ResearcherSecond Military Medical UniversityNo recent work listed
Ming-hua Zhu
Matched on OpenAlex author ID A5100518391. Sources: OpenAlex.
Their work
- Papers
- 6 (first author 0, last author 5)
- Trials
- 0
- Grants
- 0
- Labs led
- 1
- Collaborators
- 11
2012: 2 papers · 2013: 2 papers · 2014: 1 paper · 2015: none · 2016: 1 paper
Papers 6
- Upregulation of the expression of Wnt5a promotes the proliferation of pancreatic cancer cells in vitro and in a nude mouse model. Last author DOI 10.3892/mmr.2015.4642↗
- Upregulation of miR-194 contributes to tumor growth and progression in pancreatic ductal adenocarcinoma. Last author DOI 10.3892/or.2013.2960↗
- Upregulation of Wnt5a promotes epithelial-to-mesenchymal transition and metastasis of pancreatic cancer cells. Last author DOI 10.1186/1471-2407-13-496↗
- Diagnostic and biological significance of microRNA-192 in pancreatic ductal adenocarcinoma. Last author DOI 10.3892/or.2013.2420↗
- Surviving cells after treatment with gemcitabine or 5-fluorouracil for the study of de novo resistance of pancreatic cancer. Last author DOI 10.1016/j.canlet.2011.09.018↗
- Identification of NME5 as a contributor to innate resistance to gemcitabine in pancreatic cancer cells. Co-author DOI 10.1111/j.1742-4658.2012.08521.x↗
Closest collaborators
The 11 strongest of 11 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Haiji Bo · 2 shared papers, 2013–2016 · strength 0.12
- Paper Upregulation of the expression of Wnt5a promotes the proliferation of pancreatic cancer cells in vitro and in a nude mo… DOI 10.3892/mmr.2015.4642↗
- Paper Upregulation of Wnt5a promotes epithelial-to-mesenchymal transition and metastasis of pancreatic cancer cells. DOI 10.1186/1471-2407-13-496↗
- Ying Chen · 2 shared papers, 2013–2016 · strength 0.12
- Paper Upregulation of the expression of Wnt5a promotes the proliferation of pancreatic cancer cells in vitro and in a nude mo… DOI 10.3892/mmr.2015.4642↗
- Paper Upregulation of Wnt5a promotes epithelial-to-mesenchymal transition and metastasis of pancreatic cancer cells. DOI 10.1186/1471-2407-13-496↗
- Jing Zhang · 3 shared papers, 2012–2014 · strength 0.11
- Paper Upregulation of miR-194 contributes to tumor growth and progression in pancreatic ductal adenocarcinoma. DOI 10.3892/or.2013.2960↗
- Paper Diagnostic and biological significance of microRNA-192 in pancreatic ductal adenocarcinoma. DOI 10.3892/or.2013.2420↗
- Paper Surviving cells after treatment with gemcitabine or 5-fluorouracil for the study of de novo resistance of pancreatic ca… DOI 10.1016/j.canlet.2011.09.018↗
- Qinghua Liu · 3 shared papers, 2012–2014 · strength 0.11
- Paper Upregulation of miR-194 contributes to tumor growth and progression in pancreatic ductal adenocarcinoma. DOI 10.3892/or.2013.2960↗
- Paper Diagnostic and biological significance of microRNA-192 in pancreatic ductal adenocarcinoma. DOI 10.3892/or.2013.2420↗
- Paper Surviving cells after treatment with gemcitabine or 5-fluorouracil for the study of de novo resistance of pancreatic ca… DOI 10.1016/j.canlet.2011.09.018↗
- Chenyan Zhao · 3 shared papers, 2012–2014 · strength 0.11
- Paper Upregulation of miR-194 contributes to tumor growth and progression in pancreatic ductal adenocarcinoma. DOI 10.3892/or.2013.2960↗
- Paper Diagnostic and biological significance of microRNA-192 in pancreatic ductal adenocarcinoma. DOI 10.3892/or.2013.2420↗
- Paper Surviving cells after treatment with gemcitabine or 5-fluorouracil for the study of de novo resistance of pancreatic ca… DOI 10.1016/j.canlet.2011.09.018↗
- Min Shi · 2 shared papers, 2013–2014 · strength 0.08
- Shu‐Hui Zhang · 2 shared papers, 2013–2014 · strength 0.08
- Ying Chen · 1 shared paper, 2013 · strength 0.04
- Xiaoran Qin · 1 shared paper, 2012 · strength 0.03
- Fu Li · 1 shared paper, 2012 · strength 0.03
- Luyong Zhang · 1 shared paper, 2012 · strength 0.03
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.