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Waisfisz Q, Miyazato A, De Winter JP, et al. Analysis of baseline and cisplatin-inducible gene expression in Fanconi anemia cells using oligonucleotide-based microarrays. BMC Blood Disord. 2002;2(1):5doi: 10.1186/1471-2326-2-5.
Waisfisz, Q., Miyazato, A., De Winter, J. P., Liu, J. M., & Joenje, H. (2002). Analysis of baseline and cisplatin-inducible gene expression in Fanconi anemia cells using oligonucleotide-based microarrays. BMC blood disorders, 2(1), 5. https://doi.org/10.1186/1471-2326-2-5
Waisfisz, Quinten, et al. "Analysis of baseline and cisplatin-inducible gene expression in Fanconi anemia cells using oligonucleotide-based microarrays." BMC blood disorders vol. 2,1 (2002): 5. doi: https://doi.org/10.1186/1471-2326-2-5
Waisfisz Q, Miyazato A, De Winter JP, Liu JM, Joenje H. Analysis of baseline and cisplatin-inducible gene expression in Fanconi anemia cells using oligonucleotide-based microarrays. BMC Blood Disord. 2002 Nov 26;2(1):5. doi: 10.1186/1471-2326-2-5. PMID: 12450415; PMCID: PMC138804.
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BMC Blood Disord. 2002 Nov 26;2(1):5. doi: 10.1186/1471-2326-2-5.

Analysis of baseline and cisplatin-inducible gene expression in Fanconi anemia cells using oligonucleotide-based microarrays.

BMC blood disorders

Quinten Waisfisz, Akira Miyazato, Johan P De Winter, Johnson M Liu, Hans Joenje

Affiliations

  1. Department of Clinical Genetics and Human Genetics, VU University Medical Center, Amsterdam, The Netherlands. [email protected]

PMID: 12450415 PMCID: PMC138804 DOI: 10.1186/1471-2326-2-5

Abstract

BACKGROUND: Patients with Fanconi anemia (FA) suffer from multiple defects, most notably of the hematological compartment (bone marrow failure), and susceptibility to cancer. Cells from FA patients show increased spontaneous chromosomal damage, which is aggravated by exposure to low concentrations of DNA cross-linking agents such as mitomycin C or cisplatin. Five of the identified FA proteins form a nuclear core complex. However, the molecular function of these proteins remains obscure. METHODS: Oligonucleotide microarrays were used to compare the expression of approximately 12,000 genes from FA cells with matched controls. Expression profiles were studied in lymphoblastoid cell lines derived from three different FA patients, one from the FA-A and two from the FA-C complementation groups. The isogenic control cell lines were obtained by either transfecting the cells with vectors expressing the complementing cDNAs or by using a spontaneous revertant cell line derived from the same patient. In addition, we analyzed expression profiles from two cell line couples at several time points after a 1-hour pulse treatment with a discriminating dose of cisplatin. RESULTS: Analysis of the expression profiles showed differences in expression of a number of genes, many of which have unknown function or are difficult to relate to the FA defect. However, from a selected number of proteins involved in cell cycle regulation, DNA repair and chromatin structure, Western blot analysis showed that p21waf1/Cip1 was significantly upregulated after low dose cisplatin treatment in FA cells specifically (as well as being expressed at elevated levels in untreated FA cells). CONCLUSIONS: The observed increase in expression of p21waf1/Cip1 after treatment of FA cells with crosslinkers suggests that the sustained elevated levels of p21waf1/Cip1 in untreated FA cells detected by Western blot analysis likely reflect increased spontaneous damage in these cells.

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