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Citations to this article

Autophagy inhibition enhances therapy-induced apoptosis in a Myc-induced model of lymphoma
Ravi K. Amaravadi, … , Andrei Thomas-Tikhonenko, Craig B. Thompson
Ravi K. Amaravadi, … , Andrei Thomas-Tikhonenko, Craig B. Thompson
Published February 1, 2007
Citation Information: J Clin Invest. 2007;117(2):326-336. https://doi.org/10.1172/JCI28833.
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Research Article Oncology Article has an altmetric score of 19

Autophagy inhibition enhances therapy-induced apoptosis in a Myc-induced model of lymphoma

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Abstract

Autophagy is a lysosome-dependent degradative pathway frequently activated in tumor cells treated with chemotherapy or radiation. Whether autophagy observed in treated cancer cells represents a mechanism that allows tumor cells to survive therapy or a mechanism for initiating a nonapoptotic form of programmed cell death remains controversial. To address this issue, the role of autophagy in a Myc-induced model of lymphoma generated from cells derived from p53ERTAM/p53ERTAM mice (with ER denoting estrogen receptor) was examined. Such tumors are resistant to apoptosis due to a lack of nuclear p53. Systemic administration of tamoxifen led to p53 activation and tumor regression followed by tumor recurrence. Activation of p53 was associated with the rapid appearance of apoptotic cells and the induction of autophagy in surviving cells. Inhibition of autophagy with either chloroquine or ATG5 short hairpin RNA (shRNA) enhanced the ability of either p53 activation or alkylating drug therapy to induce tumor cell death. These studies provide evidence that autophagy serves as a survival pathway in tumor cells treated with apoptosis activators and a rationale for the use of autophagy inhibitors such as chloroquine in combination with therapies designed to induce apoptosis in human cancers.

Authors

Ravi K. Amaravadi, Duonan Yu, Julian J. Lum, Thi Bui, Maria A. Christophorou, Gerard I. Evan, Andrei Thomas-Tikhonenko, Craig B. Thompson

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Total citations by year

Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 Total
Citations: 7 13 16 23 28 19 28 30 38 41 36 58 62 47 48 33 31 18 9 585
Citation information
This citation data is accumulated from CrossRef, which receives citation information from participating publishers, including this journal. Not all publishers participate in CrossRef, so this information is not comprehensive. Additionally, data may not reflect the most current citations to this article, and the data may differ from citation information available from other sources (for example, Google Scholar, Web of Science, and Scopus).

Citations to this article in year 2014 (58)

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