ResearcherUniversity of North Carolina at CharlotteNo recent work listed
Mukulika Bose
Matched on ORCID iD 0000-0002-2347-7413; OpenAlex author ID A5043466920. Sources: OpenAlex.
Their work
- Papers
- 5 (first author 1, last author 0)
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 9
2019: 1 paper · 2020: 1 paper · 2021: 1 paper · 2022: 1 paper · 2023: 1 paper
Papers 5
- Targeting tumor-associated MUC1 overcomes anoikis-resistance in pancreatic cancer. Co-author DOI 10.1016/j.trsl.2022.08.010↗
- Overexpression of MUC1 Induces Non-Canonical TGF-β Signaling in Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.3389/fcell.2022.821875↗
- Repression of MUC1 Promotes Expansion and Suppressive Function of Myeloid-Derived Suppressor Cells in Pancreatic and Breast Cancer Murine Models First author DOI 10.3390/ijms22115587↗
- Tumor -Associated MUC1 Regulates TGF-β Signaling and Function in Pancreatic Ductal Adenocarcinoma Co-author DOI 10.1101/2020.04.29.068577↗
- Overcoming Immunological Resistance Enhances the Efficacy of A Novel Anti-tMUC1-CAR T Cell Treatment against Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.3390/cells8091070↗
Closest collaborators
The 9 strongest of 9 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Pinku Mukherjee · 5 shared papers, 2019–2023 · strength 0.66
- Paper Targeting tumor-associated MUC1 overcomes anoikis-resistance in pancreatic cancer. DOI 10.1016/j.trsl.2022.08.010↗
- Paper Overexpression of MUC1 Induces Non-Canonical TGF-β Signaling in Pancreatic Ductal Adenocarcinoma. DOI 10.3389/fcell.2022.821875↗
- Paper Repression of MUC1 Promotes Expansion and Suppressive Function of Myeloid-Derived Suppressor Cells in Pancreatic and Br… DOI 10.3390/ijms22115587↗
- Ru Zhou · 4 shared papers, 2019–2023 · strength 0.52
- Paper Targeting tumor-associated MUC1 overcomes anoikis-resistance in pancreatic cancer. DOI 10.1016/j.trsl.2022.08.010↗
- Paper Overexpression of MUC1 Induces Non-Canonical TGF-β Signaling in Pancreatic Ductal Adenocarcinoma. DOI 10.3389/fcell.2022.821875↗
- Paper Tumor -Associated MUC1 Regulates TGF-β Signaling and Function in Pancreatic Ductal Adenocarcinoma DOI 10.1101/2020.04.29.068577↗
- Sritama Nath · 3 shared papers, 2020–2022 · strength 0.39
- Paper Overexpression of MUC1 Induces Non-Canonical TGF-β Signaling in Pancreatic Ductal Adenocarcinoma. DOI 10.3389/fcell.2022.821875↗
- Paper Repression of MUC1 Promotes Expansion and Suppressive Function of Myeloid-Derived Suppressor Cells in Pancreatic and Br… DOI 10.3390/ijms22115587↗
- Paper Tumor -Associated MUC1 Regulates TGF-β Signaling and Function in Pancreatic Ductal Adenocarcinoma DOI 10.1101/2020.04.29.068577↗
- Priyanka Grover · 3 shared papers, 2019–2022 · strength 0.34
- Paper Overexpression of MUC1 Induces Non-Canonical TGF-β Signaling in Pancreatic Ductal Adenocarcinoma. DOI 10.3389/fcell.2022.821875↗
- Paper Tumor -Associated MUC1 Regulates TGF-β Signaling and Function in Pancreatic Ductal Adenocarcinoma DOI 10.1101/2020.04.29.068577↗
- Paper Overcoming Immunological Resistance Enhances the Efficacy of A Novel Anti-tMUC1-CAR T Cell Treatment against Pancreatic… DOI 10.3390/cells8091070↗
- Mahboubeh Yazdanifar · 3 shared papers, 2019–2022 · strength 0.34
- Paper Overexpression of MUC1 Induces Non-Canonical TGF-β Signaling in Pancreatic Ductal Adenocarcinoma. DOI 10.3389/fcell.2022.821875↗
- Paper Tumor -Associated MUC1 Regulates TGF-β Signaling and Function in Pancreatic Ductal Adenocarcinoma DOI 10.1101/2020.04.29.068577↗
- Paper Overcoming Immunological Resistance Enhances the Efficacy of A Novel Anti-tMUC1-CAR T Cell Treatment against Pancreatic… DOI 10.3390/cells8091070↗
- Shu-ta Wu · 2 shared papers, 2019–2020 · strength 0.19
- Mahnaz Sahraei · 1 shared paper, 2021 · strength 0.14
- John F. Maher · 1 shared paper, 2019 · strength 0.09
- Didier Dréau · 1 shared paper, 2019 · strength 0.09
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.