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

Khayat, André Salim; Guimarães, Adriana Costa; Calcagno, Danielle Queiroz; Seabra, Aline Damasceno; Lima, Eleonidas Moura; Leal, Mariana Ferreira; Faria, M.; Rabenhorst, Sílvia Helena Barem; Assumpção, Paulo Pimentel de; Demachki, Sâmia; Smith, Marı́lia de Arruda Cardoso; Burbano, Rommel Rodrı́guez

doi:10.1186/1471-230x-9-55

Cited by 20 publications

(24 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This finding corroborates our previous study using dual-color FISH for chr17/ TP53 in primary tumor samples, in which we observed that the frequency of cells with two chr17 and one TP53 signals was higher in the diffuse-type than in the intestinal-type GC [27]. …”

Section: Discussionsupporting

confidence: 92%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionsupporting

confidence: 92%

“…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

View full text Add to dashboard Cite

show abstract

“…It was also suggested that the loss of p53 expression leads to the suppression of IGFBP-3 in tumor cells [23]. In our population, we previously described that all gastric samples presented TP53 allelic deletions [24]. Thus, the feedback between p53 and IGFBP-3 may be lost in these samples and other pathways may be inducing IGFBP-3 expression.…”

Section: Discussionmentioning

confidence: 82%

“…We previously observed that only intestinal type gastric cancer samples presented p53 immunoreactivity [24]. Increased immunostaining of p53 can depend on either increased synthesis of wildtype protein or accumulation of mutated protein in the cell [25], which explains the significant difference in IGFBP-3 staining between intestinal (92.3%) and in diffuse type (67.9%).…”

Section: Discussionmentioning

confidence: 96%

Insulin-like growth factor binding protein-3 gene methylation and protein expression in gastric adenocarcinoma

Gigek

Leal

Lisboa

et al. 2010

Growth Hormone & IGF Research

View full text Add to dashboard Cite

“…Previously we also reported the presence of p53 immunoreactivity in all intestinal-type gastric cancer of individuals from Northern Brazil [12]. The p53 immunoreactivity usually depends on the accumulation of mutated p53 proteins in the cell, which leads to a longer half-life [36].…”

Section: Discussionmentioning

confidence: 98%

hTERT, MYC and TP53 deregulation in gastric preneoplastic lesions

et al. 2012

View full text Add to dashboard Cite

Background Gastric cancer is a serious public health problem in Northern Brazil and in the world due to its high incidence and mortality. Despite the severity of the disease, more research is needed to better understand the molecular events involved in this intestinal-type gastric carcinogenesis process. Since precancerous lesions precede intestinal-type gastric cancer, here, we evaluated the hTERT , MYC, and TP53 mRNA and protein expression, as well as TP33 copy number, in gastric preneoplastic lesions. Methods We evaluated 19 superficial gastritis, 18 atrophic gastritis, and 18 intestinal metaplasia from cancer-free individuals of Northern Brazil. Quantitative reverse transcription PCR was used to analyze the mRNA expression and immunohistochemical methods were used to assess protein immunoreactivity in tissue samples. The number of TP53 gene copies was investigated in gastric diseases by quantitative PCR. Results We observed hTERT, MYC, and p53 immunoreactivity only in intestinal metaplasia samples. The immunoreactivity of these proteins was strongly associated with each other. A significantly higher MYC mRNA expression was observed in intestinal metaplasia compared to gastritis samples. Loss of TP53 was also only detected in intestinal metaplasia specimens. Conclusions We demonstrated that hTERT, MYC, and TP53 are deregulated in intestinal metaplasia of individuals from Northern Brazil and these alterations may facilitate tumor initiation.

show abstract

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

Cited by 20 publications

References 41 publications

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

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

Insulin-like growth factor binding protein-3 gene methylation and protein expression in gastric adenocarcinoma

hTERT, MYC and TP53 deregulation in gastric preneoplastic lesions

Contact Info

Product

Resources

About