Proteolysis targeting chimeras in non-small cell lung cancer.

[1]  Zhaofu Wang,et al.  HJM-561, a potent, selective and orally bioavailable EGFR PROTAC that overcomes osimertinib-resistant EGFR triple mutations. , 2022, Molecular cancer therapeutics.

[2]  Y. Mitsuishi,et al.  Survival past five years with advanced, EGFR-mutated or ALK-rearranged non-small cell lung cancer—is there a “tail plateau” in the survival curve of these patients? , 2022, BMC cancer.

[3]  F. Kaye,et al.  BCL-XL PROTAC degrader DT2216 synergizes with sotorasib in preclinical models of KRASG12C-mutated cancers , 2022, Journal of Hematology & Oncology.

[4]  Yongyi Mao,et al.  Discovery of Potent PROTACs Targeting EGFR Mutants through the Optimization of Covalent EGFR Ligands. , 2022, Journal of medicinal chemistry.

[5]  John Paul Shen,et al.  Phase 1/2 study of ARV-110, an androgen receptor (AR) PROTAC degrader, in metastatic castration-resistant prostate cancer (mCRPC). , 2022, Journal of Clinical Oncology.

[6]  A. Adjei,et al.  Challenges in the Use of Targeted Therapies in Non–Small Cell Lung Cancer , 2022, Cancer research and treatment.

[7]  Zeyu Cai,et al.  Rational Design for Nitroreductase (NTR)-Responsive Proteolysis Targeting Chimeras (PROTACs) Selectively Targeting Tumor Tissues. , 2022, Journal of medicinal chemistry.

[8]  Jian Li,et al.  Design, Synthesis, and Biological Evaluation of Novel EGFR PROTACs Targeting Del19/T790M/C797S Mutation. , 2022, ACS medicinal chemistry letters.

[9]  F. Grossi,et al.  Current Insights on the Treatment of Anaplastic Lymphoma Kinase-Positive Metastatic Non-Small Cell Lung Cancer: Focus on Brigatinib , 2022, Clinical pharmacology : advances and applications.

[10]  Qihua Zhu,et al.  Discovery of novel potent covalent inhibitor-based EGFR degrader with excellent in vivo efficacy. , 2022, Bioorganic chemistry.

[11]  P. Xing,et al.  Front-Line Therapy in EGFR Exon 19 Deletion and 21 Leu858Arg Mutations in Advanced Non-Small Cell Lung Cancer: A Network Meta-Analysis , 2021, Evidence-based complementary and alternative medicine : eCAM.

[12]  Wen-jun Tian,et al.  Resistance mechanisms to osimertinib and emerging therapeutic strategies in nonsmall cell lung cancer , 2021, Current opinion in oncology.

[13]  Jinhua Luo,et al.  FAK-Targeting PROTAC Demonstrates Enhanced Antitumor Activity against KRAS Mutant Non-Small Cell Lung Cancer. , 2021, Experimental cell research.

[14]  Dongming Xing,et al.  VHL-based PROTACs as potential therapeutic agents: Recent progress and perspectives. , 2021, European journal of medicinal chemistry.

[15]  Fang Wu,et al.  The Resistance Mechanisms and Treatment Strategies for ALK-Rearranged Non-Small Cell Lung Cancer , 2021, Frontiers in Oncology.

[16]  A. Imagawa,et al.  Comparison Between Second- and Third-generation Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors as First-line Treatment in Patients With Non-small-cell Lung Cancer: A Retrospective Analysis , 2021, AntiCancer Research.

[17]  M. Tsao,et al.  Mechanism of drug tolerant persister cancer cells: The landscape and clinical implication for therapy. , 2021, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[18]  D. Manna,et al.  LYTACs: An Emerging Tool for the Degradation of Non‐Cytosolic Proteins , 2021, ChemMedChem.

[19]  Kristin K. Brown,et al.  The PROTACtable genome , 2021, Nature Reviews Drug Discovery.

[20]  B. Jiang,et al.  Discovery of a Brigatinib Degrader SIAIS164018 with Destroying Metastasis-Related Oncoproteins and a Reshuffling Kinome Profile. , 2021, Journal of medicinal chemistry.

[21]  R. Govindan,et al.  Sotorasib for Lung Cancers with KRAS p.G12C Mutation. , 2021, The New England journal of medicine.

[22]  J. Soh,et al.  KRAS secondary mutations that confer acquired resistance to KRAS G12C inhibitors, sotorasib and adagrasib, and overcoming strategies: insights from the in vitro experiments. , 2021, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[23]  Jinyun Dong,et al.  PROTAC: An Effective Targeted Protein Degradation Strategy for Cancer Therapy , 2021, Frontiers in Pharmacology.

[24]  Bin Yu,et al.  Indoleamine 2,3-dioxygenase 1 (IDO1) inhibitors in clinical trials for cancer immunotherapy , 2021, Journal of Hematology & Oncology.

[25]  P. Park,et al.  The origins and genetic interactions of KRAS mutations are allele- and tissue-specific , 2021, Nature Communications.

[26]  B. Jiang,et al.  Effective degradation of EGFRL858R+T790M mutant proteins by CRBN-based PROTACs through both proteosome and autophagy/lysosome degradation systems. , 2021, European journal of medicinal chemistry.

[27]  Lixia Chen,et al.  Rational Design and Synthesis of Novel Dual PROTACs for Simultaneous Degradation of EGFR and PARP. , 2021, Journal of medicinal chemistry.

[28]  N. London,et al.  The rise of covalent proteolysis targeting chimeras. , 2021, Current opinion in chemical biology.

[29]  Y. Niu,et al.  A narrative review of proteolytic targeting chimeras (PROTACs): future perspective for prostate cancer therapy , 2021, Translational andrology and urology.

[30]  O. Margalit,et al.  Long-Term Survival of Patients with Metastatic Non-Small-Cell Lung Cancer over Five Decades , 2021, Journal of oncology.

[31]  Kai Wang,et al.  Proteolysis targeting chimera (PROTAC) for epidermal growth factor receptor enhances anti‐tumor immunity in non‐small cell lung cancer , 2020, Drug development research.

[32]  Xiangshu Xiao,et al.  PROTACs to address the challenges facing small molecule inhibitors. , 2020, European journal of medicinal chemistry.

[33]  B. Cornelissen,et al.  PARP Inhibitors in Cancer Diagnosis and Therapy , 2020, Clinical Cancer Research.

[34]  Shaomeng Wang,et al.  A highly potent PROTAC androgen receptor (AR) degrader ARD-61 effectively inhibits AR-positive breast cancer cell growth in vitro and tumor growth in vivo , 2020, Neoplasia.

[35]  Haolan Lei,et al.  Discovery of potent small molecule PROTACs targeting mutant EGFR. , 2020, European journal of medicinal chemistry.

[36]  V. Dötsch,et al.  Ubiquitination in the ERAD Process , 2020, International journal of molecular sciences.

[37]  P. Jänne,et al.  Mutant-Selective Allosteric EGFR Degraders are Effective Against a Broad Range of Drug-Resistant Mutations. , 2020, Angewandte Chemie.

[38]  C. Crews,et al.  Targeted Degradation of Oncogenic KRASG12C by VHL-Recruiting PROTACs , 2020, ACS central science.

[39]  Xiaoju Wang,et al.  Discovery and biological evaluation of proteolysis targeting chimeras (PROTACs) as an EGFR degraders based on osimertinib and lenalidomide. , 2020, Bioorganic & medicinal chemistry letters.

[40]  Lin-jiang Tong,et al.  Design and synthesis of selective degraders of EGFRL858R/T790M mutant. , 2020, European journal of medicinal chemistry.

[41]  B. Jiang,et al.  Development of a Brigatinib degrader (SIAIS117) as a potential treatment for ALK positive cancer resistance. , 2020, European journal of medicinal chemistry.

[42]  D. Planchard,et al.  Novel drugs targeting EGFR and HER2 exon 20 mutations in metastatic NSCLC. , 2020, Critical reviews in oncology/hematology.

[43]  San-qi Zhang,et al.  Discovery of potent epidermal growth factor receptor (EGFR) degraders by proteolysis targeting chimera (PROTAC). , 2020, European journal of medicinal chemistry.

[44]  Xian Chen,et al.  Discovery of Potent and Selective Epidermal Growth Factor Receptor (EGFR) Bifunctional Small-molecule Degraders. , 2020, Journal of medicinal chemistry.

[45]  Ying Cheng,et al.  Overall Survival with Osimertinib in Untreated, EGFR-Mutated Advanced NSCLC. , 2019, The New England journal of medicine.

[46]  A. Ferrando,et al.  A selective BCL-XL PROTAC degrader achieves safe and potent antitumor activity , 2019, Nature Medicine.

[47]  Youwei Xu,et al.  Discovery of SIAIS178 as an effective BCR-ABL degrader by recruiting von Hippel-Lindau (VHL) E3 Ubiquitin Ligase. , 2019, Journal of medicinal chemistry.

[48]  C. Bouzin,et al.  Increased Expression and Activation of FAK in Small-Cell Lung Cancer Compared to Non-Small-Cell Lung Cancer , 2019, Cancers.

[49]  E. Giovannetti,et al.  Resistance mechanisms to osimertinib in EGFR-mutated non-small cell lung cancer , 2019, British Journal of Cancer.

[50]  Rafał Bartoszewski,et al.  Primary endothelial cell–specific regulation of hypoxia‐inducible factor (HIF)‐1 and HIF‐2 and their target gene expression profiles during hypoxia , 2019, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[51]  J. Barrett,et al.  Mechanisms of acquired resistance to first-line osimertinib: Preliminary data from the phase III FLAURA study. , 2018, Annals of oncology : official journal of the European Society for Medical Oncology.

[52]  Chi-Hoon Park,et al.  Induced protein degradation of anaplastic lymphoma kinase (ALK) by proteolysis targeting chimera (PROTAC). , 2018, Biochemical and biophysical research communications.

[53]  J. Barrett,et al.  Analysis of resistance mechanisms to osimertinib in patients with EGFR T790M advanced NSCLC from the AURA3 study. , 2018, Annals of oncology : official journal of the European Society for Medical Oncology.

[54]  C. Crews,et al.  Androgen receptor degradation by the proteolysis-targeting chimera ARCC-4 outperforms enzalutamide in cellular models of prostate cancer drug resistance , 2018, Communications Biology.

[55]  Y. Xiong,et al.  Proteolysis Targeting Chimeras (PROTACs) of Anaplastic Lymphoma Kinase (ALK). , 2018, European journal of medicinal chemistry.

[56]  P. Jänne,et al.  Chemically Induced Degradation of Anaplastic Lymphoma Kinase (ALK). , 2018, Journal of medicinal chemistry.

[57]  Yong-xiao Cao,et al.  Discovery of 2,4,6-trisubstitued pyrido[3,4-d]pyrimidine derivatives as new EGFR-TKIs. , 2018, European journal of medicinal chemistry.

[58]  Yunpeng Liu,et al.  Investigating Novel Resistance Mechanisms to Third-Generation EGFR Tyrosine Kinase Inhibitor Osimertinib in Non–Small Cell Lung Cancer Patients , 2018, Clinical Cancer Research.

[59]  B. Stockwell,et al.  Design of Small Molecules That Compete with Nucleotide Binding to an Engineered Oncogenic KRAS Allele. , 2018, Biochemistry.

[60]  Ying Cheng,et al.  Osimertinib in Untreated EGFR‐Mutated Advanced Non–Small‐Cell Lung Cancer , 2018, The New England journal of medicine.

[61]  Jing Wang,et al.  The Advantages of Targeted Protein Degradation Over Inhibition: An RTK Case Study. , 2017, Cell chemical biology.

[62]  Daniel H. Miller,et al.  Cancer-specific PERK signaling drives invasion and metastasis through CREB3L1 , 2017, Nature Communications.

[63]  F. Hirsch,et al.  Comprehensive Analysis of EGFR‐Mutant Abundance and Its Effect on Efficacy of EGFR TKIs in Advanced NSCLC with EGFR Mutations , 2017, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[64]  P. Stephens,et al.  Emergence of novel and dominant acquired EGFR solvent-front mutations at Gly796 (G796S/R) together with C797S/R and L792F/H mutations in one EGFR (L858R/T790M) NSCLC patient who progressed on osimertinib. , 2017, Lung cancer.

[65]  Dana S. Neel,et al.  Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinoma , 2017, npj Precision Oncology.

[66]  C. Crews,et al.  Targeted Protein Degradation by Small Molecules. , 2017, Annual review of pharmacology and toxicology.

[67]  A. Mansfield,et al.  S768I Mutation in EGFR in Patients with Lung Cancer , 2016, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[68]  C. Amos,et al.  The potential utility of re-mining results of somatic mutation testing: KRAS status in lung adenocarcinoma. , 2016, Cancer genetics.

[69]  Chandra Sekhar Pedamallu,et al.  Distinct patterns of somatic genome alterations in lung adenocarcinomas and squamous cell carcinomas , 2016, Nature Genetics.

[70]  R. Gibbs,et al.  Genomic analyses identify molecular subtypes of pancreatic cancer , 2016, Nature.

[71]  Abdel Kareem Azab,et al.  The role of hypoxia in cancer progression, angiogenesis, metastasis, and resistance to therapy , 2015, Hypoxia.

[72]  Dong-Wan Kim,et al.  Mechanisms of Acquired Resistance to AZD9291: A Mutation-Selective, Irreversible EGFR Inhibitor , 2015, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[73]  F. Sinicrope,et al.  The Mutant KRAS Gene Up-regulates BCL-XL Protein via STAT3 to Confer Apoptosis Resistance That Is Reversed by BIM Protein Induction and BCL-XL Antagonism* , 2015, The Journal of Biological Chemistry.

[74]  R. Govindan,et al.  Genomic alterations in lung adenocarcinoma. , 2015, The Lancet. Oncology.

[75]  L. Sequist,et al.  The Allelic Context of the C797S Mutation Acquired upon Treatment with Third-Generation EGFR Inhibitors Impacts Sensitivity to Subsequent Treatment Strategies , 2015, Clinical Cancer Research.

[76]  C. Mathers,et al.  Cancer incidence and mortality worldwide: Sources, methods and major patterns in GLOBOCAN 2012 , 2015, International journal of cancer.

[77]  C. Gambacorti-Passerini,et al.  Activity of second-generation ALK inhibitors against crizotinib-resistant mutants in an NPM-ALK model compared to EML4-ALK , 2015, Cancer medicine.

[78]  M. Ladanyi,et al.  ALK Rearrangements Are Mutually Exclusive with Mutations in EGFR or KRAS: An Analysis of 1,683 Patients with Non–Small Cell Lung Cancer , 2013, Clinical Cancer Research.

[79]  C. Crews,et al.  Chemical biology: Greasy tags for protein removal , 2012, Nature.

[80]  A. Iafrate,et al.  Mechanisms of Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancers , 2012, Science Translational Medicine.

[81]  C. Cole,et al.  COSMIC: the catalogue of somatic mutations in cancer , 2011, Genome Biology.

[82]  J. Guan,et al.  Focal adhesion kinase and its signaling pathways in cell migration and angiogenesis. , 2011, Advanced drug delivery reviews.

[83]  T. Corson,et al.  Small-Molecule Hydrophobic Tagging Induced Degradation of HaloTag Fusion Proteins , 2011, Nature chemical biology.

[84]  C. Tse,et al.  Bcl-2 family proteins are essential for platelet survival , 2007, Cell Death and Differentiation.

[85]  S. Ishikawa,et al.  Hypoxia increases the motility of lung adenocarcinoma cell line A549 via activation of the epidermal growth factor receptor pathway , 2007, Cancer science.

[86]  W. Denny,et al.  Reductive chemistry of the novel hypoxia-selective cytotoxin 5-[N,N-bis(2-chloroethyl)amino]-2,4-dinitrobenzamide. , 1995, Journal of medicinal chemistry.

[87]  Xiaojian Zhang,et al.  Development of Hypoxia-activated PROTAC Exerting More Potent Effect in Tumor Hypoxia than in Normoxia , 2021, Chemical Communications.