Characterization of four new gastric cancer cell lines

Vollmers, H. Peter; Stulle, K; Dämmrich, J.; Pfaff, Martin; Papadopoulos, Thomas; Betz, Christoph; Saal, Kim‐Ann; Müller-Hermelink, H. K.

doi:10.1007/bf02899281

Cited by 28 publications

(18 citation statements)

References 21 publications

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“…Walen (28) suggested that these morphological characteristics might be indicators of the process of in vitro immortalization, supporting the conclusion that ACP01 had been immortalized. It should be pointed out that only 14 of the 59 cell lines that have been reported are from primary tumors, and that their morphological characteristics are similar to those found in our cell line (10,14,15).…”

Section: Discussionsupporting

confidence: 81%

“…Yet, in spite of the importance of gastric cancer, relatively few such cell lines are available (12). So far, 59 lines have been cultured, 14 of which were from primary tumors (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23) and the remainder from secondary tumors or metastases (10,12,(14)(15)(16)(17). Most of these cell lines (78%) were isolated in Asia (6).…”

Section: Introductionmentioning

confidence: 99%

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Conventional cytogenetic characterization of a new cell line, ACP01, established from a primary human gastric tumor

Lima

Rissino

Harada

et al. 2004

Braz J Med Biol Res

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Gastric cancer is the second most frequent type of neoplasia and also the second most important cause of death in the world. Virtually all the established cell lines of gastric neoplasia were developed in Asian countries, and western countries have contributed very little to this area. In the present study we describe the establishment of the cell line ACP01 and characterize it cytogenetically by means of in vitro immortalization. Cells were transformed from an intestinal-type gastric adenocarcinoma (T4N2M0) originating from a 48-year-old male patient. This is the first gastric adenocarcinoma cell line established in Brazil. The most powerful application of the cell line ACP01 is in the assessment of cytotoxicity. Solid tumor cell lines from different origins have been treated with several conventional and investigational anticancer drugs. The ACP01 cell line is triploid, grows as a single, non-organized layer, similar to fibroblasts, with focus formation, heterogeneous division, and a cell cycle of approximately 40 h. Chromosome 8 trisomy, present in 60% of the cells, was the most frequent cytogenetic alteration. These data lead us to propose a multifactorial triggering of gastric cancer which evolves over multiple stages involving progressive genetic changes and clonal expansion.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Conventional cytogenetic characterization of a new cell line, ACP01, established from a primary human gastric tumor

Lima

Rissino

Harada

et al. 2004

Braz J Med Biol Res

View full text Add to dashboard Cite

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“…According to Laurén's classification, cases were classified as intestinal (n ϭ 39), diffuse (n ϭ 29), and atypical (n ϭ 22) carcinomas. Gastric carcinoma-derived cell lines GP220 (Gärtner et al, 1996), GP202 (Gärtner et al, 1996), MKN45 (Motoyama et al, 1986), KATO-III (Sekiguchi et al, 1978), L195 (Carvalho et al, 2001), St2957 (Vollmers et al, 1993), St3051 (Vollmers et al, 1993), and St23132 (Vollmers et al, 1993) were also studied. In addition, blood donors (n ϭ 98) from the same geographic region as the patients with gastric carcinoma were used as controls.…”

Section: Methodsmentioning

confidence: 99%

Loss of Heterozygosity and Promoter Methylation, but not Mutation, May Underlie Loss of TFF1 in Gastric Carcinoma

Carvalho

Kayademir

Soares

et al. 2002

Laboratory Investigation

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SUMMARY:It has been advanced that the trefoil factor (TFF) 1 gene is a candidate tumor-suppressor gene and may be involved in the development and/or progression of human gastric cancer. We aimed to clarify the putative role of TFF1 in gastric carcinogenesis. Ninety gastric carcinomas and eight gastric carcinoma-derived cell lines were screened for TFF1 mutations; subsets of the primary tumors and of the cell lines were subjected to loss of heterozygosity (LOH), immunohistochemistry, and promoter methylation analyses. TFF1 mutations were not detected in any of 90 gastric carcinomas. Eight (28%) of 28 informative cases displayed LOH at the TFF1 locus and absence of TFF1 staining by immunohistochemistry. These results indicate a frequent loss of TFF1 expression in gastric carcinomas through a mutation-independent mechanism. Extensive TFF1 promoter methylation was observed in nonexpressing gastric carcinoma-derived cell lines and tissues. Expressing cell lines, as well as normal gastric mucosa, presented little or no methylation of the promoter. Gastric carcinoma DNA presented de novo methylation of the promoter. These results point to the involvement of promoter methylation in the shutting down of TFF1. We conclude that TFF1 point mutations seem to be a rare event in gastric carcinogenesis. The loss of expression of TFF1 in a proportion of gastric carcinomas may be explained by LOH and methylation of the TFF1 promoter region. Our results further support the role of TFF1 inactivation in gastric carcinogenesis, in agreement with the results obtained in the Tff1-knockout mice model. (Lab Invest 2002, 82:1319 -1326.

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“…The gastric cancer cell line 23132 was derived from human gastric adenocarcinoma (Vollmers et al, 1993). HGT-1 (kindly provided by Dr. R. Negrini, Brescia, Italy) was chosen because of its features of gastric parietal cells (Carmosino et al, 2000;Laboisse et al, 1982).…”

Section: Cell Linesmentioning

confidence: 99%

Transcription of Sonic Hedgehog, a Potential Factor for Gastric Morphogenesis and Gastric Mucosa Maintenance, Is Up-regulated in Acidic Conditions

Dimmler

Brabletz

Hlubek

et al. 2003

Laboratory Investigation

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SUMMARY:Gastric body mucosa atrophy predisposes one to gastric cancer. Disturbances in the gastric differentiation process might play a role in the evolution of gastric atrophy. Sonic hedgehog (Shh) has recently been implicated as a crucial factor in gastric organogenesis and gland differentiation. In this study we investigated the expression of key factors in the Shh pathway, namely Shh and its receptor Patched (Ptc), in normal and pathologic stomach mucosa. Furthermore, the potential role of pH for Shh dysregulation was analyzed. Ten gastric biopsy specimens each from normal gastric mucosa, chronic nonatrophic gastritis, atrophic gastritis, and gastric cancer were included. Expression of Shh and Ptc was analyzed by immunohistochemistry. In normal body mucosa and in nonatrophic body gastritis, Shh was strongly expressed in parietal cells. Ptc was also expressed in gastric chief cells. Shh expression was almost completely lost in atrophic gastritis and in gastric cancer and absent in intestinal metaplasia. Ptc was markedly reduced in atrophy and only weakly positive in intestinal metaplasia and gastric cancer. In in vitro experiments, gastric cancer cell line 23132 was found positive for Shh. In long-term culture as well as in culture conditions with low pH, transcription of Shh in 23132 was significantly increased in quantitative reverse transcription PCR analyses. We concluded that the decreased expression of the Shh pathway in atrophic gastritis and gastric cancer might reflect altered differentiation processes within the gastric unit and contributes to the development of gastric atrophy. The increase of gastric pH might play a role in the development of gastric mucosa atrophy via reduction of Shh transcription. (Lab Invest 2003, 83:1829 -1837.

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Characterization of four new gastric cancer cell lines

Cited by 28 publications

References 21 publications

Conventional cytogenetic characterization of a new cell line, ACP01, established from a primary human gastric tumor

Conventional cytogenetic characterization of a new cell line, ACP01, established from a primary human gastric tumor

Loss of Heterozygosity and Promoter Methylation, but not Mutation, May Underlie Loss of TFF1 in Gastric Carcinoma

Transcription of Sonic Hedgehog, a Potential Factor for Gastric Morphogenesis and Gastric Mucosa Maintenance, Is Up-regulated in Acidic Conditions

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