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Träfflista för sökning "LAR1:uu ;pers:(Larsson Rolf);srt2:(2005-2009);pers:(Isaksson Anders);pers:(Dhar Sumeer);conttype:(refereed);srt2:(2007)"

Sökning: LAR1:uu > Larsson Rolf > (2005-2009) > Isaksson Anders > Dhar Sumeer > Refereegranskat > (2007)

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1.
  • Fryknäs, Mårten, et al. (författare)
  • STAT1 signaling is associated with acquired crossresistance to doxorubicin and radiation in myeloma cell lines
  • 2007
  • Ingår i: International Journal of Cancer. - 0020-7136. ; 120:1, s. 189-195
  • Tidskriftsartikel (refereegranskat)abstract
    • The myeloma cell line RPMI 8226/S and its doxorubicin resistant subline 8226/Dox40 were used as models to explore the potential importance of the STAT1 signaling pathway in drug and radiation resistance. The 40-fold doxorubicin resistant subline 8226/Dox40 was found to be crossresistant to single doses of 4 and 8 Gy of radiation. A genome-wide mRNA expression study comparing the 8226/Dox40 cell line to its parental line was performed to identify the underlying molecular mechanisms. Seventeen of the top 50 overexpressed genes have previously been implicated in the STAT1 signaling pathway. STAT1 was over expressed both at the mRNA and protein level. Moreover, analyses of nuclear extracts showed higher abundance of phosphorylated STAT1 (Tyr 701) in the resistant subline. Preexposure of the crossresistant cells to the STAT1 inhibiting drug fludarabine reduced expression of overexpressed genes and enhanced the effects of both doxorubicin and radiation. These results show that resistance to doxorubicin and radiation is associated with increased STAT1 signaling and can be modulated by fludarabine. The data support further development of therapies combining fludarabine and radiation.
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2.
  • Milani, Lili, et al. (författare)
  • Allelic imbalance in gene expression as a guide to cis-acting regulatory single nucleotide polymorphisms in cancer cells
  • 2007
  • Ingår i: Nucleic Acids Research. - 0305-1048. ; 35:5, s. e34
  • Tidskriftsartikel (refereegranskat)abstract
    • Using the relative expression levels of two SNP alleles of a gene in the same sample is an effective approach for identifying cis-acting regulatory SNPs (rSNPs). In the current study, we established a process for systematic screening for cis-acting rSNPs using experimental detection of AI as an initial approach. We selected 160 expressed candidate genes that are involved in cancer and anticancer drug resistance for analysis of AI in a panel of cell lines that represent different types of cancers and have been well characterized for their response patterns against anticancer drugs. Of these genes, 60 contained heterozygous SNPs in their coding regions, and 41 of the genes displayed imbalanced expression of the two cSNP alleles. Genes that displayed AI were subjected to bioinformatics-assisted identification of rSNPs that alter the strength of transcription factor binding. rSNPs in 15 genes were subjected to electrophoretic mobility shift assay, and in eight of these genes (APC, BCL2, CCND2, MLH1, PARP1, SLIT2, YES1, XRCC1) we identified differential protein binding from a nuclear extract between the SNP alleles. The screening process allowed us to zoom in from 160 candidate genes to eight genes that may contain functional rSNPs in their promoter regions.
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