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Caleb Cheng

As seen in: Nature, BioRxiv, Cell Press, Cell Reports Medicine, CSDN
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Articles by Caleb Cheng

A stress-adaptive lipid kinase axis defines metabolic vulnerabilities in neuroendocrine prostate cancer

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By Yang Zheng, Caleb Cheng, Yizhi Cao, Gabriel Cruz, Yuping Zhang, Radha Paturu, Somnath Mahapatra, Jing Hu, Rahul Mannan, Hüseyin Karabürk, Rupam Bhattacharyya, Yitong Yin, Yi Zhao, Wenyan Liu, Xuhong Cao, Hui Xue, Chungen Li, Zhen J Wang, Stephanie Miner, Zachery R. Reichert, Rohit Mehra, Ulka Vaishampayan, Vaibhav Sahai, Lois S. Weisman, Ke Ding, Costas A. Lyssiotis, Yuzhuo Wang, Arul M. Chinnaiyan, Yuanyuan Qiao
| Cell Press Verified
Compounds ESK981 was provided by Esanik Therapeutics. Apilimod, Torin-1, bafilomycin A1, simvastatin, atorvastatin, WX8, MK-8245, ND-646, and Q-VD-OPh were purchased from Selleck Chemicals. PIK5-33d was provided by K. Ding. U18666A, YM-53601, and NB-598 were obtained from MedChemExpress. TVB-2640 was purchased from Nantong Hi-future Biotechnology. Doxycycline hydrochloride was obtained from Thermo Fisher Scientific. Thapsigargin was purchased from Cell Signaling Technology.
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Targeting the ferritinophagy-lysosome axis as a therapeutic vulnerability in gastroenteropancreatic neuroendocrine tumors

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By Yizhi Cao, Caleb Cheng, Yitong Yin, Sarah Yee, Yang Zheng, Somnath Mahapatra, Fan Yang, Yi Zhao, Rupam Bhattacharyya, Stephanie Miner, Xuhong Cao, Rahul Mannan, Chungen Li, Vaibhav Sahai, Ke Ding, Costas A. Lyssiotis, Arul M. Chinnaiyan, Yuanyuan Qiao, Radha Paturu, Andrej Coleski, Shannon VanAken, Rüya Pakkan
| Cell Reports Medicine Verified
Keywords lysosome lipid metabolism mTOR ferritinophagy gastroenteropancreatic neuroendocrine tumor PIKfyve Introduction Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are rare malignancies arising from neuroendocrine cells in the gastrointestinal tract or pancreas and account for around 70% of all neuroendocrine tumors.1 Although uncommon, GEP-NET incidence has increased markedly over the past four decades.2 High-grade and metastatic GEP-NETs have poor prognosis, with 5-year survival...
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cs285 lecture9-CSDN博客

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By Caleb Cheng
| CSDN
🔗 GitHub 持续更新仓库（含代码+课件）： 👉 github.com/CalebCheng819/cs285 lecture9 part1 Policy gradient as softened policy iteration 我们可以换一种角度理解策略梯度：将其看作一种“软化版（softened）”的策略迭代（Policy Iteration）。 经典策略迭代结构（policy iteration）： Alternating between: 估计当前策略的值函数 VπV^\piVπ 或 Advantage； 使用估计值更新策略（例如贪心选择最优动作）。 类比： 步骤策略迭代策略梯度 值估计 准确估计 Aπ(s,a)A^\pi(s, a)Aπ(s,a) 使用样本/网络近似 Advantage 策略更新 argmax (完全采纳最优动作) 轻微调整策略参数（通过梯度） 策略梯度不会像策略迭代那样直接跳转到贪心策略，而是根据 Advantage 的大小轻微提高动作概率。 这在 Advantage 估计不准时很有用 —— 小步更新可以避免因估计误差而“走错方向”。 理论证明...
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cs285 lec4_and_lec5

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By Caleb Cheng
| CSDN
cs285 lecture4-5课程笔记（持续更新） CS285 持续更新 👉 GitHub仓库直达： https://github.com/CalebCheng819/cs285 (记得复制完整链接哦！ )可以给个🌟吗 lecture 4 part1 reward function:r(s,a)r(\mathbf{s},\mathbf{a})r(s,a)强调的是future reward，而不是right now Markov chain 主要有两部分组件： M={S,T}S−state spaceT−transition operator \begin{aligned}&\mathcal{M}=\{\mathcal{S},\mathcal{T}\}\\&\mathcal{S}-\text{state space}\\&\mathcal{T}-\text{transition operator}\end{aligned} ​M={S,T}S−state spaceT−transition operator​...
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Targeting PIKfyve-driven lipid metabolism in pancreatic cancer - Nature

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By Caleb Cheng, Jing Hu, Rahul Mannan, Rupam Bhattacharyya, Saadia A. Karim, David Maclean, Nicholas J. Rossiter, Yang Zheng, Dominik Awad, Yuping Zhang, Zhen Wang, Rohit Mehra, Vaibhav Sahai, Yatrik M Shah, Lois S. Weisman, Jennifer Morton, Yuanyuan Qiao, Costas A. Lyssiotis, Jasmine P. Wisniewski, Hüseyin Karabürk
| Nature Verified
Abstract Pancreatic ductal adenocarcinoma (PDAC) subsists in a nutrient-deregulated microenvironment, making it particularly susceptible to treatments that interfere with cancer metabolism1,2. For example, PDAC uses, and is dependent on, high levels of autophagy and other lysosomal processes3,4,5. Although targeting these pathways has shown potential in preclinical studies, progress has been hampered by the difficulty in identifying and characterizing favourable targets for drug development6.
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Targeting PIKfyve-driven lipid homeostasis as a metabolic vulnerability in pancreatic cancer

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By Caleb Cheng, Jing Hu, Rahul Mannan, Rupam Bhattacharyya
| BioRxiv
Abstract Pancreatic ductal adenocarcinoma (PDAC) subsists in a nutrient-deregulated microenvironment, making it particularly susceptible to treatments that interfere with cancer metabolism. For example, PDAC utilizes and is dependent on high levels of autophagy and other lysosomal processes. Although targeting these pathways has shown potential in preclinical studies, progress has been hampered by the challenge of identifying and characterizing favorable targets for drug development.
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Development of an orally bioavailable mSWI/SNF ATPase degrader and acquired mechanisms of resistance in prostate cancer

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By Tongchen He, Yuanyuan Qiao, Caleb Cheng, Hanbyul Cho
| BioRxiv
Abstract Mammalian switch/sucrose non-fermentable (mSWI/SNF) ATPase degraders have been shown to be effective in enhancer-driven cancers by functioning to impede oncogenic transcription factor chromatin accessibility. Here, we developed AU-24118, a first-in-class, orally bioavailable proteolysis targeting chimera (PROTAC) degrader of mSWI/SNF ATPases (SMARCA2 and SMARCA4) and PBRM1.
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