Cytogenetic characterization and evaluation of c-MYC gene amplification in PG100, a new Brazilian gastric cancer cell line

Ribeiro, Helem Ferreira; Alcântara, Diego Di Felipe Ávila; Matos, Leomá Albuquerque; Sousa, João Marcelo de Castro e; Leal, Mariana Ferreira; Smith, Marı́lia de Arruda Cardoso; Burbano, Rommel Rodrı́guez; Bahia, Marcelo de Oliveira

doi:10.1590/s0100-879x2010007500068

Cited by 21 publications

(9 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, most of the copy number changes observed in ACP02, ACP03, AGP01 and PG100 by cCGH were confirmed by aCGH. ACP02, ACP03 and AGP01 are gastric adenocarcinoma cell lines from diffuse and intestinal types and cancerous ascitic fluid and were previously established and characterized by our research group[17,18], while PG100 is a commercially available primary gastric adenocarcinoma cell line[19]. Furthermore, aCGH analysis enabled the identification of many additional chromosomal gains and losses.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Identification ofIL11RAandMELKamplification in gastric cancer by comprehensive genomic profiling of gastric cancer cell lines

Calcagno¹,

Takeno²,

Gigek³

et al. 2016

WJG

View full text Add to dashboard Cite

AIMTo identify common copy number alterations on gastric cancer cell lines.METHODSFour gastric cancer cell lines (ACP02, ACP03, AGP01 and PG100) underwent chromosomal comparative genome hybridization and array comparative genome hybridization. We also confirmed the results by fluorescence in situ hybridization analysis using the bacterial artificial chromosome clone and quantitative real time PCR analysis.RESULTSThe amplification of 9p13.3 was detected in all cell lines by both methodologies. An increase in the copy number of 9p13.3 was also confirmed by fluorescence in situ hybridization analysis. Moreover, the interleukin 11 receptor alpha (IL11RA) and maternal embryonic leucine zipper kinase (MELK) genes, which are present in the 9p13.3 amplicon, revealed gains of the MELK gene in all the cell lines studied. Additionally, a gain in the copy number of IL11RA and MELK was observed in 19.1% (13/68) and 55.9% (38/68) of primary gastric adenocarcinoma samples, respectively.CONCLUSIONThe characterization of a small gain region at 9p13.3 in gastric cancer cell lines and primary gastric adenocarcinoma samples has revealed MELK as a candidate target gene that is possibly related to the development of gastric cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Additionally, we used the GC cell line, PG100, obtained from the Rio de Janeiro Cell Bank (Rio de Janeiro, RJ, Brazil), which was previously characterized cytogenetically by our group[19]. All cell lines were cultured according to Lima et al[20].…”

Section: Methodsmentioning

confidence: 99%

Identification ofIL11RAandMELKamplification in gastric cancer by comprehensive genomic profiling of gastric cancer cell lines

Calcagno¹,

Takeno²,

Gigek³

et al. 2016

WJG

View full text Add to dashboard Cite

show abstract

“…MYC also consistently represses genes involved in cell growth arrest and cell adhesion and also has a direct role in the control of DNA replication [23]. MYC amplification has been observed in gastric cancer cell lines and primary stomach tumors [8], [14], [15], [19], [24], [25], [26], [27], [28], [29], [30].…”

Section: Discussionmentioning

confidence: 99%

Experimental Gastric Carcinogenesis in Cebus apella Nonhuman Primates

et al. 2011

View full text Add to dashboard Cite

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.

show abstract

“…85,86 Many studies reported that a significant increase in MYC copy number can be detected in the carcinogenic process of GC and in gastric cell lines. [87][88][89][90][91][92] The amplification of MYC has also been suggested with independent prognostic value on overall survival. 93 In addition, MYC CNVs has a tight connection with the clinicopathological features of GC.…”

Section: Chromosomementioning

confidence: 99%

Gastric cancer and gene copy number variation: emerging cancer drivers for targeted therapy

2015

View full text Add to dashboard Cite

Gastric cancer (GC) is among the most common malignancy in the world with poor prognosis and limited treatment options. It has been established that gastric carcinogenesis is caused by a complex interaction between host and environmental factors. Copy number variation (CNV) refers to a form of genomic structural variation that results in abnormal gene copy numbers, including gene amplification, gain, loss and deletion. DNA CNV is an important influential factor for the expression of both protein-coding and non-coding genes, affecting the activity of various signaling pathways. CNV arises as a result of preferential selection that favors cancer development, and thus, targeting the amplified 'driver genes' in GC may provide novel opportunities for personalized therapy. The detection of CNVs in chromosomal or mitochondrial DNA from tissue or blood samples may assist the diagnosis, prognosis and targeted therapy of GC. In this review, we discuss the recent CNV discoveries that shed light on the molecular pathogenesis of GC, with a specific emphasis on CNVs that display diagnostic, prognostic or therapeutic significances in GC.

show abstract

Cytogenetic characterization and evaluation of c-MYC gene amplification in PG100, a new Brazilian gastric cancer cell line

Cited by 21 publications

References 17 publications

Identification ofIL11RAandMELKamplification in gastric cancer by comprehensive genomic profiling of gastric cancer cell lines

Identification ofIL11RAandMELKamplification in gastric cancer by comprehensive genomic profiling of gastric cancer cell lines

Experimental Gastric Carcinogenesis in Cebus apella Nonhuman Primates

Gastric cancer and gene copy number variation: emerging cancer drivers for targeted therapy

Contact Info

Product

Resources

About