Pancreatic Cancer Research

ResearcherPhilipps University of MarburgActive in the last 2 years

Elisabeth Heßmann

ORCID-verified (high confidence, 0.95), identity_conf@1As of 6 November 2026

Matched on ORCID iD 0000-0002-9462-1291; OpenAlex author ID A5045288328. Sources: OpenAlex.

Their work

Papers
48 (first author 1, last author 5)
Trials
0
Grants
0
Labs led
1
Collaborators
168
Papers, trials and grants by year

2014: 1 paper · 2015: 3 papers · 2016: 3 papers · 2017: 3 papers · 2018: 1 paper · 2019: 3 papers · 2020: 2 papers · 2021: 6 papers · 2022: 4 papers · 2023: 3 papers · 2024: 6 papers · 2025: 5 papers · 2026: 8 papers

Papers 48

  1. The Protein Phosphatase Inhibitor LB100 Targets the Mesenchymal Lineage of Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.1002/mco2.70794↗
  2. Author Correction: Combined inhibition of BET family proteins and histone deacetylases as a potential epigenetics-based therapy for pancreatic ductal adenocarc… Co-author DOI 10.1038/s41591-026-04234-8↗
  3. A CXCR4 targeting peptide delivered by silica nanoparticles eliminates migrating cancer stem cells in pancreatic ductal adenocarcinoma. Co-author DOI 10.1038/s41598-026-48584-2↗
  4. Targeting Mutual Dependence of Phosphatidylinositol-3-Kinase α/δ and Small Ubiquitin-Like Modifier Signaling in Pancreatic Cancer. Co-author DOI 10.1053/j.gastro.2025.08.018↗
  5. GSK3βhigh/NFATc1high subtype targeting overcomes therapy resistance in pancreatic cancer through transcriptional induction of homologous recombination repair. Co-author DOI 10.1136/gutjnl-2025-336227↗
  6. Targeting PRMT5 Inhibitor-Induced Adaptation in Pancreatic Cancer with the RBM39 Degrader Indisulam. Co-author DOI 10.1158/2767-9764.crc-25-0670↗
  7. Spatially-resolved subtype progression reveals metabolic vulnerabilities in pancreatic ductal adenocarcinoma. Co-author DOI 10.1186/s12943-026-02628-3↗
  8. Loss of the Y chromosome drives basal identity and metastatic potential via epigenetic reprogramming in pancreatic cancer Co-author DOI 10.64898/2026.10.06.756936↗
  9. KRAS G 12C-inhibitor-based combination therapies for pancreatic cancer: insights from drug screening. Co-author DOI 10.1002/1878-0261.13725↗
  10. Simultaneous targeting of KRAS and CDK4 synergistically induces durable growth arrest in pancreatic cancer cells. Co-author DOI 10.1038/s41419-025-08362-w↗
  11. Spatial tumor immune heterogeneity facilitates subtype co-existence and therapy response in pancreatic cancer. Co-author DOI 10.1038/s41467-024-55330-7↗
  12. TP53 missense-specific transcriptional plasticity drives resistance against cell cycle inhibitors in pancreatic cancer. Co-author DOI 10.1126/sciadv.adu2339↗
  13. Glucocorticoid receptor suppresses GATA6-mediated RNA polymerase II pause release to modulate classical subtype identity in pancreatic cancer. Co-author DOI 10.1136/gutjnl-2024-334374↗
  14. A Novel AMPK Inhibitor Sensitizes Pancreatic Cancer Cells to Ferroptosis Induction. Co-author DOI 10.1002/advs.202307695↗
  15. Expression of gemcitabine metabolizing enzymes and stromal components reveal complexities of preclinical pancreatic cancer models for therapeutic testing. Co-author DOI 10.1016/j.neo.2024.101002↗
  16. Author Correction: Combined inhibition of BET family proteins and histone deacetylases as a potential epigenetics-based therapy for pancreatic ductal adenocarc… Co-author DOI 10.1038/s41591-024-03054-y↗
  17. An NFATc1/SMAD3/cJUN Complex Restricted to SMAD4-Deficient Pancreatic Cancer Guides Rational Therapies. Last author DOI 10.1053/j.gastro.2023.10.026↗
  18. A single-cell strategy for the identification of intronic variants related to mis-splicing in pancreatic cancer. Co-author DOI 10.1093/nargab/lqae057↗
  19. A Concept for Mining Transitive Sequential Patterns from Pancreatic Cancer Patient Journeys. Co-author DOI 10.3233/shti240862↗
  20. Epigenetic control of pancreatic cancer metastasis. Co-author DOI 10.1007/s10555-023-10132-z↗
  21. Interactive enhancer hubs (iHUBs) mediate transcriptional reprogramming and adaptive resistance in pancreatic cancer. Co-author DOI 10.1136/gutjnl-2022-328154↗
  22. Identification of a ΔNp63-Dependent Basal-Like A Subtype-Specific Transcribed Enhancer Program (B-STEP) in Aggressive Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.1158/1541-7786.mcr-22-0916↗
  23. AP1/Fra1 confers resistance to MAPK cascade inhibition in pancreatic cancer. Co-author DOI 10.1007/s00018-022-04638-y↗
  24. Epigenetic Therapeutic Strategies to Target Molecular and Cellular Heterogeneity in Pancreatic Cancer. First author DOI 10.1159/000519859↗
  25. Axon guidance receptor ROBO3 modulates subtype identity and prognosis via AXL-associated inflammatory network in pancreatic cancer. Co-author DOI 10.1172/jci.insight.154475↗
  26. TP53-Status-Dependent Oncogenic EZH2 Activity in Pancreatic Cancer. Last author DOI 10.3390/cancers14143451↗
  27. TNF-α-producing macrophages determine subtype identity and prognosis via AP1 enhancer reprogramming in pancreatic cancer. Co-author DOI 10.1038/s43018-021-00258-w↗
  28. New Insights Into Pancreatic Cancer: Notes from a Virtual Meeting. Co-author DOI 10.1053/j.gastro.2021.04.082↗
  29. Synergistic targeting and resistance to PARP inhibition in DNA damage repair-deficient pancreatic cancer. Co-author DOI 10.1136/gutjnl-2019-319970↗
  30. STIM1 Mediates Calcium-Dependent Epigenetic Reprogramming in Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-20-2874↗
  31. HSP90 Inhibition Synergizes with Cisplatin to Eliminate Basal-like Pancreatic Ductal Adenocarcinoma Cells. Co-author DOI 10.3390/cancers13246163↗
  32. Chromatin-Independent Interplay of NFATc1 and EZH2 in Pancreatic Cancer. Last author DOI 10.3390/cells10123463↗
  33. Microenvironmental Determinants of Pancreatic Cancer. Co-author DOI 10.1152/physrev.00042.2019↗
  34. EZH2 Regulates Pancreatic Cancer Subtype Identity and Tumor Progression via Transcriptional Repression of GATA6. Last author DOI 10.1158/0008-5472.can-20-0672↗
  35. Cytosolic 5'-nucleotidase 1A is overexpressed in pancreatic cancer and mediates gemcitabine resistance by reducing intracellular gemcitabine metabolites. Co-author DOI 10.1016/j.ebiom.2019.01.037↗
  36. Aberrant NFATc1 signaling counteracts TGFβ-mediated growth arrest and apoptosis induction in pancreatic cancer progression. Last author DOI 10.1038/s41419-019-1682-2↗
  37. Preclinical Evaluation of 1,2-Diamino-4,5-Dibromobenzene in Genetically Engineered Mouse Models of Pancreatic Cancer. Co-author DOI 10.3390/cells8060563↗
  38. Utilizing High Resolution Ultrasound to Monitor Tumor Onset and Growth in Genetically Engineered Pancreatic Cancer Models. Co-author DOI 10.3791/56979↗
  39. Histone deacetylase class-I inhibition promotes epithelial gene expression in pancreatic cancer cells in a BRD4- and MYC-dependent manner. Co-author DOI 10.1093/nar/gkx212↗
  40. Epigenetic treatment of pancreatic cancer: is there a therapeutic perspective on the horizon? Co-author DOI 10.1136/gutjnl-2016-312539↗
  41. ATM Deficiency Generating Genomic Instability Sensitizes Pancreatic Ductal Adenocarcinoma Cells to Therapy-Induced DNA Damage. Co-author DOI 10.1158/0008-5472.can-17-0634↗
  42. MYC in pancreatic cancer: novel mechanistic insights and their translation into therapeutic strategies. Co-author DOI 10.1038/onc.2015.216↗
  43. NFATc4 Regulates Sox9 Gene Expression in Acinar Cell Plasticity and Pancreatic Cancer Initiation. Co-author DOI 10.1155/2016/5272498↗
  44. GSK-3β Governs Inflammation-Induced NFATc2 Signaling Hubs to Promote Pancreatic Cancer Progression. Co-author DOI 10.1158/1535-7163.mct-15-0309↗
  45. Loss of ATM accelerates pancreatic cancer formation and epithelial-mesenchymal transition. Co-author DOI 10.1038/ncomms8677↗
  46. Combined inhibition of BET family proteins and histone deacetylases as a potential epigenetics-based therapy for pancreatic ductal adenocarcinoma. Co-author DOI 10.1038/nm.3952↗
  47. Antithetical NFATc1-Sox2 and p53-miR200 signaling networks govern pancreatic cancer cell plasticity. Co-author DOI 10.15252/embj.201489574↗
  48. Inflammation-induced NFATc1-STAT3 transcription complex promotes pancreatic cancer initiation by KrasG12D. Co-author DOI 10.1158/2159-8290.cd-13-0593↗

Closest collaborators

The 25 strongest of 168 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Volker Ellenrieder · 33 shared papers, 2014–2026 · strength 4.25
  2. Günter Schneider · 14 shared papers, 2016–2026 · strength 2.39
  3. Shiv K. Singh · 16 shared papers, 2014–2026 · strength 1.92
  4. Carolin Schneider · 9 shared papers, 2022–2026 · strength 1.60
  5. Steven A. Johnsen · 12 shared papers, 2017–2026 · strength 1.44
  6. Matthias Wirth · 9 shared papers, 2015–2026 · strength 1.41
  7. Albrecht Neeße · 14 shared papers, 2014–2024 · strength 1.40
  8. Dieter Saur · 8 shared papers, 2021–2026 · strength 1.37
  9. Michael B. Ghadimi · 7 shared papers, 2024–2026 · strength 1.32
  10. Jens Thomas Siveke · 12 shared papers, 2014–2026 · strength 1.24
  11. Jochen Gaedcke · 11 shared papers, 2015–2025 · strength 1.14
  12. Ulrich Sax · 6 shared papers, 2024–2026 · strength 1.11
  13. Lukas Krauß · 6 shared papers, 2022–2026 · strength 1.07
  14. Maximilian Reichert · 7 shared papers, 2021–2026 · strength 1.05
  15. Stephan A. Hahn · 8 shared papers, 2015–2026 · strength 0.96
  16. Constanza Tapia Contreras · 5 shared papers, 2024–2026 · strength 0.92
  17. Zeynab Najafova · 6 shared papers, 2017–2026 · strength 0.83
  18. Marian Grade · 5 shared papers, 2022–2026 · strength 0.83
  19. Christian Schneeweis · 5 shared papers, 2022–2026 · strength 0.83
  20. Lukas Klein · 5 shared papers, 2021–2026 · strength 0.82
  21. Xin Wang · 6 shared papers, 2020–2025 · strength 0.79
  22. Lena‐Christin Conradi · 4 shared papers, 2025–2026 · strength 0.77
  23. Lennart Versemann · 5 shared papers, 2020–2024 · strength 0.74
  24. Shilpa Patil · 7 shared papers, 2018–2022 · strength 0.73
  25. Feda H. Hamdan · 6 shared papers, 2019–2024 · strength 0.68

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.