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The gene expression profiles of medulloblastoma cell lines resistant to preactivated cyclophosphamide.

Publication ,  Journal Article
Bacolod, MD; Lin, SM; Johnson, SP; Bullock, NS; Colvin, M; Bigner, DD; Friedman, HS
Published in: Curr Cancer Drug Targets
May 2008

The total expression profiles of two medulloblastoma cell lines resistant to the preactivated form of cyclophosphamide (4-hydroperoxycyclophosphamide, 4-HC) were examined using the Affymetrix GeneChip U133A array. Our primary objective was to look for possible genes, other than the well-studied aldehyde dehydrogenases (ALDH) that may be involved in cyclophosphamide (CP) resistance in medulloblastomas. We present here the lists of the most highly upregulated [30 for D341 MED (4-HCR); 20 for D283 MED (4-HCR)] and downregulated [19 for D341 MED (4-HCR); 15 for D283 MED (4-HCR)] genes which may be involved in conferring CP-resistance to the two medullobalstoma cell lines. The lists of genes from the two sublines almost had no overlap, suggesting different mechanisms of CP-resistance. One of the most noteworthy upregulated gene is TAP1 [90-fold increase in D341 MED (4-HCR) relative to D341 MED]. TAP1, a protein belonging to the ABC transporter family is normally involved in major histocompatibility class I (MHC I) antigen processing. This suggests the possible role of multidrug resistance (MDR), albeit atypical (which means it does not involve the usual MDR1 and MRP glycoproteins), in medulloblastoma's CP-resistance. Apart from TAP1, a number of other genes involved in MHC1 processing were upregulated in D341 MED (4HCR). D341 MED (4-HCR) also had a 20-fold increase in the expression of the aldo-keto reductase gene, AKR1B10, which may deactivate the reactive cyclophosphamide metabolite, aldophosphamide. For D283 MED (4-HCR), the most notable increase in expression is that of ALDH1B1, a member of the aldehyde dehydrogenase (ALDH) family of proteins.

Duke Scholars

Published In

Curr Cancer Drug Targets

DOI

EISSN

1873-5576

Publication Date

May 2008

Volume

8

Issue

3

Start / End Page

172 / 179

Location

Netherlands

Related Subject Headings

  • Phenotype
  • Oncology & Carcinogenesis
  • Oligonucleotide Array Sequence Analysis
  • Medulloblastoma
  • Humans
  • Genotype
  • Gene Expression Regulation, Neoplastic
  • Gene Expression Regulation, Enzymologic
  • Gene Expression Profiling
  • Drug Resistance, Neoplasm
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Bacolod, M. D., Lin, S. M., Johnson, S. P., Bullock, N. S., Colvin, M., Bigner, D. D., & Friedman, H. S. (2008). The gene expression profiles of medulloblastoma cell lines resistant to preactivated cyclophosphamide. Curr Cancer Drug Targets, 8(3), 172–179. https://doi.org/10.2174/156800908784293631
Bacolod, M. D., S. M. Lin, S. P. Johnson, N. S. Bullock, M. Colvin, D. D. Bigner, and H. S. Friedman. “The gene expression profiles of medulloblastoma cell lines resistant to preactivated cyclophosphamide.Curr Cancer Drug Targets 8, no. 3 (May 2008): 172–79. https://doi.org/10.2174/156800908784293631.
Bacolod MD, Lin SM, Johnson SP, Bullock NS, Colvin M, Bigner DD, et al. The gene expression profiles of medulloblastoma cell lines resistant to preactivated cyclophosphamide. Curr Cancer Drug Targets. 2008 May;8(3):172–9.
Bacolod, M. D., et al. “The gene expression profiles of medulloblastoma cell lines resistant to preactivated cyclophosphamide.Curr Cancer Drug Targets, vol. 8, no. 3, May 2008, pp. 172–79. Pubmed, doi:10.2174/156800908784293631.
Bacolod MD, Lin SM, Johnson SP, Bullock NS, Colvin M, Bigner DD, Friedman HS. The gene expression profiles of medulloblastoma cell lines resistant to preactivated cyclophosphamide. Curr Cancer Drug Targets. 2008 May;8(3):172–179.

Published In

Curr Cancer Drug Targets

DOI

EISSN

1873-5576

Publication Date

May 2008

Volume

8

Issue

3

Start / End Page

172 / 179

Location

Netherlands

Related Subject Headings

  • Phenotype
  • Oncology & Carcinogenesis
  • Oligonucleotide Array Sequence Analysis
  • Medulloblastoma
  • Humans
  • Genotype
  • Gene Expression Regulation, Neoplastic
  • Gene Expression Regulation, Enzymologic
  • Gene Expression Profiling
  • Drug Resistance, Neoplasm