Preloader

Identifying transcriptional programs underlying cancer drug response with TraCe-seq

  • 1.

    Chapman, P. B. et al. Improved survival with vemurafenib in melanoma with BRAF V600E mutation. N. Engl. J. Med. 364, 2507–2516 (2011).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 2.

    Lito, P., Rosen, N. & Solit, D. B. Tumor adaptation and resistance to RAF inhibitors. Nat. Med. 19, 1401–1409 (2013).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 3.

    Choi, Y. L. et al. EML4–ALK mutations in lung cancer that confer resistance to ALK inhibitors. N. Engl. J. Med. 363, 1734–1739 (2010).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 4.

    Gorre, M. E. et al. Clinical resistance to STI-571 cancer therapy caused by BCR–ABL gene mutation or amplification. Science 293, 876–880 (2001).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 5.

    Kobayashi, S. et al. EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. N. Engl. J. Med. 352, 786–792 (2005).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 6.

    Pao, W. et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med 2, e73 (2005).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar 

  • 7.

    Yauch, R. L. et al. Epithelial versus mesenchymal phenotype determines in vitro sensitivity and predicts clinical activity of erlotinib in lung cancer patients. Clin. Cancer Res. 11, 8686–8698 (2005).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 8.

    Davies, A. H., Beltran, H. & Zoubeidi, A. Cellular plasticity and the neuroendocrine phenotype in prostate cancer. Nat. Rev. Urol. 15, 271–286 (2018).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 9.

    Kitai, H. et al. Epithelial-to-mesenchymal transition defines feedback activation of receptor tyrosine kinase signaling induced by MEK inhibition in KRAS-mutant lung cancer. Cancer Discov. 6, 754–769 (2016).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 10.

    Uramoto, H. et al. Epithelial-mesenchymal transition in EGFR-TKI acquired resistant lung adenocarcinoma. Anticancer Res. 30, 2513–2517 (2010).

    CAS 
    PubMed 

    Google Scholar 

  • 11.

    Burslem, G. M. & Crews, C. M. Proteolysis-targeting chimeras as therapeutics and tools for biological discovery. Cell 181, 102–114 (2020).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 12.

    Verma, R., Mohl, D. & Deshaies, R. J. Harnessing the power of proteolysis for targeted protein inactivation. Mol. Cell 77, 446–460 (2020).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 13.

    Olson, C. M. et al. Pharmacological perturbation of CDK9 using selective CDK9 inhibition or degradation. Nat. Chem. Biol. 14, 163–170 (2018).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 14.

    You, I. et al. Discovery of an AKT degrader with prolonged inhibition of downstream signaling. Cell Chem. Biol. 27, 66–73 (2020).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 15.

    Dixit, A. et al. Perturb-seq: dissecting molecular circuits with scalable single-cell RNA profiling of pooled genetic screens. Cell 167, 1853–1866 (2016).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 16.

    Weinreb, C., Rodriguez-Fraticelli, A., Camargo, F. D. & Klein, A. M. Lineage tracing on transcriptional landscapes links state to fate during differentiation. Science 367, eaaw3381 (2020).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 17.

    Lynch, T. J. et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N. Engl. J. Med. 350, 2129–2139 (2004).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 18.

    Paez, J. G. et al. EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science 304, 1497–1500 (2004).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 19.

    Sankar, K., Gadgeel, S. M. & Qin, A. Molecular therapeutic targets in non-small cell lung cancer. Expert Rev. Anticancer Ther. 20, 647–661 (2020).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 20.

    Soria, J. C. et al. Osimertinib in untreated EGFR-mutated advanced non-small-cell lung cancer. N. Engl. J. Med. 378, 113–125 (2018).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 21.

    Leonetti, A. et al. Resistance mechanisms to osimertinib in EGFR-mutated non-small cell lung cancer. Br. J. Cancer 121, 725–737 (2019).

    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 22.

    Buckley, D. et al. Targeting the von Hippel–Lindau E3 ubiquitin ligase using small molecules to disrupt the VHL/HIF-1α interaction. J. Am. Chem. Soc. 134, 4465–4468 (2012).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 23.

    Bondeson, D. P. et al. Catalytic in vivo protein knockdown by small-molecule PROTACs. Nat. Chem. Biol. 11, 611–617 (2015).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 24.

    Shah, K. N. et al. Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer. Nat. Med. 25, 111–118 (2019).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 25.

    Sharma, S. V. et al. A chromatin-mediated reversible drug-tolerant state in cancer cell subpopulations. Cell 141, 69–80 (2010).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 26.

    Byers, L. A. et al. An epithelial–mesenchymal transition gene signature predicts resistance to EGFR and PI3K inhibitors and identifies Axl as a therapeutic target for overcoming EGFR inhibitor resistance. Clin. Cancer Res. 19, 279–290 (2013).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 27.

    Okura, N. et al. ONO-7475, a novel AXL inhibitor, suppresses the adaptive resistance to initial EGFR-TKI treatment in EGFR-mutated non-small cell lung cancer. Clin. Cancer Res. 26, 2244–2256 (2020).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 28.

    Taniguchi, H. et al. AXL confers intrinsic resistance to osimertinib and advances the emergence of tolerant cells. Nat. Commun. 10, 259 (2019).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar 

  • 29.

    Zhang, Z. et al. Activation of the AXL kinase causes resistance to EGFR-targeted therapy in lung cancer. Nat. Genet. 44, 852–860 (2012).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 30.

    Hata, A. N. et al. Tumor cells can follow distinct evolutionary paths to become resistant to epidermal growth factor receptor inhibition. Nat. Med. 22, 262–269 (2016).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 31.

    Wagle, M. C. et al. A transcriptional MAPK pathway activity score (MPAS) is a clinically relevant biomarker in multiple cancer types. NPJ Precis. Oncol. 2, 7 (2018).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar 

  • 32.

    Jia, Y. et al. Overcoming EGFR(T790M) and EGFR(C797S) resistance with mutant-selective allosteric inhibitors. Nature 534, 129–132 (2016).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 33.

    To, C. et al. Single and dual targeting of mutant EGFR with an allosteric inhibitor. Cancer Discov. 9, 926–943 (2019).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 34.

    Hetz, C., Zhang, K. & Kaufman, R. J. Mechanisms, regulation and functions of the unfolded protein response. Nat. Rev. Mol. Cell Biol. 21, 421–438 (2020).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 35.

    Marciniak, S. J. et al. CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum. Genes Dev. 18, 3066–3077 (2004).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 36.

    Walter, P. & Ron, D. The unfolded protein response: from stress pathway to homeostatic regulation. Science 334, 1081–1086 (2011).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 37.

    Timosenko, E. et al. Nutritional stress induced by tryptophan-degrading enzymes results in ATF4-dependent reprogramming of the amino acid transporter profile in tumor cells. Cancer Res. 76, 6193–6204 (2016).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 38.

    Rabouw, H. H. et al. Small molecule ISRIB suppresses the integrated stress response within a defined window of activation. Proc. Natl Acad. Sci. USA 116, 2097–2102 (2019).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 39.

    Stockwell, S. et al. Mechanism-based screen for G1/S checkpoint activators identifies a selective activator of EIF2AK3/PERK signaling. PLoS ONE 7, e28568 (2012).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 40.

    Bruch, J. et al. PERK activation mitigates tau pathology in vitro and in vivo. EMBO Mol. Med. 9, 371–384 (2017).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 41.

    Yu, M. et al. A resource for cell line authentication, annotation and quality control. Nature 520, 307–311 (2015).

    CAS 
    PubMed 
    Article 

    Google Scholar 

  • 42.

    Galdeano, C. et al. Structure-guided design and optimization of small molecules targeting the protein–protein interaction between the von Hippel–Lindau (VHL) E3 ubiquitin ligase and the hypoxia inducible factor (HIF) ɑ subunit with in vitro nanomolar affinities. J. Med. Chem. 57, 8657–8663 (2014).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 43.

    Blaquiere, N. et al. Preparation of (4-hydroxypyrrolodin-2-yl)-hydroxamate compounds and methods of use thereof as modulators of targeted ubiquitination. WO2019084026 (2019).

  • 44.

    Schnur, R. C. et al. Preparation of N-phenylquinazoline-4-amines as neoplasm inhibitors. WO9630347 (1996).

  • 45.

    Blaquiere, N. et al. Hetero-bifunctional degrader compounds and their use as modulators of targeted ubiquination (VHL). WO2019183523 (2019).

  • 46.

    Yu, G., Wang, L. G., Han, Y. & He, Q. Y. clusterProfiler: an R package for comparing biological themes among gene clusters. OMICS 16, 284–287 (2012).

    CAS 
    PubMed 
    PubMed Central 
    Article 

    Google Scholar 

  • 47.

    Street, K. et al. Slingshot: cell lineage and pseudotime inference for single-cell transcriptomics. BMC Genomics 19, 477 (2018).

    PubMed 
    PubMed Central 
    Article 
    CAS 

    Google Scholar 

  • Source link