often under-diagnosed. The symptoms can appear very late and about 25% of the patients are diagnosed at metastatic stage. Familial adenomatous polyposis (FAP) is an inherited colorectal cancer syndrome, characterized by the early onset of hundred to thousands of adenomatous polyps in the colon and rectum. Left untreated, there is a nearly 100% cumulative risk of progression to CRC by the age of 35-40 years, as well as an increased risk of various other malignancies. CRC can be prevented by the identification of the high risk population and by the timely implementation of rigid screening programs which will lead to special medico-surgical interventions. [less ▲]

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See detailAcute myeloid leukaemia with 8p11 (MYST3) rearrangement : an integrated cytologic, cytogenetic and molecular study by the groupe francophone de cytogénétique hématologique
Gervais, C.; Murati, A.; Helias, C. et al

in Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K (2008), 22(8), 1567-1575

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See detailMolecular cytogenetic study of 126 unselected T-ALL cases reveals high incidence of TCR beta locus rearrangements and putative new T-cell oncogenes
Cauwelier, B.; Dastugue, N.; Cools, J. et al

in Leukemia (2006), 20(7), 1238-1244

Chromosomal aberrations of T-cell receptor (TCR) gene loci often involve the TCR alpha delta (14q11) locus and affect various known T-cell oncogenes. A systematic fluorescent in situ hybridization (FISH ... [more ▼]

Chromosomal aberrations of T-cell receptor (TCR) gene loci often involve the TCR alpha delta (14q11) locus and affect various known T-cell oncogenes. A systematic fluorescent in situ hybridization (FISH) screening for the detection of chromosomal aberrations involving the TCR loci, TCRad (14q11), TCR beta (7q34) and TCR gamma (7p14), has not been conducted so far. Therefore, we initiated a screening of 126 T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma cases and 19 T-ALL cell lines using FISH break-apart assays for the different TCR loci. Genomic rearrangements of the TCR beta locus were detected in 24/ 126 cases (19%), most of which (58.3%) were not detected upon banding analysis. Breakpoints in the TCR alpha delta locus were detected in 22/ 126 cases (17.4%), whereas standard cytogenetics only detected 14 of these 22 cases. Cryptic TCR alpha delta/ TCR beta chromosome aberrations were thus observed in 22 of 126 cases (17.4%). Some of these chromosome aberrations target new putative T-cell oncogenes at chromosome 11q24, 20p12 and 6q22. Five patients and one cell line carried chromosomal rearrangements affecting both TCR beta and TCR alpha delta loci. In conclusion, this study presents the first inventory of chromosomal rearrangements of TCR loci in T-ALL, revealing an unexpected high number of cryptic chromosomal rearrangements of the TCR beta locus and further broadening the spectrum of genes putatively implicated in T-cell oncogenesis. [less ▲]

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See detailPAX5/IGH rearrangement is a recurrent finding in a subset of aggressive B-NHL with complex chromosomal rearrangements
Poppe, B.; De Paepe, P.; Michaux, L. et al

in Genes Chromosomes & Cancer (2005), 44(2), 218-223

We present an extensive characterization of 10 B-cell lymphomas with a t(9; 14)(p I 3;q32). The presence of the PAX5/IGH gene rearrangement was demonstrated by fluorescence in situ hybridization (FISH ... [more ▼]

We present an extensive characterization of 10 B-cell lymphomas with a t(9; 14)(p I 3;q32). The presence of the PAX5/IGH gene rearrangement was demonstrated by fluorescence in situ hybridization (FISH) using a validated probe set, whereas complex karyotypic changes were reassessed by multiplex-FISH (M-FISH). Pathologic and clinical review revealed the presence of this rearrangement in 4 histiocyte-rich, T-cell-rich B-cell lymphomas (HRTR-BCLs) and 2 posttransplantation diffuse large B-cell lymphomas (PTLD-DLBCLs). In contrast to initial observations describing this translocation in lymphoplasmacytic lymphoma (LPL) and LPL-derived large B-cell lymphoma, our data showed a wide morphologic and clinical spectrum associated with the PAX5/IGH rearrangement, pointing to an association between this aberration and a subset of de novo DLBCLs presenting with advanced disease and adverse prognosis. In addition, the recurrent incidence of this rearrangement in both HRTR-BCL (4 cases) and PTLD-DLBCL (2 cases) was previously unrecognized and is intriguing. (c) 2005 Wiley-Liss, Inc. [less ▲]

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See detailExpression analyses identify MLL as a prominent target of 11q23 amplification and support an etiologic role for MLL gain of function in myeloid malignancies
Poppe, B.; Vandesompele, J.; Schoch, C. et al

in Blood (2004), 103(1), 229-235

MLL amplification was recently recognized as a recurrent aberration in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), associated with adverse prognosis and karyotype complexity. Here we ... [more ▼]

MLL amplification was recently recognized as a recurrent aberration in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), associated with adverse prognosis and karyotype complexity. Here we present detailed results of fluorescence in situ hybridization (FISH) and expression analyses of MLL and 5 selected 11q candidate oncogenes (CBL, DDX6, ETS1, FLI1, and PLZF) in 31 patient samples and one cell line with 11q23 gain. FISH analyses revealed that the 11q23 amplicon invariably encompassed MLL, DDX6, ETS1, and FLI1, whereas expression analyses identified MLL and DDX6 as the most differentially expressed genes among samples with and without 11q23 copy gain or amplification. In MLL-amplified samples, a significant transcriptional up-regulation of MEIS1, PROML1, ADAM10, NKG2D, and ITPA was noted. Further analyses, designed to elucidate a possible role of the 11q overexpressed genes (MLL, DDX6, FLI1, and ETS1) in unselected MDS and AML samples, revealed a significant upregulation of MLL in MDS. Our findings confirm the MLL gene as a prominent target of 11q23 amplification and provide further evidence for an etiologic role for MLL gain of function in myeloid malignancies. In addition, our results indicate that the transcriptional program associated with MLL rearrangements and MLL overexpression displays significant similarities. [less ▲]

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See detailt(5;14)/HOX11L2-positive T-cell acute lymphoblastic leukemia. A collaborative study of the Groupe Francais de Cytogenetique Hematologique (GFCH)
Berger, R.; Dastugue, N.; Busson, M. et al

in Leukemia (2003), 17(9), 1851-1857

To accurately estimate the incidence of HOX11L2 expression, and determine the associated cytogenetic features, in T-cell acute lymphoblastic leukemia (T-ALL), the Groupe Francais de Cytogenetique ... [more ▼]

To accurately estimate the incidence of HOX11L2 expression, and determine the associated cytogenetic features, in T-cell acute lymphoblastic leukemia (T-ALL), the Groupe Francais de Cytogenetique Hematologique (GFCH) carried out a retrospective study of both childhood and adult patients. In total, 364 patients were included ( 211 children less than or equal to15 years and 153 adults), and 67 ( 18.5%) [ 47 children ( 22.4%) and 20 adults (13.1%)] were shown to either harbor the t(5; 14) q35; q32) translocation or express the HOX11L2 gene or both. Most of the common hematological parameters did not show significant differences within positive and negative populations, whereas the incidence of CD1a+/CD10+ and cytoplasmic CD3+ patients was significantly higher in positive than in negative children. Out of the 63 positive patients investigated by conventional cytogenetics, 32 exhibited normal karyotype, whereas the others 31 showed clonal chromosome abnormalities, which did not include classical T-ALL specific translocations. Involvement of the RANBP17/HOX11L2 locus was ascertained by fluorescence in situ hybridization in six variant or alternative (three-way translocation or cytogenetic partner other than 14q32) translocations out of the 223 patients. Our results also show that HOX11L2 expression essentially occurs as a result of a 5q35 rearrangement, but is not associated with another identified T-ALL specific recurrent genetic abnormality, such as SIL-TAL fusion or HOX11 expression. [less ▲]

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