Lorena Heinst
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View article: Supplementary Table S1 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Table S1 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Table S1. Primary antibodies.
View article: Supplementary Figure S2 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Figure S2 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Figure S2. Dose dependent sensitivity of MLS cells to pharmacologic inhibition of WEE 1 activity and cellular localization.
View article: Supplementary Figure S6 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Figure S6 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Figure S6. CDK 2 expression exacerbates replication stress in MLS.
View article: Supplementary Table S5 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Table S5 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Table S5. Densitometric analysis of western blot results (Figure 3A). WEE1 activity is required for genomic integrity and survival of MLS 402-91 (left) and MLS 1765-92 (right) cells.
View article: Supplementary Table S4 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Table S4 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Table S4. Statistical correlation analysis by means of χ².
View article: Supplementary Table S3 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Table S3 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Table S3. Individual clinicopathological characteristics and semi-quantitative immunohistochemistry results of MLS patients (n=49).
View article: Supplementary Figure S3 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Figure S3 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Figure S3. Supplementary Figure S3. In vivo efficacy of WEE 1 inhibition in MLS CAM xenografts.
View article: Supplementary Table S7 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Table S7 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Table S7. Densitometric analysis of western blot results (Supplementary figure S2). Dose-dependent sensitivity of MLS cells to pharmacologic inhibition of WEE1 activity and cellular localization.
View article: Supplementary Figure S1 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Figure S1 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Figure S1. WEE 1 expression correlates with histological grade of MLS.
View article: Supplementary Figure S4 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Figure S4 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Figure S4. Concurrent expression of WEE 1 signaling pathway and G 1 /S effectors and correlation of P Thr 160 CDK 2 with the histological grade of MLS.
View article: Data from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Data from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Purpose:The pathognomonic FUS::DDIT3 fusion protein drives myxoid liposarcoma (MLS) tumorigenesis via aberrant transcriptional activation of oncogenic signaling. As FUS::DDIT3 has so far not been pharmacologically tractable to selectively …
View article: Supplementary Table S6 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Table S6 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Table S6. MK-1775 IC50 values of liposarcoma cell lines.
View article: Supplementary Table S2 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Table S2 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Table S2. Clinicopathological characteristics of patients with myxoid liposarcoma (n=49).
View article: Supplementary Figure S5 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma
Supplementary Figure S5 from Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma Open
Supplementary Figure S5. Causal relationship between FUS::DDIT3-modulated G1/S cell cycle checkpoint regulation and requirement for WEE1 activity.
View article: Figure S6 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S6 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S6 shows that the mutual activation of YAP1/TAZ and β-catenin in SySa cells is impeded by knockdown of BAF complex subunits.
View article: Figure S4 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S4 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S4 shows that induction of hyperactive YAP1/TAZ or β-catenin variants does not alter the other’s protein levels.
View article: Figure S5 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S5 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S5 shows that there is no interdependency between YAP1/TAZ and β-catenin activation in control cell lines.
View article: Figure S4 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S4 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S4 shows that induction of hyperactive YAP1/TAZ or β-catenin variants does not alter the other’s protein levels.
View article: Figure S1 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S1 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S1 shows that the SS18-SSX fusion protein regulates TEAD- and TCF-mediated transcriptional activity, both being important for SySa cell viability.
View article: Figure S1 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S1 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S1 shows that the SS18-SSX fusion protein regulates TEAD- and TCF-mediated transcriptional activity, both being important for SySa cell viability.
View article: Figure S2 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S2 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S2 shows that inhibition of YAP1, TAZ or β-catenin via siRNA-mediated knockdown or inhibitor treatment reduces each other's transcriptional activity.
View article: Figure S5 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S5 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S5 shows that there is no interdependency between YAP1/TAZ and β-catenin activation in control cell lines.
View article: Figure S3 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S3 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S3 shows a reciprocal regulation of YAP1/TAZ-TEAD and β-catenin-TCF in SySa cells via luciferase assays.
View article: Figure S3 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S3 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S3 shows a reciprocal regulation of YAP1/TAZ-TEAD and β-catenin-TCF in SySa cells via luciferase assays.
View article: Figure S6 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S6 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S6 shows that the mutual activation of YAP1/TAZ and β-catenin in SySa cells is impeded by knockdown of BAF complex subunits.
View article: Figure S2 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Figure S2 from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Figure S2 shows that inhibition of YAP1, TAZ or β-catenin via siRNA-mediated knockdown or inhibitor treatment reduces each other's transcriptional activity.
View article: Data from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Data from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma Open
Synovial sarcoma (SySa), a rare malignant soft tissue tumor, is characterized by a specific chromosomal translocation t(X;18). The resulting chimeric SS18-SSX fusion protein drives SySa pathogenesis by integrating into the BAF complex and …
View article: Exploiting WEE1 kinase activity as FUS::DDIT3-dependent therapeutic vulnerability in myxoid liposarcoma
Exploiting WEE1 kinase activity as FUS::DDIT3-dependent therapeutic vulnerability in myxoid liposarcoma Open
The pathognomonic FUS::DDIT3 fusion protein drives myxoid liposarcoma (MLS) tumorigenesis via aberrant transcriptional activation of oncogenic signaling. Since FUS::DDIT3 has so far not been pharmacologically tractable to selectively targe…
View article: 1253P Analytic validation and implementation of OncoDEEP: A pan-cancer comprehensive genomic profiling NGS assay for assessing homologous recombination deficiency (HRD)
1253P Analytic validation and implementation of OncoDEEP: A pan-cancer comprehensive genomic profiling NGS assay for assessing homologous recombination deficiency (HRD) Open
View article: Figure S5 from Interdependence of SS18-SSX–driven YAP1 and β-Catenin Activation in Synovial Sarcoma
Figure S5 from Interdependence of SS18-SSX–driven YAP1 and β-Catenin Activation in Synovial Sarcoma Open
Figure S5 shows that there is no interdependency between YAP1/TAZ and β-catenin activation in control cell lines.