ResearcherUniversity of North Carolina at CharlotteNo recent work listed
Sritama Nath
Matched on OpenAlex author ID A5076013481. Sources: OpenAlex.
Their work
- Papers
- 9 (first author 2, last author 0)
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 13
2011: 1 paper · 2012: 1 paper · 2013: 1 paper · 2014: 1 paper · 2015: 1 paper · 2016: none · 2017: none · 2018: 1 paper · 2019: none · 2020: 1 paper · 2021: 1 paper · 2022: 1 paper
Papers 9
- 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 Co-author DOI 10.3390/ijms22115587↗
- Tumor -Associated MUC1 Regulates TGF-β Signaling and Function in Pancreatic Ductal Adenocarcinoma First author DOI 10.1101/2020.04.29.068577↗
- SMAD4-independent activation of TGF-β signaling by MUC1 in a human pancreatic cancer cell line. First author DOI 10.18632/oncotarget.23966↗
- Mucin 1 Regulates Cox-2 Gene in Pancreatic Cancer. Co-author DOI 10.1097/mpa.0000000000000371↗
- Pancreatic Cancer Cells Isolated from Muc1-Null Tumors Favor the Generation of a Mature Less Suppressive MDSC Population. Co-author DOI 10.3389/fimmu.2014.00067↗
- MUC1 induces drug resistance in pancreatic cancer cells via upregulation of multidrug resistance genes. Co-author DOI 10.1038/oncsis.2013.16↗
- MUC1 regulates PDGFA expression during pancreatic cancer progression. Co-author DOI 10.1038/onc.2011.651↗
- MUC1 enhances invasiveness of pancreatic cancer cells by inducing epithelial to mesenchymal transition. Co-author DOI 10.1038/onc.2010.526↗
Closest collaborators
The 13 strongest of 13 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Pinku Mukherjee · 9 shared papers, 2011–2022 · strength 0.68
- 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 · 5 shared papers, 2013–2022 · strength 0.45
- 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 SMAD4-independent activation of TGF-β signaling by MUC1 in a human pancreatic cancer cell line. DOI 10.18632/oncotarget.23966↗
- Mukulika Bose · 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↗
- Ru Zhou · 3 shared papers, 2018–2022 · 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 SMAD4-independent activation of TGF-β signaling by MUC1 in a human pancreatic cancer cell line. DOI 10.18632/oncotarget.23966↗
- Mahboubeh Yazdanifar · 2 shared papers, 2020–2022 · strength 0.25
- Mahnaz Sahraei · 4 shared papers, 2011–2021 · strength 0.23
- Paper Repression of MUC1 Promotes Expansion and Suppressive Function of Myeloid-Derived Suppressor Cells in Pancreatic and Br… DOI 10.3390/ijms22115587↗
- Paper MUC1 induces drug resistance in pancreatic cancer cells via upregulation of multidrug resistance genes. DOI 10.1038/oncsis.2013.16↗
- Paper MUC1 regulates PDGFA expression during pancreatic cancer progression. DOI 10.1038/onc.2011.651↗
- Lopamudra Das Roy · 5 shared papers, 2011–2015 · strength 0.20
- Paper Mucin 1 Regulates Cox-2 Gene in Pancreatic Cancer. DOI 10.1097/mpa.0000000000000371↗
- Paper Pancreatic Cancer Cells Isolated from Muc1-Null Tumors Favor the Generation of a Mature Less Suppressive MDSC Populatio… DOI 10.3389/fimmu.2014.00067↗
- Paper MUC1 induces drug resistance in pancreatic cancer cells via upregulation of multidrug resistance genes. DOI 10.1038/oncsis.2013.16↗
- Amritha Kidiyoor · 3 shared papers, 2012–2014 · strength 0.11
- Paper Pancreatic Cancer Cells Isolated from Muc1-Null Tumors Favor the Generation of a Mature Less Suppressive MDSC Populatio… DOI 10.3389/fimmu.2014.00067↗
- Paper MUC1 induces drug resistance in pancreatic cancer cells via upregulation of multidrug resistance genes. DOI 10.1038/oncsis.2013.16↗
- Paper MUC1 regulates PDGFA expression during pancreatic cancer progression. DOI 10.1038/onc.2011.651↗
- Shu-ta Wu · 1 shared paper, 2020 · strength 0.10
- Dahlia M. Besmer · 3 shared papers, 2011–2014 · strength 0.10
- Paper Pancreatic Cancer Cells Isolated from Muc1-Null Tumors Favor the Generation of a Mature Less Suppressive MDSC Populatio… DOI 10.3389/fimmu.2014.00067↗
- Paper MUC1 regulates PDGFA expression during pancreatic cancer progression. DOI 10.1038/onc.2011.651↗
- Paper MUC1 enhances invasiveness of pancreatic cancer cells by inducing epithelial to mesenchymal transition. DOI 10.1038/onc.2010.526↗
- Jennifer M. Curry · 1 shared paper, 2014 · strength 0.04
- Didier Dréau · 1 shared paper, 2014 · strength 0.04
- Sun‐Il Hwang · 1 shared paper, 2011 · strength 0.02
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.