Changes of the p16 gene but not the p53 gene in human chondrosarcoma tissues

Asp, Julia; Sangiorgi, Luca; Inerot, Sven; Lindahl, Anders; Molendini, Lara; Benassi, Maria Serena; Picci, Piero

doi:10.1002/(sici)1097-0215(20000315)85:6<782::aid-ijc7>3.0.co;2-o

Cited by 66 publications

(47 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies of the p14 ARF and p16 INK4A gene have been reported previously (Asp et al, 2000(Asp et al, , 2001a(Asp et al, , 2001b. Alterations in the p16 INK4A have been found in 6 of 22 human CS tissues, which were all grade 2 and 3 tumors; the majority of the alterations were increases in methylation rather than homozygous deletions of the gene.…”

Section: Gil-benso Et Almentioning

confidence: 85%

See 1 more Smart Citation

Establishment and Characterization of a Continuous Human Chondrosarcoma Cell Line, ch-2879: Comparative Histologic and Genetic Studies with Its Tumor of Origin

Gil-Benso

López‐Ginés

Löpez‐Guerrero

et al. 2003

Laboratory Investigation

View full text Add to dashboard Cite

SUMMARY:Chondrosarcomas are malignant cartilage-forming tumors that represent the second most common malignant solid tumor of bone. These biologically poorly understood neoplasms vary considerably in clinical presentation and biologic behavior. Chemotherapy and radiation therapy are generally ineffective. Here we describe the establishment and characterization of a new human chondrosarcoma cell line named ch-2879, and we compare the cell line with its tumor of origin. The cell line was established from a recurrent grade 3 chondrosarcoma of the chest wall and characterized by growth kinetics and morphologic studies. Immunocytochemistry and RT-PCR were performed to examine the expression of cartilage-specific phenotypes. Genetic characterization was performed using cytogenetics, fluorescence in situ hybridization, flow cytometry, and molecular techniques for analysis of the genes implicated in cell cycle control, amplification of MDM2, CDK4, and Cyclin D1, and mutations in the p53 gene. ch-2879 cells were subcultured for more than 80 passages. They expressed vimentin, HNK-1, HBA-71, Ki-67, cyclin D1, Fli-1, S-100, p21, p27, and p53 and were negative for cytokeratin, EMA, p14, p16, MDM2, Rb, and c-erb-b2 antigens. Cytogenetically the recurrent tumor showed a hyperhaploid karyotype with clonal numerical and structural abnormalities. The sole structural abnormality was a chromosome derivative of a t(1;21) translocation. The cell line at passage 3 showed two populations: the hyperhaploid and an exactly duplicated, hypotriploid population. After the 18th passage, only the hypotriploid population was present. The cells expressed collagen 2. Molecular comparison of the primary and recurrent tumor evidenced an in vivo molecular change consisting of a deletion of 9p21 genes in the recurrence, probably caused by a selection process. Because of its gene expression profile, including expression of genes implicated in chondrogenesis in uncoated plastic dishes, this cell line may prove useful for cellular and molecular studies as well as studies of chondrosarcoma characterization and treatment. (Lab Invest 2003, 83:877-887).

show abstract

Section: Gil-benso Et Almentioning

confidence: 85%

“…On the contrary, only a few reports have analyzed alterations in the 9p21 locus genes. These studies showed that hypermethylation of the p16 INK4A gene is found predominantly in high-grade CS (Asp et al, 2000(Asp et al, , 2001b.…”

mentioning

confidence: 97%

Establishment and Characterization of a Continuous Human Chondrosarcoma Cell Line, ch-2879: Comparative Histologic and Genetic Studies with Its Tumor of Origin

Gil-Benso

López‐Ginés

Löpez‐Guerrero

et al. 2003

Laboratory Investigation

View full text Add to dashboard Cite

show abstract

“…DNA hypermethylation contributes to the development of CS via various cell pathways, including cell cycle, apoptosis, cell adherence and cell-to-cell interaction [25][26][27][28]. For example, P16 INK4a , a well-known tumor suppressor gene, was found to be hypermethylated in the promoter region in CS [26].…”

Section: Dna Hypermethylation and Abnormalities In Csmentioning

confidence: 99%

“…For example, P16 INK4a , a well-known tumor suppressor gene, was found to be hypermethylated in the promoter region in CS [26]. P16…”

Section: Dna Hypermethylation and Abnormalities In Csmentioning

confidence: 99%

See 1 more Smart Citation

Aberrant DNA Methylations in Chondrosarcoma

Liu

Shen

et al. 2016

Epigenomics

View full text Add to dashboard Cite

Chondrosarcoma (CS) is the second most common primary malignant bone tumor. Unlike other bone tumors, CS is highly resistant to conventional chemotherapy and radiotherapy, thus resulting in poor patient outcomes. There is an urgent need to establish alternative therapies for CS. However, the etiology and pathogenesis of CS still remain elusive. Recently, DNA methylation-associated epigenetic changes have been found to play a pivotal role in the initiation and development of human cancers, including CS, by regulating target gene expression in different cellular pathways. Elucidating the mechanisms of DNA methylation alteration may provide biomarkers for diagnosis and prognosis, as well as novel treatment options for CS. We have conducted a critical review to summarize the evidence regarding aberrant DNA methylation patterns as diagnostic biomarkers, predictors of progression and potential treatment strategies in CS.

show abstract

Proteomics approach in classifying the biochemical basis of the anticancer activity of the new olomoucine-derived synthetic cyclin-dependent kinase inhibitor, bohemine

Kovářová¹,

Hajdúch

Korinkova

et al. 2000

Electrophoresis

View full text Add to dashboard Cite

The aim of this study was to use two-dimensional electrophoresis (2-DE) coupled with multivariate principal component analysis (PCA) to characterize the quantitative changes in the protein composition of the CEM T-lymphoblastic leukemia cell line after treatment with bohemine (BOH), a synthetic olomoucin-derived cyclin-dependent kinase inhibitor (CDKI). Cell classification, reflecting protein patterns, clearly distinguished two main groups: one group consists of 9, 12 and 24 h treated BOH cells while the second is represented by the 0 and 24 h control untreated cells and the 6 h BOH-exposed CEM lymphoblasts. Discriminant protein spots differentially expressed in the BOH-treated CEM cells were selected for identification by matrix assisted laser desorption/ionization-mass spectrometry (MALDI-MS) or electrospray ionization-tandem MS (ESI-MS/MS). Five of the selected protein spots were unequivocally identified as alpha-enolase, triosephosphate isomerase, eukaryotic initiation factor 5A, and alpha- and beta-subunits of Rho GDP-dissociation inhibitor 1. These proteins, all significantly downregulated in CEM T-lymphoblast leukemia in the course of BOH treatment, are known to play an important role in cellular functions such as glycolysis, protein biosynthesis, and cytoskeleton rearrangement. These results indicate that the cellular effects of olomoucine-derived CDKIs are not dependent on their ability to inhibit CDKs and could be mediated by several factors such as a decrease in protein synthesis and/or glycolysis which in turn diminishes the ability of cancer cells to function.

show abstract

Changes of the p16 gene but not the p53 gene in human chondrosarcoma tissues

Cited by 66 publications

References 19 publications

Establishment and Characterization of a Continuous Human Chondrosarcoma Cell Line, ch-2879: Comparative Histologic and Genetic Studies with Its Tumor of Origin

Establishment and Characterization of a Continuous Human Chondrosarcoma Cell Line, ch-2879: Comparative Histologic and Genetic Studies with Its Tumor of Origin

Aberrant DNA Methylations in Chondrosarcoma

Proteomics approach in classifying the biochemical basis of the anticancer activity of the new olomoucine-derived synthetic cyclin-dependent kinase inhibitor, bohemine

Contact Info

Product

Resources

About