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Träfflista för sökning "WFRF:(O'Hare Michael) srt2:(2010-2014)"

Sökning: WFRF:(O'Hare Michael) > (2010-2014)

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1.
  • Jia, Min, et al. (författare)
  • Proteome profiling of immortalization-to-senescence transition of human breast epithelial cells identified MAP2K3 as a senescence-promoting protein which is downregulated in human breast cancer
  • 2010
  • Ingår i: PROTEOMICS - Clinical Applications. - : Wiley. - 1862-8346 .- 1862-8354. ; 4:10-11, s. 816-828
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: Immortalization is one of the first changes in cells undergoing carcinogenic transformation. Proteome profiling of the immortalization-senescence transition is expected to provide insights into the molecular mechanisms of early tumorigenesis. Experimental design: 2-DE and MALDI-MS were used to identify proteins in primary human breast epithelial cells, relevant to the immortalization-senescence transition. Cell and molecular biology and immunohistochemistry were used to validate involvement of mitogen-activated protein kinase kinase 3 (MAP2K3) in the immortalization-senescence transition. Results: We identified 71 proteins whose expression changed upon induction of senescence. The identified proteins include regulators of cell growth, death, cell assembly and organization. Analysis of the network formed by the identified proteins suggested that the immortalization-to-senescence transition could affect regulators of the cell cycle, protein synthesis, transport, post-translational modifications, DNA recombination and repair, and lipid and amino acid metabolism. We observed that MAP2K3 was downregulated in immortal human breast epithelial cells and that upregulation of MAP2K3 expression promoted cell senescence. Decreased expression of MAP2K3 was observed in human breast infiltrating ductal carcinomas, as compared to non-cancerous human breast tissues. Conclusion and clinical relevance: We described a proteome profile of the immortalization-to-senescence transition for human breast epithelial cells, and identified MAP2K3 as a protein that promotes senescence in these cells.
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2.
  • Zabriskie, Matthew S., et al. (författare)
  • BCR-ABL1 Compound Mutations Combining Key Kinase Domain Positions Confer Clinical Resistance to Ponatinib in Ph Chromosome-Positive Leukemia
  • 2014
  • Ingår i: Cancer Cell. - : Elsevier BV. - 1535-6108 .- 1878-3686. ; 26:3, s. 428-442
  • Tidskriftsartikel (refereegranskat)abstract
    • Ponatinib is the only currently approved tyrosine kinase inhibitor (TKI) that suppresses all BCR-ABL1 single mutants in Philadelphia chromosome-positive (Ph+) leukemia, including the recalcitrant BCR-ABL1(T315I) mutant. However, emergence of compound mutations in a BCR-ABL1 allele may confer ponatinib resistance. We found that clinically reported BCR-ABL1 compound mutants center on 12 key positions and confer varying resistance to imatinib, nilotinib, dasatinib, ponatinib, rebastinib, and bosutinib. T315I-inclusive compound mutants confer high-level resistance to TKIs, including ponatinib. In vitro resistance profiling was predictive of treatment outcomes in Ph+ leukemia patients. Structural explanations for compound mutation-based resistance were obtained through molecular dynamics simulations. Our findings demonstrate that BCR-ABL1 compound mutants confer different levels of TKI resistance, necessitating rational treatment selection to optimize clinical outcome.
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