ResearcherUniversity of California, Los AngelesActive in the last 2 years
Keke Liang
Matched on ORCID iD 0000-0002-0007-6326; OpenAlex author ID A5038792983. Sources: OpenAlex.
Their work
- Papers
- 8 (first author 1, last author 2)
- Trials
- 0
- Grants
- 0
- Labs led
- 1
- Collaborators
- 20
2020: 3 papers · 2021: 1 paper · 2022: 1 paper · 2023: 1 paper · 2024: 2 papers
Papers 8
- The prognostic value of myosteatosis in pancreatic cancer: A systematic review and meta-analysis. Last author DOI 10.1016/j.clnu.2024.10.017↗
- Artificial intelligence to predict T4 stage of pancreatic ductal adenocarcinoma using CT imaging. Last author DOI 10.1016/j.compbiomed.2024.108125↗
- MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell-intrinsic Amplification of Type I IFN Signaling. First author DOI 10.1158/1078-0432.ccr-22-3322↗
- Reprogramming of nucleotide metabolism by interferon confers dependence on the replication stress response pathway in pancreatic cancer cells. Co-author DOI 10.1016/j.celrep.2021.110236↗
- NAD+ depletion by type I interferon signaling sensitizes pancreatic cancer cells to NAMPT inhibition. Co-author DOI 10.1073/pnas.2012469118↗
- Identification of dissociation factors in pancreatic Cancer using a mass spectrometry-based proteomic approach. Co-author DOI 10.1186/s12885-020-6522-3↗
- The miR-1224-5p/ELF3 Axis Regulates Malignant Behaviors of Pancreatic Cancer via PI3K/AKT/Notch Signaling Pathways. Co-author DOI 10.2147/ott.s248507↗
- Multi-omics analysis based on integrated genomics, epigenomics and transcriptomics in pancreatic cancer. Co-author DOI 10.2217/epi-2019-0374↗
Closest collaborators
The 20 strongest of 20 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Xiaodong Tan · 4 shared papers, 2020–2024 · strength 0.56
- Paper Artificial intelligence to predict T4 stage of pancreatic ductal adenocarcinoma using CT imaging. DOI 10.1016/j.compbiomed.2024.108125↗
- Paper Multi-omics analysis based on integrated genomics, epigenomics and transcriptomics in pancreatic cancer. DOI 10.2217/epi-2019-0374↗
- Paper Identification of dissociation factors in pancreatic Cancer using a mass spectrometry-based proteomic approach. DOI 10.1186/s12885-020-6522-3↗
- Qi Miao · 2 shared papers, 2024 · strength 0.43
- Lingming Kong · 3 shared papers, 2020 · strength 0.38
- Paper Multi-omics analysis based on integrated genomics, epigenomics and transcriptomics in pancreatic cancer. DOI 10.2217/epi-2019-0374↗
- Paper Identification of dissociation factors in pancreatic Cancer using a mass spectrometry-based proteomic approach. DOI 10.1186/s12885-020-6522-3↗
- Paper The miR-1224-5p/ELF3 Axis Regulates Malignant Behaviors of Pancreatic Cancer via PI3K/AKT/Notch Signaling Pathways. DOI 10.2147/ott.s248507↗
- Peng Liu · 3 shared papers, 2020 · strength 0.38
- Paper Multi-omics analysis based on integrated genomics, epigenomics and transcriptomics in pancreatic cancer. DOI 10.2217/epi-2019-0374↗
- Paper Identification of dissociation factors in pancreatic Cancer using a mass spectrometry-based proteomic approach. DOI 10.1186/s12885-020-6522-3↗
- Paper The miR-1224-5p/ELF3 Axis Regulates Malignant Behaviors of Pancreatic Cancer via PI3K/AKT/Notch Signaling Pathways. DOI 10.2147/ott.s248507↗
- Timothy R. Donahue · 3 shared papers, 2021–2023 · strength 0.36
- Paper MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell-intrinsic Amplification of Type I IFN Signal… DOI 10.1158/1078-0432.ccr-22-3322↗
- Paper Reprogramming of nucleotide metabolism by interferon confers dependence on the replication stress response pathway in p… DOI 10.1016/j.celrep.2021.110236↗
- Paper NAD+ depletion by type I interferon signaling sensitizes pancreatic cancer cells to NAMPT inhibition. DOI 10.1073/pnas.2012469118↗
- Evan R. Abt · 3 shared papers, 2021–2023 · strength 0.36
- Paper MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell-intrinsic Amplification of Type I IFN Signal… DOI 10.1158/1078-0432.ccr-22-3322↗
- Paper Reprogramming of nucleotide metabolism by interferon confers dependence on the replication stress response pathway in p… DOI 10.1016/j.celrep.2021.110236↗
- Paper NAD+ depletion by type I interferon signaling sensitizes pancreatic cancer cells to NAMPT inhibition. DOI 10.1073/pnas.2012469118↗
- Caius Gabriel Radu · 3 shared papers, 2021–2023 · strength 0.36
- Paper MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell-intrinsic Amplification of Type I IFN Signal… DOI 10.1158/1078-0432.ccr-22-3322↗
- Paper Reprogramming of nucleotide metabolism by interferon confers dependence on the replication stress response pathway in p… DOI 10.1016/j.celrep.2021.110236↗
- Paper NAD+ depletion by type I interferon signaling sensitizes pancreatic cancer cells to NAMPT inhibition. DOI 10.1073/pnas.2012469118↗
- Jason M. Link · 2 shared papers, 2022–2023 · strength 0.26
- Paper MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell-intrinsic Amplification of Type I IFN Signal… DOI 10.1158/1078-0432.ccr-22-3322↗
- Paper Reprogramming of nucleotide metabolism by interferon confers dependence on the replication stress response pathway in p… DOI 10.1016/j.celrep.2021.110236↗
- Razmik Ghukasyan · 2 shared papers, 2021–2023 · strength 0.25
- Hongbo Chen · 1 shared paper, 2024 · strength 0.24
- Jing Cui · 2 shared papers, 2021–2022 · strength 0.21
- David W. Dawson · 2 shared papers, 2021–2022 · strength 0.21
- Joon Y. Park · 1 shared paper, 2023 · strength 0.15
- Haoyi Jin · 1 shared paper, 2020 · strength 0.13
- Bing Song · 1 shared paper, 2020 · strength 0.13
- Yunhao Wu · 1 shared paper, 2020 · strength 0.13
- Yang Gao · 1 shared paper, 2020 · strength 0.12
- Johannes Czernin · 1 shared paper, 2022 · strength 0.11
- Irmina A. Elliott · 1 shared paper, 2021 · strength 0.10
- Alexandra M. Moore · 1 shared paper, 2021 · strength 0.10
How to reach this person
A chain of introductions through people who have published, run trials or held grants together (warm_path@1: fewest links first, then the strongest). Built from public records only; no contact details are kept.