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Iwanicki, Marcin

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Iwanicki

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Marcin

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Iwanicki, Marcin

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2009 - 200912010 - 20172

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Author's Publications: search.filters.isAuthorOfPublication.b837396d-b3da-4bbd-854d-80c9278036e8

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Now showing 1 - 3 of 3
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    Gene Expression Signature of Normal Cell-of-Origin Predicts Ovarian Tumor Outcomes
    (Public Library of Science, 2013) Merritt, Melissa A.; Bentink, Stefan; Schwede, Matthew; Iwanicki, Marcin; Quackenbush, John; Woo, Terri; Agoston, Elin S.; Reinhardt, Ferenc; Crum, Christopher; Berkowitz, Ross; Mok, Samuel C.; Witt, Abigail E.; Jones, Michelle A.; Wang, Bin; Ince, Tan A.
    The potential role of the cell-of-origin in determining the tumor phenotype has been raised, but not adequately examined. We hypothesized that distinct cells-of-origin may play a role in determining ovarian tumor phenotype and outcome. Here we describe a new cell culture medium for in vitro culture of paired normal human ovarian (OV) and fallopian tube (FT) epithelial cells from donors without cancer. While these cells have been cultured individually for short periods of time, to our knowledge this is the first long-term culture of both cell types from the same donors. Through analysis of the gene expression profiles of the cultured OV/FT cells we identified a normal cell-of-origin gene signature that classified primary ovarian cancers into OV-like and FT-like subgroups; this classification correlated with significant differences in clinical outcomes. The identification of a prognostically significant gene expression signature derived solely from normal untransformed cells is consistent with the hypothesis that the normal cell-of-origin may be a source of ovarian tumor heterogeneity and the associated differences in tumor outcome.
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    Starved epithelial cells uptake extracellular matrix for survival
    (Nature Publishing Group, 2017) Muranen, Taru; Iwanicki, Marcin; Curry, Natasha L.; Hwang, Julie; DuBois, Cory D.; Coloff, Jonathan L.; Hitchcock, Daniel S.; Clish, Clary B.; Brugge, Joan; Kalaany, Nada
    Extracellular matrix adhesion is required for normal epithelial cell survival, nutrient uptake and metabolism. This requirement can be overcome by oncogene activation. Interestingly, inhibition of PI3K/mTOR leads to apoptosis of matrix-detached, but not matrix-attached cancer cells, suggesting that matrix-attached cells use alternate mechanisms to maintain nutrient supplies. Here we demonstrate that under conditions of dietary restriction or growth factor starvation, where PI3K/mTOR signalling is decreased, matrix-attached human mammary epithelial cells upregulate and internalize β4-integrin along with its matrix substrate, laminin. Endocytosed laminin localizes to lysosomes, results in increased intracellular levels of essential amino acids and enhanced mTORC1 signalling, preventing cell death. Moreover, we show that starved human fibroblasts secrete matrix proteins that maintain the growth of starved mammary epithelial cells contingent upon epithelial cell β4-integrin expression. Our study identifies a crosstalk between stromal fibroblasts and epithelial cells under starvation that could be exploited therapeutically to target tumours resistant to PI3K/mTOR inhibition.
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    Transcriptional Regulation of Metastatic [Id]entity by KLF17
    (BioMed Central, 2009) Iwanicki, Marcin; Brugge, Joan
    A novel in vivo screening approach has identified KLF17 as a key metastasis suppressor gene that acts through regulation of Id1 transcription factor-dependent induction of the epithelial-to-mesenchymal transition.