No single ALK mutations confer high-level resistance to lorlatinib.

Slides:



Advertisements
Similar presentations
Gleevec vs. BMS Druker vs. Sawyers
Advertisements

Chronic myelogenous leukemia Uncommon disease Highly lethal when ineffectively Rxd Most pts are in their 50s+60s The molecular understanding of this disease.
Clinicopathologic Features of EML4-ALK Mutant Lung Cancer Shaw AT et al. ASCO 2009; Abstract (Poster)
Resensitization to Crizotinib by the Lorlatinib ALK Resistance Mutation L1198F R1. 임빈 / prof. 김시영
Defining Epidermal Growth Factor Receptor exon 20 mutant sensitivity to tyrosine kinase inhibition Danny Rayes.
Phase I/II Study of Lorlatinib in Advanced ALK+ or ROS1+ NSCLC
Enhanced DNA damage in IDH1 mutant glioma cells.
Unità Clinica di Diagnostica Istopatologica e Molecolare
Clonal evolution of resistance to sequential ALK inhibitor therapy.
Summary of genetic alterations in resistant biopsies among patients progressing on ceritinib or alectinib. Summary of genetic alterations in resistant.
Carlos L. Arteaga, Jeffrey A. Engelman  Cancer Cell 
Recent Advances in Targeting ROS1 in Lung Cancer
Distribution of phosphorylation sites identified in the cytosolic phosphoproteome.A, numbers of approved phosphopeptides, previously phosphorylated peptides,
Fig. 4. Functional annotation of VUS in EGFR.
Fig. 2. Mutant KRAS mediates resistance to PARPi and sensitivity to PARPi and MEKi Mutant KRAS mediates resistance to PARPi and sensitivity to PARPi and.
RAS/RAF pathway-activated ovarian cancer cells exhibit MEK dependence and synergistic induction of apoptosis with combined MEK/AKT inhibition. RAS/RAF.
AKT dependence of ovarian cancer cell lines.
Volume 28, Issue 1, Pages (July 2015)
ASSIGNMENT 10 Use the UP and DOWN tags as provided and query the LINCS. These are the KRAS-DEP (UP) and KRAS-IND (DOWN) gene signatures from Singh et al.
Volume 2, Issue 2, Pages (August 2002)
Multiple Acquired Resistance Mutations of the ALK Tyrosine Kinase Domain after Sequential Use of ALK Inhibitors  Hsin-Yi Wang, MD  Journal of Thoracic.
Volume 1, Issue 5, Pages (June 2002)
The EGF receptor confers BRAF inhibitor resistance in BRAF-mutant melanoma cells. The EGF receptor confers BRAF inhibitor resistance in BRAF-mutant melanoma.
MAPKKK5-induced cell death is independent of Ser-289 phosphorylation.
Recent Advances in Targeting ROS1 in Lung Cancer
Volume 27, Issue 3, Pages (March 2015)
Quantification of drug cross-resistance between mutants selected for I-BET151 resistance and F0002 resistance. Quantification of drug cross-resistance.
Heterogeneity of Genetic Changes Associated with Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancer  Soyeon Kim, PhD, Tae Min Kim, MD, PhD,
Volume 14, Issue 4, Pages (February 2016)
Daniel B. Costa, MD, PhD, Susumu Kobayashi, MD, PhD 
Oncogenic ALK signaling.
Mohammad Azam, Robert R. Latek, George Q. Daley  Cell 
Volume 14, Issue 2, Pages (August 2008)
A and B, CO-1686–resistant NCI-H1975 cell clones, COR1-1 and COR10-1 display a reduced dependence on EGFR signaling for survival. A and B, CO-1686–resistant.
Disruption of the svkA gene encoding severin kinase.
Schematic design of the SSM
Mutant BRAF Melanomas—Dependence and Resistance
ALK resistance mutations predict for sensitivity to lorlatinib in patient-derived cell line models of acquired resistance to ceritinib. ALK resistance.
VP16-E2 is a more potent transcriptional activator than Gal4-VP16.
Identification of NSC as a FADD-kinase inhibitor.
The SFKs confer BRAF inhibitor resistance in BRAF-mutant melanoma cells. The SFKs confer BRAF inhibitor resistance in BRAF-mutant melanoma cells. A, phospho-protein.
Protein expression profile in a dasatinib-resistant cell line.
Colony-forming capacity of CD34+ cells with and without CLL-1 expression. Colony-forming capacity of CD34+ cells with and without CLL-1 expression. CD34+
The Pathway to Progress Against Chronic Myelogenous Leukemia.
Pancreatic cancer cell lines are sensitive to knockdown of outlier kinases. Pancreatic cancer cell lines are sensitive to knockdown of outlier kinases.
Saturation analysis and the discovery of actionability of mutational hotspots. Saturation analysis and the discovery of actionability of mutational hotspots.
ADNs are largely distinct from CDNs
Location of common clinically relevant mutations in EGFR
Incorporation of the TSTA system into a single plasmid.
Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. LNCaP,
KRAS mutation leads to resistance to combined RAF/EGFR and RAF/MEK inhibition. KRAS mutation leads to resistance to combined RAF/EGFR and RAF/MEK inhibition.
History of ALK in oncology.
High-throughput drug screen (HTDS) reveals ARS1620 and PI3K pathway inhibitors synergies and a heterogeneous pattern of RTK synergies. High-throughput.
The Ser124 site of Cdc25A is required for Cdc25A degradation in response to I3C induction. The Ser124 site of Cdc25A is required for Cdc25A degradation.
MEK1F53L mutation drives clinical acquired resistance to combined RAF/MEK inhibition. MEK1F53L mutation drives clinical acquired resistance to combined.
Combined inhibition of coamplified RTKs is required for response.
Although equivalent experimental systems have been employed in a variety of assessments to determine BCR-ABL1 kinase domain mutation sensitivity on the.
Establishment of HeLa/rtTAA/TRE-N1-IC cell line.
Validation of MYC-driven drug responses.
Blocking αvβ3/galectin-3 binding with GCS-100 selectively kills KRAS-addicted lung cancer cells. Blocking αvβ3/galectin-3 binding with GCS-100 selectively.
Crizotinib-resistant NPM-ALK mutants retain sensitivity to ganetespib.
A, Schematic diagram of identified splice variants of PD-L1.
Detection of protein levels of Cdc25AWT and its mutation derivatives in breast cancer cells with I3C treatment. Detection of protein levels of Cdc25AWT.
An isogenic cell line screen reveals genomic drivers of drug response.
Investigation of reactivity of D14 HLA-A
THZ1 in combination with targeted therapy enhances cell death and hinders the establishment of drug-resistant colonies in diverse oncogene-addicted cellular.
Ceritinib is a potent ALK inhibitor in crizotinib-naïve models.
Response and resistance to savolitinib and osimertinib in a patient with EGFR-mutant NSCLC harboring MET amplification. Response and resistance to savolitinib.
TRK inhibitor binding to acquired resistance mutations.
Genotype-specific combinatorial drug sensitivities in melanoma.
Presentation transcript:

No single ALK mutations confer high-level resistance to lorlatinib. No single ALK mutations confer high-level resistance to lorlatinib. A, For reference are shown previously reported IC50 values of first-, second-, and third-generation ALK inhibitors on cellular ALK phosphorylation in Ba/F3 cells expressing nonmutant or mutant EML4–ALK (adapted from ref. 12). B, Scheme of ENU mutagenesis screen using Ba/F3 cells. C, Summary of the type and number of ALK kinase domain mutations identified in the mutagenesis screen using Ba/F3 cells harboring nonmutant EML4–ALK (either variant 1 or variant 3). Numerous crizotinib-resistant clones were identified, as shown at right. In contrast, no lorlatinib-resistant clones were identified at comparable and clinically achievable drug concentrations, as shown at left. Shown are combined data from two independent experiments. Satoshi Yoda et al. Cancer Discov 2018;8:714-729 ©2018 by American Association for Cancer Research