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Apeng Chen

As seen in: Nature, BioRxiv
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Articles by Apeng Chen

SLC25A20 promotes tumor growth by reprogramming energy metabolism in lung adenocarcinoma

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By Xing Liu, Xiaoyu Song, Ye Wang, Min Zhang, Shaodi Wen, Yahui Cao, Changhua Yi, Man Tian, Apeng Chen, Cong Gan, Mingxin Ni
| Nature Verified
Abstract Accumulating evidence has shown that the dysfunction of mitochondria, the multifunctional organelles in various cellular processes, is a pivotal event in the development of various diseases, including human cancers. The molecular alterations in tumors that promote metabolic diversity and distinct targetable dependencies remain poorly defined.
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Development of a human glioblastoma model using humanized DRAG mice for immunotherapy

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By Rashmi Srivastava, Alireza Labani-Motlagh, Apeng Chen, Fan Yang
| BioRxiv
Thank you for your interest in spreading the word about bioRxiv. NOTE: Your email address is requested solely to identify you as the sender of this article. Your Email * Your Name * Send To * Enter multiple addresses on separate lines or separate them with commas. Message Subject (Your Name) has forwarded a page to you from bioRxiv Message Body (Your Name) thought you would like to see this page from the bioRxiv website.
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Author Correction: Loss of MAT2A compromises methionine metabolism and represents a vulnerability in H3K27M mutant glioma by modulating the epigenome - Nature Cancer

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By Srinidhi Varadharajan, Allison R. Cheney, Apeng Chen, Robert F Koncar, Michal Zapotocky, Xiuxing Wang, Claudia L. Kleinman, Costas A. Lyssiotis, Nada Jabado, Sameer Agnihotri
| Nature Verified
Correction to: Nature Cancer https://doi.org/10.1038/s43018-022-00348-3, published online 14 April 2022.
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Loss of MAT2A compromises methionine metabolism and represents a vulnerability in H3K27M mutant glioma by modulating the epigenome - Nature Cancer

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By Srinidhi Varadharajan, Allison R. Cheney, Apeng Chen, Robert F Koncar, Michal Zapotocky, Xiuxing Wang, Claudia L. Kleinman, Costas A. Lyssiotis, Nada Jabado, Sameer Agnihotri
| Nature Verified
Abstract Diffuse midline gliomas (DMGs) bearing driver mutations of histone 3 lysine 27 (H3K27M) are incurable brain tumors with unique epigenomes. Here, we generated a syngeneic H3K27M mouse model to study the amino acid metabolic dependencies of these tumors. H3K27M mutant cells were highly dependent on methionine.
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