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. 2019 Nov 20;21(12):1143–1150. doi: 10.1016/j.neo.2019.09.002

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© 2019 Neoplasia Press, Inc.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

PMC Copyright notice

ATM-directed DNA damage repair in DOX treated cells. MMTV-PyMT;Apc^+/+ and MMTV-PyMT;Apc^Min/+ cells were treated for 24 hrs with DOX and PTX. Protein was isolated and western blots were used to determine expression of DNA damage repair components. A) No change was observed in ATR phosphorylation (Thr1989) in either cell line following treatment. B) ATM activation was measured via phosphorylation of ATM (Ser1981). Increased phosphorylation of ATM was observed in DOX treated MMTV-PyMT;Apc^+/+ cells, but not in DOX treated MMTV-PyMT;Apc^Min/+ cells. C) DOX treated MMTV-PyMT;Apc^+/+ cells expressed increased phosphorylation of Chk1 (Ser345), which is absent in MMTV-PyMT;Apc^Min/+ cells. D) Increased phosphorylation of Chk2 (Thr68) was observed in DOX treated MMTV-PyMT;Apc^+/+ cells, with no change observed in DOX treated MMTV-PyMT;Apc^Min/+ cells. *P < 0.05 comparing MMTV-PyMT;Apc^Min/+ or MMTV-PyMT;Apc^+/+ cells treated to solvent control and **P < 0.05 comparing MMTV-PyMT;Apc^Min/+ to MMTV-PyMT;Apc^+/+ cells.