Numerical aberrations of chromosomes 11 and 17 in colorectal adenocarcinomas

Tagawa, Yutaka; Sawai, Terumitsu; Nakagoe, Tohru; Morinaga, Masafumi; Yasutake, Toru; Ayabe, Hiroyoshi; Tomita, Masaru

doi:10.1007/bf00311787

Cited by 10 publications

(10 citation statements)

References 35 publications

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“…We have already reported the presence of a significant relationship (P Ͻ 0.005) in colorectal cancer between an increased number of aberrations in chromosome 17 and DNA aneuploidy. 20 The present results showed no relationship between these two features in HNPCC. Although the reason for this finding is not clear at present, the numerical changes in chromosome 17, which are small relative to the total DNA content, may not necessarily be reflected in total nuclear DNA content.…”

Section: Discussioncontrasting

confidence: 75%

Chromosome instability evaluated by fluorescence in situ hybridization in hereditary non-polyposis colorectal cancer

Sawai

Sasano

Tsuji

et al. 1998

Journal of Gastroenterology

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Numerical aberrations of chromosome 17 and nuclear DNA content were compared in patients with hereditary non-polyposis colorectal cancer (HNPCC) and those with sporadic colorectal cancer (SCRC). During a period of 22 years, 30 cases (3.2%) from 28 families satisfied the Japanese clinical criteria of HNPCC. Using freshly frozen tissue samples, we investigated chromosomal aberration with fluorescence in situ hybridization with alpha satellite DNA probe for chromosome 17. Flow cytometric quantification of nuclear DNA content showed DNA aneuploidy in 9 of 15 patients (60.0%) with HNPCC and in 160 of 234 patients (68.4%) with SCRC, there was no significant difference between HNPCC and SCRC. The mean proportion of nuclei with aneusomy 17 (numerical chromosome aberration index: NCAI) in 14 patients with HNPCC was significantly higher than that in 42 patients with SCRC (46.8 +/- 5.0% vs 39.0 +/- 10.3%, P < 0.01). NCAI increased in proportion with the progression of the disease in SCRC (26.1% in stage I, 33.3% in stage II, 38.8% in stage IIIa, 42.7% in stage IIIb, and 46.2% in stage IV, P < 0.01), whereas NCAI in HNPCC was high in all stages (43.5%-49.2%). The proportion of patients with multiple numerical aberration of chromosome 17 was significantly higher in HNPCC (9/14) than among SCRC (11/42). Our data suggest that chromosome 17 is present in an unstable condition in HNPCC.

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Section: Discussioncontrasting

confidence: 75%

Chromosome instability evaluated by fluorescence in situ hybridization in hereditary non-polyposis colorectal cancer

Sawai

Sasano

Tsuji

et al. 1998

Journal of Gastroenterology

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“…S4i). This is suggestive of a pattern of chromosomal acquisitions potentially relevant for colorectal cancer progression (Tagawa et al 1996). It remains to be examined if the extent of Lamin stoichiometry correlates with the extent of these chromosomal gains during colorectal cancer progression (Belt et al 2011; Roth et al 2010).…”

Section: Discussionmentioning

confidence: 90%

Chromosomal aneuploidies induced upon Lamin B2 depletion are mislocalized in the interphase nucleus

et al. 2016

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Chromosome territories assume non-random positions in the interphase nucleus with gene-rich chromosomes localized toward the nuclear interior and gene-poor chromosome territories toward the nuclear periphery. Lamins are intermediate filament proteins of the inner nuclear membrane required for the maintenance of nuclear structure and function. Here, we show using whole-genome expression profiling that Lamin A/C or Lamin B2 depletion in an otherwise diploid colorectal cancer cell line (DLD1) deregulates transcript levels from specific chromosomes. Further, three-dimensional fluorescence in situ hybridization (3D-FISH) analyses of a subset of these transcriptionally deregulated chromosome territories revealed that the diploid chromosome territories in Lamin-depleted cells largely maintain conserved positions in the interphase nucleus in a gene-density-dependent manner. In addition, chromosomal aneuploidies were induced in ~25 % of Lamin A/C or Lamin B2-depleted cells. Sub-populations of these aneuploid cells consistently showed a mislocalization of the gene-rich aneuploid chromosome 19 territory toward the nuclear periphery, while gene-poor aneuploid chromosome 18 territory was mislocalized toward the nuclear interior predominantly upon Lamin B2 than Lamin A/C depletion. In addition, a candidate gene locus ZNF570 (Chr.19q13.12) significantly overexpressed upon Lamin B2 depletion was remarkably repositioned away from the nuclear lamina. Taken together, our studies strongly implicate an overarching role for Lamin B2 in the maintenance of nuclear architecture since loss of Lamin B2 relieves the spatial positional constraints required for maintaining conserved localization of aneuploid chromosome territories in the interphase nucleus.Electronic supplementary materialThe online version of this article (doi:10.1007/s00412-016-0580-y) contains supplementary material, which is available to authorized users.

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“…5F). DISCUSSION We elected to analyze the changes in chromosome 11 because we have noticed a correlation between this chromosome and colorectal cancer, indicating that numerical and structural aberrations of this chromosome are closely associated with the biological grade of malignancy (24,35). Furthermore, the importance of this chromosome is reflected by the presence, on the same chromosome, of the cyclin D1 gene, which plays an important role in the cell cycle (14).…”

Section: Formation Of Pericentromeres and Entire Chromatinmentioning

confidence: 99%

Differences in spatial localization and chromatin pattern during different phases of cell cycle between normal and cancer cells

et al. 1997

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We studied differences in chromatin patterns and the spatial localization of centromeres of chromosome 11 during the cell cycle between normal peripheral blood lymphocytes (PBL) and human promyclocytic leukemia cells (HL‐60) using fluorescence in situ hybridization. The pericentromeres in both cells were located at the periphery during Gq (quiescent) phase, but moved towards the nuclear center in G1 and mid‐S phase. During G2, the pericentromeres of PBL continued to move towards the nuclear center whereas those of HL‐60 returned to the periphery. The angle defining the spatial location of two pericentromeres, in reference to the center of the nucleus, increased in PBL cells from a mean of 67° during Gq phase to 106° during G1 phase (P < 0.01), and the two pericentromeres remained wide apart throughout the entire cell cycle. In HL‐60, the angle also increased during G1, but then decreased during mid‐S and G2 phases. Both cells exhibited pericentromeric signals during Gq that were round and compact, and the entire chromatin was loosely condensed. The signal became more loose and dispersed during the G1 and mid‐S phases. The pericentromere signal varied during G2 and was generally rod‐like or bipartite with condensation of the entire chromatin or chromosome‐like. Our results suggest that subtle but important differences in spatial localization of pericentromeres are present during the interphase between normal PBL and HL‐60 cells. Cytometry 27:327–335, 1997. © 1997 Wiley‐Liss, Inc.

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Numerical aberrations of chromosomes 11 and 17 in colorectal adenocarcinomas

Cited by 10 publications

References 35 publications

Chromosome instability evaluated by fluorescence in situ hybridization in hereditary non-polyposis colorectal cancer

Chromosome instability evaluated by fluorescence in situ hybridization in hereditary non-polyposis colorectal cancer

Chromosomal aneuploidies induced upon Lamin B2 depletion are mislocalized in the interphase nucleus

Differences in spatial localization and chromatin pattern during different phases of cell cycle between normal and cancer cells

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