⌘+K

Pulse Explore Clubs Researchers Journals

Home Clubs Explore

May 29, 2024Pharmacology

Transcription factor E2F8 activates PDK1-mediated DNA damage repair to enhance cisplatin resistance in lung adenocarcinoma

Hongliang Li Junxia Sun Haibo Hu Yi Wang

View Full Paper

Ask AI

Bookmark

Share

Abstract

Cisplatin (DDP) is the commonest chemo drug in lung adenocarcinoma (LUAD) treatment, and DDP resistance is a significant barrier to therapeutic therapy. This study attempted to elucidate the impact of PDK1 on DDP resistance in LUAD and its mechanism.

Discussion

No takes yet. Share an insight, caveat, or question.

Cite This Study

Li et al. (2024) studied this question.

synapsesocial.com/papers/68e67e28b6db64358760829f https://doi.org/10.1159/000537819

View Full Paper

Ask AI

Bookmark

Share

Keep reading

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1Cisplatin-mediated activation of NF-κB promotes lung cancer stem cell formation via DNA repair pathways2025
2TP53 mitigates cisplatin resistance in non-small cell lung cancer by mediating the effects of resistant cell-derived exosome mir-424-5p2024 · 4 citations
3Integrated analysis reveals critical cisplatin-resistance regulators E2F7 contributed to tumor progression and metastasis in lung adenocarcinoma2024 · 13 citations
4PDPK1 activates BIRC3 via NFKB1 to promote radiotherapy resistance in lung adenocarcinomaOriginal Research · 2026 · 1 citations
5Metabolic reprogramming and cisplatin resistance: the emerging role of Pyruvate Dehydrogenase Kinases (PDKs)Review · 2026