Journal: Cancer prevention research (Philadelphia, Pa.)

Article Title: Notch1 mutations are drivers of oral tumorigenesis

doi: 10.1158/1940-6207.CAPR-14-0257

Figure Lengend Snippet: A. Schematic depiction of mutations in NOTCH1 identified in 22 tumor-normal pairs. Indel mutation is not included. EGF: epidermal growth factor; HD: heterodimerization domain; LNR: Lin12-Notch repeats; TM: transmembrane domain; RAM: recombination signal-binding protein - Jkappa-associated module; ANK: ankyrin repeats domain; TAD: transactivation domain; PEST: region rich in proline (P), glutamine (E), serine (S) and threonine (T) residues. B. Summary of nonsynonymous mutations found in this group. C. Shows a ratio of tumors with mutated NOTCH1. D. Distribution of nonsynonymous mutations among NOTCH1 functional domains. E. Schematic depiction of NOTCH1 mutations identified in 28 tumors without matched normal control. F. Summary of nonsynonymous mutations found in this group. G. Shows a ratio of tumors with mutated NOTCH1 identified in unmatched OSCCs. H. Distribution of NOTCH1 mutations (showed in E) across functional domains. I. Schematic depiction of all NOTCH1 nonsynonymous mutations found in 50 Chinese OCSS patients (A and E combined). Black bars show regions where most gain-of-function mutations were reported in hematologic malignancies. J. Summary of nonsynonymous mutations found in 50 OSCC tumors. K. Percentage of tumors with mutated NOTCH1 among 50 Chinese patients. L. Overall mutations distribution across NOTCH1 functional domains. M. Table of most frequently mutated exons. N. List of NOTCH1 mutations found in this study that have been previously observed in solid tumors and hematopoietic malignancies.

Article Snippet: Notch1 amplification 108 primers pairs were designed by Fluidigm (San Francisco, USA) to cover all 34 exons of the NOTCH1 and exon–intron boundaries ( Supp.

Techniques: Mutagenesis, Binding Assay, Functional Assay, Control

Journal: Cancer prevention research (Philadelphia, Pa.)

Article Title: Notch1 mutations are drivers of oral tumorigenesis

doi: 10.1158/1940-6207.CAPR-14-0257

Figure Lengend Snippet: A. Schematic depiction of mutations in NOTCH1 identified in 45 leukoplakia samples. B. Summary of nonsynonymous mutations found in this cohort. C. Percentage of tumors with mutated NOTCH1. D. Summary of nonsynonymous mutations distribution across NOTCH1 functional domains. E. List of NOTCH1 mutations found in leukoplakia patients that have been previously observed in solid tumors and hematopoietic malignancies. F. Table demonstrates higher prevalence of NOTCH1 mutations in patients that were diagnosed with moderate or severe dysplasia. G. Schematic depiction of nonsynonymous mutations found in 50 Chinese OSCC tumors (top) and leukoplakia patients (bottom). Blue triangles show overlapping mutations that were found in both cohorts. Dashed bracket indicates mutations in ‘ligand binding’ domain and its boundaries. Black bars show regions where most gain-of-function mutations were reported in hematologic malignancies. H. List of mutations overlapping between OSCC and leukoplakia. I. Table shows higher prevalence of overlapping mutations in patients diagnosed with moderate or severe leukoplakia. J. Table shows mutations distribution per exon in OSCC and leukoplakia. Cells highlighted with cyan indicate most frequently mutated exons in OSCC, leukoplakia or combined.

Article Snippet: Notch1 amplification 108 primers pairs were designed by Fluidigm (San Francisco, USA) to cover all 34 exons of the NOTCH1 and exon–intron boundaries ( Supp.

Techniques: Functional Assay, Ligand Binding Assay

Journal: Cancer prevention research (Philadelphia, Pa.)

Article Title: Notch1 mutations are drivers of oral tumorigenesis

doi: 10.1158/1940-6207.CAPR-14-0257

Figure Lengend Snippet: A. Schematic depiction of all NOTCH1 mutations identified in Chinese OSCC tumors to date (Top-triangles) and all mutations identified in Caucasian patients with HNSCC (Bottom-diamonds). B. Summary of nonsynonymous mutations within the codding region found in both ethnicities. C. Number and percentage of tumors with mutated NOTCH1 in Chinese and Caucasian patients. D. Table displays differences in mutations distribution across functional domains of NOTCH1 in Chinese and Caucasians samples. E. Mutations distribution per exon in Chinese and Caucasian patients. Cells highlighted in cyan indicate most frequently mutated exons in Chinese (lighter) and Caucasian (darker) tumors. F. Mutations clusterization in distinct functional modules of NOTCH1 in Chinese (red bars, top) and Caucasian (purple bars, bottom) tumors. G. List of mutations that were found in Caucasian tumors by two or more independent studies (left). Mutations in the same codon that were seen in Chinese and Caucasians patients (right).

Article Snippet: Notch1 amplification 108 primers pairs were designed by Fluidigm (San Francisco, USA) to cover all 34 exons of the NOTCH1 and exon–intron boundaries ( Supp.

Techniques: Functional Assay

Journal: bioRxiv

Article Title: Finding the right tool: a comprehensive evaluation of microglial inducible cre mouse models

doi: 10.1101/2023.04.17.536878

Figure Lengend Snippet:

Article Snippet: Primers: PGK1 (Probe #108) , Integrated DNA Technologies , F: TAC CTG CTG GCT GGA TGG R: CAC AGC CTC GGC ATA TTT CT.

Techniques: Recombinant, RNA Sequencing Assay, Isolation, Software, Microscopy