Genomic alterations in diffuse-type gastric cancer as shown by high-resolution comparative genomic hybridization

Takeno, Sylvia Satomi; Leal, Mariana Ferreira; Lisboa, Luara Carolina Frias; Lipay, Mônica Vannucci Nunes; Khayat, André Salim; Assumpção, Paulo Pimentel de; Burbano, Rommel Rodrı́guez; Smith, Marı́lia de Arruda Cardoso

doi:10.1016/j.cancergencyto.2008.09.007

Cited by 17 publications

(10 citation statements)

References 34 publications

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“…This result corroborates our previous conventional and molecular cytogenetic studies, which demonstrated that chr17 aneusomy is not a frequent in GC samples of individual from Northern Brazil [7,35,36]. …”

Section: Discussionsupporting

confidence: 92%

Interrelationship between TP53gene deletion, protein expression and chromosome 17 aneusomy in gastric adenocarcinoma

et al. 2009

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BackgroundThis study evaluates the existence of numerical alterations of chromosome 17 and TP53 gene deletion in gastric adenocarcinoma. The p53 protein expression was also evaluated, as well as, possible associations with clinicopathological characteristics.MethodsDual-color fluorescence in situ hybridization and immunostaining were performed in twenty gastric cancer samples of individuals from Northern Brazil.ResultsDeletion of TP53 was found in all samples. TP53 was inactivated mainly by single allelic deletion, varying to 7–39% of cells/case. Aneusomy of chromosome 17 was observed in 85% of cases. Chromosome 17 monosomy and gain were both observed in about half of cases. Cells with gain of chromosome 17 frequently presented TP53 deletion. The frequency of cells with two chr17 and one TP53 signals observed was higher in diffuse than in intestinal-type GC. Immunoreactivity of p53 was found only in intestinal-type samples. The frequency of cells with two chr17 and two TP53 signals found was higher in samples with positive p53 expression than in negative cases in intestinal-type GC.ConclusionWe suggest that TP53 deletion and chromosome 17 aneusomy is a common event in GC and other TP53 alterations, as mutation, may be implicated in the distinct carcinogenesis process of diffuse and intestinal types.

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Section: Discussionsupporting

confidence: 92%

Interrelationship between TP53gene deletion, protein expression and chromosome 17 aneusomy in gastric adenocarcinoma

et al. 2009

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“…Abud et al described that the number of macrophages increased in cultures of bone marrow cells treated with Canova [46], corroborating previous in vivo and in vitro studies which showed macrophage activation by Canova treatment [47], [48], [49], [50], [51], [52]. According to Abud et al, Canova-active macrophages induce the production of lymphocytes and erythrocytes [46].…”

Section: Discussionsupporting

confidence: 60%

Experimental Gastric Carcinogenesis in Cebus apella Nonhuman Primates

et al. 2011

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The evolution of gastric carcinogenesis remains largely unknown. We established two gastric carcinogenesis models in New-World nonhuman primates. In the first model, ACP03 gastric cancer cell line was inoculated in 18 animals. In the second model, we treated 6 animals with N-methyl-nitrosourea (MNU). Animals with gastric cancer were also treated with Canova immunomodulator. Clinical, hematologic, and biochemical, including C-reactive protein, folic acid, and homocysteine, analyses were performed in this study. MYC expression and copy number was also evaluated. We observed that all animals inoculated with ACP03 developed gastric cancer on the 9th day though on the 14th day presented total tumor remission. In the second model, all animals developed pre-neoplastic lesions and five died of drug intoxication before the development of cancer. The last surviving MNU-treated animal developed intestinal-type gastric adenocarcinoma observed by endoscopy on the 940th day. The level of C-reactive protein level and homocysteine concentration increased while the level of folic acid decreased with the presence of tumors in ACP03-inoculated animals and MNU treatment. ACP03 inoculation also led to anemia and leukocytosis. The hematologic and biochemical results corroborate those observed in patients with gastric cancer, supporting that our in vivo models are potentially useful to study this neoplasia. In cell line inoculated animals, we detected MYC immunoreactivity, mRNA overexpression, and amplification, as previously observed in vitro. In MNU-treated animals, mRNA expression and MYC copy number increased during the sequential steps of intestinal-type gastric carcinogenesis and immunoreactivity was only observed in intestinal metaplasia and gastric cancer. Thus, MYC deregulation supports the gastric carcinogenesis process. Canova immunomodulator restored several hematologic measurements and therefore, can be applied during/after chemotherapy to increase the tolerability and duration of anticancer treatments.

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“…Although primary tumors of individuals from Northern Brazil present clonal crh17 trisomy or monosomy by FISH analysis [27], chr17 aneusomy is not the most frequent alteration within primary tumors of our population [7, 22, 28]. …”

Section: Discussionmentioning

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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Genomic alterations in diffuse-type gastric cancer as shown by high-resolution comparative genomic hybridization

Cited by 17 publications

References 34 publications

Interrelationship between TP53gene deletion, protein expression and chromosome 17 aneusomy in gastric adenocarcinoma

Interrelationship between TP53gene deletion, protein expression and chromosome 17 aneusomy in gastric adenocarcinoma

Experimental Gastric Carcinogenesis in Cebus apella Nonhuman Primates

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

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