ResearcherWayne State UniversityActive in the last 2 years
Bin Bao
Matched on ORCID iD 0000-0001-9312-5096; OpenAlex author ID A5101427104, A5102482537. Sources: OpenAlex.
Their work
- Papers
- 23
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 28
2011: 7 papers · 2012: 5 papers · 2013: 3 papers · 2014: 3 papers · 2015: none · 2016: none · 2017: none · 2018: 2 papers · 2019: none · 2020: none · 2021: none · 2022: none · 2023: none · 2024: none · 2025: 2 papers · 2026: 1 paper
Papers 23
- XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant pancreatic ductal adenocarcinoma. Co-author DOI 10.1016/j.canlet.2026.218804↗
- Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcinoma Co-author DOI 10.1101/2025.11.21.689857↗
- PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer Co-author DOI 10.64898/2025.12.06.692635↗
- Retraction notice to "Increased Ras GTPase activity is regulated by miRNAs that can be attenuated by CDF treatment in pancreatic cancer cells" [Cancer Lett. 31… Co-author DOI 10.1016/j.canlet.2017.11.030↗
- Retraction notice to "Notch-1 induces Epithelial-mesenchymal transition consistent with cancer stem cell phenotype in pancreatic cancer cells". Co-author DOI 10.1016/j.canlet.2018.03.020↗
- Deregulation of miR-146a expression in a mouse model of pancreatic cancer affecting EGFR signaling. Co-author DOI 10.1016/j.canlet.2014.05.013↗
- Pancreatic cancer stem-like cells display aggressive behavior mediated via activation of FoxQ1. Co-author DOI 10.1074/jbc.m113.532887↗
- Differentially expressed miRNAs in cancer-stem-like cells: markers for tumor cell aggressiveness of pancreatic cancer. Co-author DOI 10.1089/scd.2013.0551↗
- Activated K-Ras and INK4a/Arf deficiency promote aggressiveness of pancreatic cancer by induction of EMT consistent with cancer stem cell phenotype. Co-author DOI 10.1002/jcp.24162↗
- Pancreatic cancer stem cells: emerging target for designing novel therapy. Co-author DOI 10.1016/j.canlet.2012.03.018↗
- Selective inhibitors of nuclear export block pancreatic cancer cell proliferation and reduce tumor growth in mice. Co-author DOI 10.1053/j.gastro.2012.10.036↗
- Inactivation of Ink4a/Arf leads to deregulated expression of miRNAs in K-Ras transgenic mouse model of pancreatic cancer. Co-author DOI 10.1002/jcp.24036↗
- RETRACTED: Increased Ras GTPase activity is regulated by miRNAs that can be attenuated by CDF treatment in pancreatic cancer cells. Co-author DOI 10.1016/j.canlet.2012.01.013↗
- Metformin inhibits cell proliferation, migration and invasion by attenuating CSC function mediated by deregulating miRNAs in pancreatic cancer cells. Co-author DOI 10.1158/1940-6207.capr-11-0299↗
- Hypoxia-induced aggressiveness of pancreatic cancer cells is due to increased expression of VEGF, IL-6 and miR-21, which can be attenuated by CDF treatment. Co-author DOI 10.1371/journal.pone.0050165↗
- Genistein inhibits cell growth and induces apoptosis through up-regulation of miR-34a in pancreatic cancer cells. Co-author DOI 10.2174/138945012804545597↗
- Over-expression of FoxM1 leads to epithelial-mesenchymal transition and cancer stem cell phenotype in pancreatic cancer cells. Co-author DOI 10.1002/jcb.23150↗
- The complexities of obesity and diabetes with the development and progression of pancreatic cancer. Co-author DOI 10.1016/j.bbcan.2010.11.003↗
- Notch-1 induces epithelial-mesenchymal transition consistent with cancer stem cell phenotype in pancreatic cancer cells. Co-author DOI 10.1016/j.canlet.2011.03.012↗
- Anti-tumor activity of a novel compound-CDF is mediated by regulating miR-21, miR-200, and PTEN in pancreatic cancer. Co-author DOI 10.1371/journal.pone.0017850↗
- Activated K-ras and INK4a/Arf deficiency cooperate during the development of pancreatic cancer by activation of Notch and NF-κB signaling pathways. Co-author DOI 10.1371/journal.pone.0020537↗
- Aberrant epigenetic grooming of miRNAs in pancreatic cancer: a systems biology perspective. Co-author DOI 10.2217/epi.11.97↗
- Network modeling of CDF treated pancreatic cancer cells reveals a novel c-myc-p73 dependent apoptotic mechanism. Co-author PMID 21904657↗
Closest collaborators
The 25 strongest of 28 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Asfar Sohail Azmi · 15 shared papers, 2011–2026 · strength 0.97
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Amro Aboukameel · 11 shared papers, 2011–2026 · strength 0.89
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Fazlul H. Sarkar · 20 shared papers, 2011–2018 · strength 0.75
- Paper Retraction notice to "Increased Ras GTPase activity is regulated by miRNAs that can be attenuated by CDF treatment in p… DOI 10.1016/j.canlet.2017.11.030↗
- Paper Retraction notice to "Notch-1 induces Epithelial-mesenchymal transition consistent with cancer stem cell phenotype in p… DOI 10.1016/j.canlet.2018.03.020↗
- Paper Pancreatic cancer stem cells: emerging target for designing novel therapy. DOI 10.1016/j.canlet.2012.03.018↗
- Ramzi M. Mohammad · 7 shared papers, 2011–2026 · strength 0.69
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Shadan S. Ali · 16 shared papers, 2011–2018 · strength 0.61
- Paper Retraction notice to "Increased Ras GTPase activity is regulated by miRNAs that can be attenuated by CDF treatment in p… DOI 10.1016/j.canlet.2017.11.030↗
- Paper Retraction notice to "Notch-1 induces Epithelial-mesenchymal transition consistent with cancer stem cell phenotype in p… DOI 10.1016/j.canlet.2018.03.020↗
- Paper Deregulation of miR-146a expression in a mouse model of pancreatic cancer affecting EGFR signaling. DOI 10.1016/j.canlet.2014.05.013↗
- Sahar F. Bannoura · 3 shared papers, 2025–2026 · strength 0.55
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Md. Hafiz Uddin · 3 shared papers, 2025–2026 · strength 0.55
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Boris Pasche · 3 shared papers, 2025–2026 · strength 0.55
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Mohammed Najeeb Al Hallak · 3 shared papers, 2025–2026 · strength 0.55
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Husain Yar Khan · 3 shared papers, 2025–2026 · strength 0.55
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Muhammad Wasif Saif · 3 shared papers, 2025–2026 · strength 0.55
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Bassel F. El‐Rayes · 3 shared papers, 2025–2026 · strength 0.55
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Sanjeev Banerjee · 15 shared papers, 2011–2018 · strength 0.51
- Paper Retraction notice to "Notch-1 induces Epithelial-mesenchymal transition consistent with cancer stem cell phenotype in p… DOI 10.1016/j.canlet.2018.03.020↗
- Paper Deregulation of miR-146a expression in a mouse model of pancreatic cancer affecting EGFR signaling. DOI 10.1016/j.canlet.2014.05.013↗
- Paper Differentially expressed miRNAs in cancer-stem-like cells: markers for tumor cell aggressiveness of pancreatic cancer. DOI 10.1089/scd.2013.0551↗
- Philip A. Philip · 8 shared papers, 2011–2025 · strength 0.47
- Paper PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic Cancer DOI 10.64898/2025.12.06.692635↗
- Paper Retraction notice to "Increased Ras GTPase activity is regulated by miRNAs that can be attenuated by CDF treatment in p… DOI 10.1016/j.canlet.2017.11.030↗
- Paper Deregulation of miR-146a expression in a mouse model of pancreatic cancer affecting EGFR signaling. DOI 10.1016/j.canlet.2014.05.013↗
- P. A. Philip · 2 shared papers, 2025–2026 · strength 0.37
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Eliza Wright Beal · 2 shared papers, 2025–2026 · strength 0.37
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Anthony Frank Shields · 2 shared papers, 2025–2026 · strength 0.37
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Azeddine Atfi · 2 shared papers, 2025–2026 · strength 0.37
- Paper XPO1 inhibition enhances the efficacy and durability of RAS-targeted therapy in preclinical models of KRASG12D mutant p… DOI 10.1016/j.canlet.2026.218804↗
- Paper Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcino… DOI 10.1101/2025.11.21.689857↗
- Yiwei Li · 9 shared papers, 2011–2018 · strength 0.33
- Paper Retraction notice to "Notch-1 induces Epithelial-mesenchymal transition consistent with cancer stem cell phenotype in p… DOI 10.1016/j.canlet.2018.03.020↗
- Paper Pancreatic cancer stem cells: emerging target for designing novel therapy. DOI 10.1016/j.canlet.2012.03.018↗
- Paper Differentially expressed miRNAs in cancer-stem-like cells: markers for tumor cell aggressiveness of pancreatic cancer. DOI 10.1089/scd.2013.0551↗
- Subhash Padhyé · 5 shared papers, 2011–2018 · strength 0.21
- Paper Retraction notice to "Increased Ras GTPase activity is regulated by miRNAs that can be attenuated by CDF treatment in p… DOI 10.1016/j.canlet.2017.11.030↗
- Paper RETRACTED: Increased Ras GTPase activity is regulated by miRNAs that can be attenuated by CDF treatment in pancreatic c… DOI 10.1016/j.canlet.2012.01.013↗
- Paper Hypoxia-induced aggressiveness of pancreatic cancer cells is due to increased expression of VEGF, IL-6 and miR-21, whic… DOI 10.1371/journal.pone.0050165↗
- Zhiwei Peter Wang · 5 shared papers, 2011–2018 · strength 0.19
- Paper Retraction notice to "Notch-1 induces Epithelial-mesenchymal transition consistent with cancer stem cell phenotype in p… DOI 10.1016/j.canlet.2018.03.020↗
- Paper Activated K-Ras and INK4a/Arf deficiency promote aggressiveness of pancreatic cancer by induction of EMT consistent wit… DOI 10.1002/jcp.24162↗
- Paper Over-expression of FoxM1 leads to epithelial-mesenchymal transition and cancer stem cell phenotype in pancreatic cancer… DOI 10.1002/jcb.23150↗
- Lucio Miele · 5 shared papers, 2011–2018 · strength 0.18
- Paper Retraction notice to "Notch-1 induces Epithelial-mesenchymal transition consistent with cancer stem cell phenotype in p… DOI 10.1016/j.canlet.2018.03.020↗
- Paper Genistein inhibits cell growth and induces apoptosis through up-regulation of miR-34a in pancreatic cancer cells. DOI 10.2174/138945012804545597↗
- Paper Over-expression of FoxM1 leads to epithelial-mesenchymal transition and cancer stem cell phenotype in pancreatic cancer… DOI 10.1002/jcb.23150↗
- Steve H. Kim · 1 shared paper, 2025 · strength 0.17
- Murray Korc · 3 shared papers, 2011–2013 · strength 0.09
- Paper Activated K-Ras and INK4a/Arf deficiency promote aggressiveness of pancreatic cancer by induction of EMT consistent wit… DOI 10.1002/jcp.24162↗
- Paper Inactivation of Ink4a/Arf leads to deregulated expression of miRNAs in K-Ras transgenic mouse model of pancreatic cance… DOI 10.1002/jcp.24036↗
- Paper Activated K-ras and INK4a/Arf deficiency cooperate during the development of pancreatic cancer by activation of Notch a… DOI 10.1371/journal.pone.0020537↗
- Zhiwei Wang · 2 shared papers, 2011–2012 · strength 0.05
- Paper Genistein inhibits cell growth and induces apoptosis through up-regulation of miR-34a in pancreatic cancer cells. DOI 10.2174/138945012804545597↗
- Paper Anti-tumor activity of a novel compound-CDF is mediated by regulating miR-21, miR-200, and PTEN in pancreatic cancer. DOI 10.1371/journal.pone.0017850↗
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.