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201520212024

论文（91）

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1Supplementary Table 13 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Federica Pecci,Seshiru Nakazawa,Biagio Ricciuti,Guilherme Harada,Jessica K. Lee,Joao V. Alessi,Adriana Barrichello,Victor R. Vaz,Giuseppe Lamberti,Alessandro Di Federico,Malini M. Gandhi, Dimitris Gazgalis,

Concurrent driver mutations according to oncogenic / likely oncogenic MET TKD mutations detected in cohort #2.

2026

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2Supplementary Figure 10 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

MET TKD mutations in NSCLC cohort of Caris Life Sciences. (A) Flowchart of the NSCLC subgroup in the Caris Life Sciences dataset. (B) Prevalence of MET TKD mutations in NSCLC cases in the Caris Life Sciences dataset (MET TKD mutations in 280 unique patients). (C) Lollipop plot of the oncogenic / likely oncogenic MET TKD mutations detected in NSCLC cases in the Caris Life Sciences dataset (35 oncogenic / likely oncogenic MET TKD mutations in 35 unique patients). (D) concurrent driver alterations (information available for 24 cases, unavailable for 11 cases) and (E) concurrent MET amplification status (information available for 33 cases, unavailable for 2 cases) of NSCLC cases harboring oncogenic / likely oncogenic MET TKD mutations in the Caris Life Sciences dataset.

2026

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3Supplementary Figure 20 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Equilibration of interactions that drives ATP affinity in the presence MET R1170Q mutant. (A) Representative structure of ATP bound MET R1170Q with the regions of interest highlighted [hinge site (green), and mutation site (blue)]. (B) Mutation at position 1170 facilitates the formation of a hydrogen bonding network. (C) Interatomic distances for non solvent mediated hydrogen bonding.

2026

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4Supplementary Table 24 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Single trajectory generalized Born and surface area solvation (MM/GBSA) calculated free energy of ATP binding into the orthosteric pocket.

2026

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5Supplementary Table 4 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

List of missense mutations with unknown biologic function and their pathogenicity scores using all three in silico tools in cohort #1

2026

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6Supplementary Table 14 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Concurrent genomic drivers in cases with oncogenic / likely oncogenic MET tyrosine kinase domain (TKD) mutations and co-occurring MET gene amplification in cohort #2.

2026

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7Supplementary Table 20 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Clinicopathologic and genomic characteristics of 171 cases of cancers other than NSCLC harboring oncogenic / likely oncogenic MET TKD mutations in cohort #2.

2026

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8Supplementary Methods from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Additional information regarding the methods used in this study

2026

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9Supplementary Table 11 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Detailed genomic characteristics for each case of NSCLC with oncogenic / likely oncogenic MET tyrosine kinase domain (TKD) mutations in cohort #1.

2026

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10Supplementary Table 17 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Comparison of clinicopathologic characteristics between NSCLCs with oncogenic / likely oncogenic MET tyrosine kinase domain (TKD) mutations without other concurrent drivers and NSCLCs with MET exon 14 alterations in the Caris Life Sciences cohort.

2026

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11Supplementary Table 18 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Detailed clinicopathologic and genomic characteristics of the 61 cases with a malignancy other than NSCLC harboring an oncogenic / likely oncogenic MET TKD mutation in cohort #1.

2026

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12Supplementary Figure 12 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Sensitivity pattern of MET TKD mutations in 293T cells. (A) ERK-mediated transcriptional activation assessed by luciferase assay in 293T cells co-transfected with MET WT or TKD mutant constructs, an ERK activation reporter vector (pGL4.33), and a control co-reporter vector (pRL-TK). The lower panel shows western blot analysis of transfected samples. (B) Western blot analysis of MET and ERK1/2 phosphorylation in response to 1 μM crizotinib. MET TKD mutants showing sensitivity and resistance to crizotinib are colored in green and orange, respectively.

2026

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13Supplementary Table 2 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Frequency of MET tyrosine kinase domain (TKD) mutations in cohort #1 according to amino acid residue, out of a total of 711 MET TKD mutations.

2026

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14Supplementary Figure 4 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Type and frequency of MET TKD mutations across cancer types in cohort #1. (A) Frequency of MET TKD mutations in various cancer types in cohort #1 according to OncoKB status; the numbers above each bar indicate the number of cases with MET TKD mutations (regardless OncoKB annotations) out of the total of cases of each cancer type. (B) Detailed oncogenic / likely oncogenic MET TKD mutations according to cancer type in cohort #1.

2026

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15Supplementary Table 8 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Prevalence of MET tyrosine kinase domain (TKD) mutations across cancer types in cohort #2.

2026

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16Supplementary Table 26 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Mutagenic primers used for mutagenesis.

2026

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17Supplementary Figure 15 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

In vitro analysis of MET H1094Y and F1200I mutations in PC9 cells. (A) Establishment of NSCLC cancer cell lines expressing MET TKD mutations. PC9 cells were transduced with wild-type (WT) MET (as control) and MET H1094Y and F1200I. (B) Growth inhibition assay of PC9 cells in response to EGFR inhibition with osimertinib. (C) Cell proliferation and relative apoptosis were monitored under EGFR inhibition with osimertinib (300 nM). (D) Phosphorylation of MET, EGFR, AKT, and ERK was analyzed in PC9 cells expressing MET TKD mutants. PC9 cells were treated with osimertinib (1 μM) with or without capmatinib (1 μM) for 48 hrs. (E) IC50 values of PC9 cells (upper table) and Ba/F3 cells (lower table) expressing MET TKD mutants in response to MET TKIs. PC9 cells were treated with gradient dose of MET TKI combined with a fixed dose of osimertinib (100 nM) for 72 hrs.

2026

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18Supplementary Table 9 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Prevalence of MET tyrosine kinase domain (TKD) mutations across tumor in “other cancers” from Supplementary Table 8.

2026

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19Supplementary Table 23 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Oncogenic / likely oncogenic MET TKD mutations in RCC compared to those detected in NSCLC in cohort #2.

2026

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20Supplementary Figure 6 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

MET TKD mutations in NSCLC in cohort #1 and #2. (A) Flowchart of the NSCLC subgroup in cohort #1 (123 MET TKD mutations in 120 unique patients); (B) Prevalence of MET TKD mutations in NSCLC cases according to each dataset in cohort #1; (C) Lollipop plot of the oncogenic / likely oncogenic MET TKD mutations detected in NSCLC cases of cohort #1 (47 oncogenic / likely oncogenic MET TKD mutations in 44 unique patients); (D) Flowchart of the NSCLC subgroup in cohort #2 (590 MET TKD mutations in 586 unique patients); (E) Prevalence of MET TKD mutations in NSCLC cases according to cohort #2 (590 MET TKD mutations in 586 unique patients); (F) Lollipop plot of the oncogenic / likely oncogenic MET TKD mutations detected in NSCLC cases of cohort #2 (129 oncogenic / likely oncogenic MET TKD mutations in 129 unique patients).

2026

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