• 14 Hits
  • 検索条件 : 絞込み (MeSH = Adenocarcinoma of Lung / pathology)
生物種 リソース名 タイトル
ヒト・動物細胞 293T(RCB2202) Reciprocal expression of trefoil factor-1 and thyroid transcription factor-1 in lung adenocarcinomas.
ヒト・動物細胞 II-18(RCB2093) Chloride Intracellular Channel 1 Expression Is Associated With Poor Prognosis of Lung Adenocarcinoma.
ヒト・動物細胞 LU99(RCB1900) , LU65(RCB1967) , IA-LM(RCB0554) The KRASG12C Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients.
ヒト・動物細胞 PC-9(RCB4455) Suppression of tumor immune microenvironment via microRNA-1 after epidermal growth factor receptor-tyrosine kinase inhibitor resistance acquirement in lung adenocarcinoma.
ヒト・動物細胞 PC-9(RCB4455) Inhibition of heat shock protein 90 destabilizes receptor tyrosine kinase ROR1 in lung adenocarcinoma.
ヒト・動物細胞 PC-9(RCB4455) Conditional Ror1 knockout reveals crucial involvement in lung adenocarcinoma development and identifies novel HIF-1α regulator.
ヒト・動物細胞 A549 (Pro)renin receptor/ATP6AP2 is required for autophagy and regulates proliferation in lung adenocarcinoma cells.
ヒト・動物細胞 A549 ZO-2 Suppresses Cell Migration Mediated by a Reduction in Matrix Metalloproteinase 2 in Claudin-18-Expressing Lung Adenocarcinoma A549 Cells.
ヒト・動物細胞 PC-9(RCB4455) Cancer exosomal microRNAs from gefitinib-resistant lung cancer cells cause therapeutic resistance in gefitinib-sensitive cells.
ヒト・動物細胞 LC-2/ad(RCB0440) , SP2/0-Ag14(RCB0209) Prognostic significance of IMMT expression in surgically-resected lung adenocarcinoma.
ヒト・動物細胞 PC-9(RCB4455) The impact of PRDX4 and the EGFR mutation status on cellular proliferation in lung adenocarcinoma.
ヒト・動物細胞 PC-9(RCB4455) AXL confers intrinsic resistance to osimertinib and advances the emergence of tolerant cells.
ヒト・動物細胞 PC-9(RCB4455) , RERF-LC-KJ(RCB1313) Cytoplasmic expression of epithelial cell transforming sequence 2 in lung adenocarcinoma and its implications for malignant progression.
ヒト・動物細胞 TE-4(RCB2097) Small molecule inhibitors and CRISPR/Cas9 mutagenesis demonstrate that SMYD2 and SMYD3 activity are dispensable for autonomous cancer cell proliferation.