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ILSC Monthly Seminar: December 2011

2013

January: Michael Taylor
February: Marna Yandeau-Nelson
March: Paul Lockman
April: Martin Gruebele

2012

January: David D. Thomas
February: Elizabeth Austin-Minor
March: Juliette Lecomte
April: David Millar
May: Lukas Tamm
September: David Millar
September: Dongping Zhong
October: Jonathan V. Rocheleau
November: Yevgenya Grinblat
December: Michael Graner

2011

January: Clay Carter
February (a): Anne Kenworthy
February (b): Jennifer Liang
March: Joe Johnson
April: Marco Ciufolini
May: Gary Pielak
October: Matthew Andrews
December: Andrew Skildum

2010

November: Rui Wang
October: Marshall Hampton

Manipulating Mitochondria Makes Malignancy More Manageable

Speaker: Dr. Andrew Skildum; Assistant Professor, Department of Biomedical Sciences, School of Medicine-Duluth

Time/Place: Thursday, Dec. 15th at 3:00 pm, 130 SMed

Abstract: Treatment outcomes for patients with breast cancer depend on their cancer cells' sensitivity to non-specific cytotoxic agents (e.g. the chemothrapy drug doxorubicin) and molecularly targeted agents (e.g. the antiestrogen Tamoxifen). Using an in vitro model of acquired resistance to antiestrogen, we have shown that antiestrogen resistant breast cancer cells have de novo resistance to doxorubicin relative to antiestrogen sensitive cells. Furthermore, antiestrogen resistant cells have increased mitochondrial capacity, mitochondrial DNA, and expression of Tfam, the major regulator of mitochondrial DNA transcription and replication. Resistance to doxorubicin is ameliorated by pharmacologically achievable concentrations of troglitazone, a PPARy agonist that increases mitochondrial superoxide. Based on these data, we hypothesize that drug sensitivity is inversely proportional to mitochondrial capacity. To test this hypothesis, we are manipulating the mitochondrial capacity of breast cancer cells. We predict that decreasing the mitochondrial capacity of drug resistant cells by interrupting Tfam expression will restore sensitivity to doxorubicin. Conversely, we predict that increasing mitochondrial capacity by adapting drug-sensitive cells to growth using non-fermentable carbon sources will result in resistance to doxorubicin. The development and confirmation of these models and the current status of the project will be discussed.

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