Publications by authors named "Yun-Jian Huang"

Article Synopsis
  • Advanced non-small cell lung cancer (NSCLC) patients with anaplastic lymphoma kinase (ALK) rearrangement can benefit from the ALK inhibitor crizotinib, but this response varies among patients.
  • A study of 66 NSCLC patients undergoing crizotinib treatment revealed that specific mutations in the ALK gene negatively impacted disease control rates and overall survival.
  • Results indicated that patients with ALK mutations experienced poorer responses to crizotinib, with lower progression-free survival and overall survival compared to those without mutations.
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Background: ALK rearrangement-advanced NSCLC patients respond to crizotinib. ALK rearrangement is currently determined with RT-PCR. VENTANA IHC is a standard method to identify ALK protein overexpression in NSCLC; however, VENTANA IHC has rarely been used to determine the response to crizotinib in Chinese patients with NSCLC and ALK overexpression.

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Background: c-MET has recently been identified as a promising novel target in non-small cell lung cancer (NSCLC). We detected the consistency of c-MET gene amplification in metastatic lymph nodes and tumor tissues of NSCLC patients and discuss the clinical application value of c-MET gene amplification in metastatic lymph nodes.

Methods: Real-time fluorescent quantitative PCR was used to test tumor tissues in 368 NSCLC patients and 178 paired metastatic lymph node samples.

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Aim: To explore the effect of VEGF inhibitor SU5416 on podocytopathy of rats with type I diabetic nephropathy.

Methods: Thirty male SD rats were randomly divided into three groups: normal control group(NC), diabetic nephropathy group(DN) and diabetic nephropathy treated with SU5416 group(SU5416). Rats with DN were induced by STZ.

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Aim: To investigate whether Smad6 and Smad7 can regulate TGF-beta-induced epithelial-mesenchymal transition in human renal proximal tubule epithelial cells.

Methods: Two recombinant adeno-associated viruses (AAV) expressing Smad6 and Smad7 genes were produced without helper virus and then they were delivered into human renal proximal tubule epithelial cells (HKCs). The cells were randomly divided into normal controls, TGF-beta1-treated group, Smad7-infected control, LacZ-infected control, TGF-beta1+Smad7 group or TGF-beta1+Smad6 group, and TGF-beta1 + LacZ group.

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Aim: To construct the adeno-associated virus(AAV) vectors of Smad 6 and Smad 7 genes and observe their expressions in human renal tubule epithelial cells.

Methods: The plasmids pcDNA3-Smad 6/flag and pcDNA3-Smad 7/flag were digested with BamH I and Xho I. Then the Smad 6/flag and Smad 7/flag gene fragments were cloned into plasmid pAAV-MCS, respectively to construct the recombinant pAAV-Smad 6/flag and pAAV-Smad 7/flag plasmids.

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