ResearcherUniversity of CopenhagenActive in the last 2 years
Dominika Czaplińska
Matched on OpenAlex author ID A5076479884. Sources: OpenAlex.
Their work
- Papers
- 4 (first author 0, last author 1)
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 9
2021: 1 paper · 2022: none · 2023: 1 paper · 2024: 1 paper · 2025: none · 2026: 1 paper
Papers 4
- Microenvironmental acidosis drives PARP- and ATM inhibitor resistance in p53 deficient pancreatic cancer. Co-author DOI 10.1016/j.isci.2026.115112↗
- Adaptation to an acid microenvironment promotes pancreatic cancer organoid growth and drug resistance. Co-author DOI 10.1016/j.celrep.2024.114409↗
- Crosstalk between tumor acidosis, p53 and extracellular matrix regulates pancreatic cancer aggressiveness. Co-author DOI 10.1002/ijc.34367↗
- Metabolic reprogramming by driver mutation-tumor microenvironment interplay in pancreatic cancer: new therapeutic targets. Last author DOI 10.1007/s10555-021-10004-4↗
Closest collaborators
The 9 strongest of 9 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Henriette Berg Andersen · 4 shared papers, 2021–2026 · strength 0.83
- Paper Microenvironmental acidosis drives PARP- and ATM inhibitor resistance in p53 deficient pancreatic cancer. DOI 10.1016/j.isci.2026.115112↗
- Paper Adaptation to an acid microenvironment promotes pancreatic cancer organoid growth and drug resistance. DOI 10.1016/j.celrep.2024.114409↗
- Paper Metabolic reprogramming by driver mutation-tumor microenvironment interplay in pancreatic cancer: new therapeutic targe… DOI 10.1007/s10555-021-10004-4↗
- Renata Ialchina · 4 shared papers, 2021–2026 · strength 0.83
- Paper Microenvironmental acidosis drives PARP- and ATM inhibitor resistance in p53 deficient pancreatic cancer. DOI 10.1016/j.isci.2026.115112↗
- Paper Adaptation to an acid microenvironment promotes pancreatic cancer organoid growth and drug resistance. DOI 10.1016/j.celrep.2024.114409↗
- Paper Metabolic reprogramming by driver mutation-tumor microenvironment interplay in pancreatic cancer: new therapeutic targe… DOI 10.1007/s10555-021-10004-4↗
- Stine F. Pedersen · 4 shared papers, 2021–2026 · strength 0.83
- Paper Microenvironmental acidosis drives PARP- and ATM inhibitor resistance in p53 deficient pancreatic cancer. DOI 10.1016/j.isci.2026.115112↗
- Paper Adaptation to an acid microenvironment promotes pancreatic cancer organoid growth and drug resistance. DOI 10.1016/j.celrep.2024.114409↗
- Paper Metabolic reprogramming by driver mutation-tumor microenvironment interplay in pancreatic cancer: new therapeutic targe… DOI 10.1007/s10555-021-10004-4↗
- Arnaud Stigliani · 3 shared papers, 2023–2026 · strength 0.64
- Paper Microenvironmental acidosis drives PARP- and ATM inhibitor resistance in p53 deficient pancreatic cancer. DOI 10.1016/j.isci.2026.115112↗
- Paper Adaptation to an acid microenvironment promotes pancreatic cancer organoid growth and drug resistance. DOI 10.1016/j.celrep.2024.114409↗
- Paper Crosstalk between tumor acidosis, p53 and extracellular matrix regulates pancreatic cancer aggressiveness. DOI 10.1002/ijc.34367↗
- Albin Sandelin · 3 shared papers, 2023–2026 · strength 0.64
- Paper Microenvironmental acidosis drives PARP- and ATM inhibitor resistance in p53 deficient pancreatic cancer. DOI 10.1016/j.isci.2026.115112↗
- Paper Adaptation to an acid microenvironment promotes pancreatic cancer organoid growth and drug resistance. DOI 10.1016/j.celrep.2024.114409↗
- Paper Crosstalk between tumor acidosis, p53 and extracellular matrix regulates pancreatic cancer aggressiveness. DOI 10.1002/ijc.34367↗
- Luis A. Pardo · 1 shared paper, 2026 · strength 0.28
- Frauke Alves · 1 shared paper, 2023 · strength 0.15
- Joanna Napp · 1 shared paper, 2023 · strength 0.15
- Mette Flinck · 1 shared paper, 2023 · strength 0.15
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.