Numerical aberrations of chromosome 8 detected by conventional cytogenetics and fluorescence in situ hybridization in individuals from northern Brazil with gastric adenocarcinoma

Assumpção, Paulo Pimentel de; Ishak, Geraldo; Chen, Elizabeth; Takeno, Sylvia Satomi; Leal, Mariana Ferreira; Guimarães, Adriana Costa; Calcagno, Danielle Queiroz; Khayat, André Salim; Demachki, Sâmia; Smith, Marı́lia de Arruda Cardoso; Burbano, Rommel Rodrı́guez

doi:10.1016/j.cancergencyto.2006.03.019

Cited by 28 publications

(19 citation statements)

References 27 publications

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“…Xia et al [11] described trisomies of chromosomes 8 and 9 as a cytogenetic subgroup of gastric cancer. Panani et al [10] suggested that chromosome 8 trisomy could be related to tumours with better prognosis, although some authors had described it in advanced cases [3,8,13,20]. Xiao et al [8] have also observed trisomy 8 in a case with minimal chromosomal changes, suggesting that this abnormality might be a non-random event in gastric tumorigenesis.…”

Section: Discussionmentioning

confidence: 92%

Aneuploidy of chromosome 8 detected by fluorescence in situ hybridisation in ACP01 cell line gastric adenocarcinoma

et al. 2006

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Gastric cancer is the third most frequent type of neoplasia and the second most important cause of death in the world. ACP01 is the first gastric adenocarcinoma cell line developed in Brazil. To evaluate chromosomal aberrations implicated in gastric carcinogenesis, we analysed three different passages (6th, 12th and 35th) of ACP01 cell line by fluorescence in situ hybridisation using chromosome 8 alpha-satellite probe. Most of the chromosome 8 alterations found involved a numerical increase of this chromosome. Chromosome 8 trisomy was detected in all cases, varying from 37% (6th passage) to 67% (35th passage), and chromosome 8 tetrasomy (also observed in all passages) varied from 2.5% (6th passage) to 30% (35th passage). The presence of five signals for chromosome 8 was observed in all passages with the highest frequency found in the 12th passage (20%). Our results confirm that trisomy of chromosome 8 is a common biological phenomenon in adenocarcinoma of stomach and can be used as a gastric mucosa malignancy marker. Although gastric tumours are frequent neoplasias, papers on their cytogenetics are scarce in the literature. It is, therefore, necessary to conduct new studies aiming to identify peculiar genetic characteristics of a tumour, which might help in diagnosis and prognosis of this disease, besides allowing more accurate therapeutic conduct to be established.

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Section: Discussionmentioning

confidence: 92%

Aneuploidy of chromosome 8 detected by fluorescence in situ hybridisation in ACP01 cell line gastric adenocarcinoma

et al. 2006

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“…Copy number gains are frequently detected along chromosome 8 in gastric tumors [43,48,56,[68][69][70][71][72][73] . Suzuki et al [43] described that chromosome 8 copy number was significantly higher in differentiated than undifferentiated types of GC.…”

Section: Mechanisms Of Myc Deregulation In Gastric Cancermentioning

confidence: 99%

MYC and gastric adenocarcinoma carcinogenesis

Calcagno¹,

Leal²,

Assumpção³

et al. 2008

WJG

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MYC is an oncogene involved in cell cycle regulation, cell growth arrest, cell adhesion, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function. It has been described as a key element of several carcinogenesis processes in humans. Many studies have shown an association between MYC deregulation and gastric cancer. MYC deregulation is also seen in gastric preneoplastic lesions and thus it may have a role in early gastric carcinogenesis. Several studies have suggested that amplification is the main mechanism of MYC deregulation in gastric cancer.In the present review, we focus on the deregulation of the MYC oncogene in gastric adenocarcinoma c a r c i n o g e n e s i s , i n c l u d i n g i t s a s s o c i a t i o n w i t h Helicobacter pylori (H pylori ) MYC AND CANCERMYC gene was found to be the cellular homolog of retroviral v-myc oncogene about 30 years ago [12][13][14] . It is located on chromosomal region 8q24.1, has 3 exons [15,16] and encodes a nuclear phosphoprotein [17] . MYC has to heteromerize with MAX, a protein expressed constitutively, to acquire DNA-binding activity. MYC/MAX dimmers are made viable by a basic region helix-loop-helix leucine-zipper motif (bHLHZip), conserved sequences in the carboxyl terminus of both proteins. MYC/MAX dimmers bind to E-box sequence CACGTG in the promoters of specific target genes and stimulate their transcription [18] . MYC has an effect on up to about 15% of genes in genomes of many organisms, from flies to humans [19] . Groups of genes involved in cell cycle regulation, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function are over-represented in the Myc target gene network.MYC also consistently represses genes involved in cell growth arrest and cell adhesion [20] . Dominguez-Sola et al [21] recently showed that Myc interacts with the prereplicative complex and localizes to early sites of DNA synthesis. Thus, it also has a direct role in the control of DNA replication.MYC regulates transcription from its targets through several mechanisms, including recruitment of histone acetylases, chromatin modulating proteins, basal transcription factors and DNA methyltransferase [22][23][24][25][26] . Protein products of MYC target genes g o on to mediate the downstream effects of MYC on cell biology. MYC is then rapidly degraded, and the pathway switches to a transcriptionally repressive state when MAX dimerizes with a group of related bHLH-Zip proteins, the MAD family, that act as MYC antagonists [27] ( Figure 1).MYC expression might be regulated transcriptionally (initiation and elongation), post-transcriptionally (mRNA stability and translation) or post-translationally (protein stability) [28] . MYC is generally recognized as an important regulator of proliferation, growth, differentiation and apoptosis [29,30] . Therefore, it is also accepted that the deregulation of MYC expression is a major event in cancer pathogenesis or progression. Deregulated expression of a wild-type MYC protein is suff...

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“…Chromosomal instability is one of the two major genomic instability pathways observed in gastric cancer (GC) [1], the fourth most frequent type of cancer and second most frequent cause of cancer mortality worldwide [2]. However, due to the difficulty in obtaining high-quality chromosome preparations in these neoplasias, the evaluation of chromosomal alterations is complicated [3–7]. …”

Section: Introductionmentioning

confidence: 99%

MYC, TP53, and Chromosome 17 Copy‐Number Alterations in Multiple Gastric Cancer Cell Lines and in Their Parental Primary Tumors

Leal

Calcagno

Costa

et al. 2011

BioMed Research International

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We evaluated whether MYC, TP53, and chromosome 17 copy-number alterations occur in ACP02, ACP03, and AGP01 gastric cancer cell lines and in their tumor counterpart. Fluorescence in situ hybridization for MYC and TP53 genes and for chromosome 17 was applied in the 6th, 12th, 60th, and 85th passages of the cell lines and in their parental primary tumors. We observed that three and four MYC signals were the most common alterations in gastric cell lines and tumors. ACP02 presented cells with two copies of chr17 and loss of one copy of TP53 more frequently than ACP03 and AGP01. Only ACP03 and AGP01 presented clonal chr17 trisomy with three or two TP53 copies. The frequency of MYC gain, TP53 loss, and chromosome 17 trisomy seems to increase in gastric cell lines compared to their parental tumors. Our findings reveal that these cell lines retain, in vitro, the genetic alterations presented in their parental primary tumors.

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Numerical aberrations of chromosome 8 detected by conventional cytogenetics and fluorescence in situ hybridization in individuals from northern Brazil with gastric adenocarcinoma

Cited by 28 publications

References 27 publications

Aneuploidy of chromosome 8 detected by fluorescence in situ hybridisation in ACP01 cell line gastric adenocarcinoma

Aneuploidy of chromosome 8 detected by fluorescence in situ hybridisation in ACP01 cell line gastric adenocarcinoma

MYC and gastric adenocarcinoma carcinogenesis

MYC, TP53, and Chromosome 17 Copy‐Number Alterations in Multiple Gastric Cancer Cell Lines and in Their Parental Primary Tumors

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