A5050077108- Lung Cancer Treatments and Mutations
- Lung Cancer Research Studies
- Cytokine Signaling Pathways and Interactions
- Cancer therapeutics and mechanisms
- Cancer-related molecular mechanisms research
- Chronic Lymphocytic Leukemia Research
- Lymphoma Diagnosis and Treatment
- Peptidase Inhibition and Analysis
- Cancer Mechanisms and Therapy
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- RNA modifications and cancer
Southern Medical University
2024
Sun Yat-sen University
2024
Tianjin Medical University General Hospital
2023
Although somatic mutations were explored in depth, limited biomarkers found to predict the resistance of EGFR tyrosine kinase inhibitors (EGFR-TKI). Previous studies reported N6-methyladenosine (m6A) levels regulated response EGFR-TKIs; whether germline variants located m6A sites affected EGFR-TKIs is still unknown.
<p>Figure S1. USP36 expression level predicted response of EGFR-TKIs in EGFR-mutant NSCLC.</p>
<p>Figure S3. G > A rs3744797 affects USP36 m6A level by silicon prediction.</p>
<p>Figure S2. High USP36 expression level promoted migration and proliferation of EGFRmutant NSCLC</p>
<p>Figure S2. High USP36 expression level promoted migration and proliferation of EGFRmutant NSCLC</p>
<div>AbstractPurpose:<p>Although somatic mutations were explored in depth, limited biomarkers found to predict the resistance of EGFR tyrosine kinase inhibitors (EGFR-TKI). Previous studies reported N6-methyladenosine (m6A) levels regulated response EGFR-TKIs; whether germline variants located m6A sites affected EGFR-TKIs is still unknown.</p>Experimental Design:<p>Patients with non–small cell lung cancer (NSCLC) EGFR-activating mutation enrolled investigate...
<p>Figure S4. The protein stability of USP36 and knock-down METTL3, METTL14, WTAP or YTHDF2 by siRNAs, cell-based xenograft treated with osimertinib in vivo</p>
<p>Figure S3. G > A rs3744797 affects USP36 m6A level by silicon prediction.</p>
<p>Figure S4. The protein stability of USP36 and knock-down METTL3, METTL14, WTAP or YTHDF2 by siRNAs, cell-based xenograft treated with osimertinib in vivo</p>
<div>AbstractPurpose:<p>Although somatic mutations were explored in depth, limited biomarkers found to predict the resistance of EGFR tyrosine kinase inhibitors (EGFR-TKI). Previous studies reported N6-methyladenosine (m6A) levels regulated response EGFR-TKIs; whether germline variants located m6A sites affected EGFR-TKIs is still unknown.</p>Experimental Design:<p>Patients with non–small cell lung cancer (NSCLC) EGFR-activating mutation enrolled investigate...
<p>Figure S1. USP36 expression level predicted response of EGFR-TKIs in EGFR-mutant NSCLC.</p>