Thomas Stricker
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View article: A rising tide lifts all boats in the personalized cancer care continuum for mNSCLC: bridging inequities in NGS fosters equity in targeted treatment
A rising tide lifts all boats in the personalized cancer care continuum for mNSCLC: bridging inequities in NGS fosters equity in targeted treatment Open
Background Next-generation sequencing (NGS) testing in patients with metastatic non-small cell lung cancer (mNSCLC) identifies actionable driver oncogenes (ADO) and targeted treatment (TT). Potential inequities were evaluated in NGS testin…
View article: Supplementary Table 1 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 1 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 1. Sequencing statistics and quality control metrics.
View article: Supplementary Table 3 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 3 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 3. Number of somatic non-synonymous variants detected in each specimen in exome sequencing data.
View article: Data from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Data from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Purpose:Desmoid tumors are bland fibroblastic tumors that do not metastasize but have a high rate of local recurrence. Previously published studies proposed two different transcriptomic signatures to predict relapse. Molecular heterogeneit…
View article: Supplementary Table 8 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 8 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 8. Antibodies used for immunohistochemistry.
View article: Supplementary Table 15 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 15 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 15. Expression of MLH1, MSH2, MSH6 and PMS2 proteins evaluated by immunohistochemistry in duplicate cores of primary and recurrent tumor specimens obtained from 2 patients.
View article: Supplementary Table 2 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 2 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 2. DNA copy number alterations detected in primary and recurrent tumor specimens of 3 patients.
View article: Supplementary Table 12 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 12 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 12. Validation of clonal and subclonal variants detected in exome sequencing data of Patients 1 and 2 using RNA-seq data.
View article: Supplementary Table 9 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 9 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 9. Differentially expressed genes between primary desmoid tumors from patients who did and did not develop local recurrence after surgery.
View article: Supplementary Table 4 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 4 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 4. RNA-seq paired reads mapped to protein coding genes in 31 specimens from 20 primary desmoid tumors.
View article: Supplementary Table 13 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 13 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 13. Variant allele fraction of clonal and subclonal point mutations supported by RNA-seq reads in Patient 1 (in genomic positions supported by >10 reads coverage and present in both forward and reverse reads).
View article: Supplementary Table 14 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 14 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 14. Variant allele fraction of clonal and subclonal point mutations supported by RNA-seq reads in Patient 2 (in genomic positions supported by >10 reads coverage and present in both forward and reverse reads).
View article: Supplementary Table 11 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 11 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 11. Expression of EFL1, HDAC6, TFG, and hnRNPC proteins evaluated by immunohistochemistry in duplicate cores of primary tumor specimens obtained from 14 patients.
View article: Supplementary Table 10 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 10 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 10. Summary of selected clinicopathological features of patient cohorts in the present study (De Bellis et al.) and in the previous studies published by Salas et al. and Kohsaka et al.
View article: Supplementary Table 5 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 5 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 5. Normalized gene expression values of the 10% most variable genes in tumor specimens from Patient 1.
View article: Supplementary Figure 2 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Figure 2 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Figure 2. Validation of the S45F mutation in the CTNNB1 gene in recurrent tumor specimen STT8702 of Patient 3.
View article: Supplementary Figure 1 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Figure 1 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Figure 1. Validation of variable expression of selected candidate prognostic markers at the protein level.
View article: Supplementary Table 7 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 7 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 7. Normalized gene expression values of the 10% most variable genes in tumor specimens from Patient 3.
View article: Supplementary Table 6 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Supplementary Table 6 from Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Supplementary Table 6. Normalized gene expression values of the 10% most variable genes in tumor specimens from Patient 2.
View article: Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors
Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors Open
Purpose: Desmoid tumors are bland fibroblastic tumors that do not metastasize but have a high rate of local recurrence. Previously published studies proposed two different transcriptomic signatures to predict relapse. Molecular heterogenei…
View article: Clinical Value of Timely Targeted Therapy for Patients With Advanced Non–Small Cell Lung Cancer With Actionable Driver Oncogenes
Clinical Value of Timely Targeted Therapy for Patients With Advanced Non–Small Cell Lung Cancer With Actionable Driver Oncogenes Open
Background A recent real-world study observed that 24% of patients with advanced non–small cell lung cancer (aNSCLC) with actionable driver oncogenes (ADOs) initiated nontargeted therapies before biomarker test results became available. Th…
View article: Identifying the effectiveness of 3D culture systems to recapitulate breast tumor tissue in situ
Identifying the effectiveness of 3D culture systems to recapitulate breast tumor tissue in situ Open
View article: Molecular signature incorporating the immune microenvironment enhances thyroid cancer outcome prediction
Molecular signature incorporating the immune microenvironment enhances thyroid cancer outcome prediction Open
View article: Correction to: The World Health Organization COVID-19 surveillance database
Correction to: The World Health Organization COVID-19 surveillance database Open
View article: Table S3 from AACR Project GENIE: Powering Precision Medicine through an International Consortium
Table S3 from AACR Project GENIE: Powering Precision Medicine through an International Consortium Open
Table S3
View article: Supplemental Methods, Supplemental Tables 1-2, Supplemental Figures 1-4 from AACR Project GENIE: Powering Precision Medicine through an International Consortium
Supplemental Methods, Supplemental Tables 1-2, Supplemental Figures 1-4 from AACR Project GENIE: Powering Precision Medicine through an International Consortium Open
Supplemental Methods. Supplemental Table 1: ââ,¬â€¹Genomic Data Characterization by Center. Supplemental Table 2: ââ,¬â€¹Gene Panels Submitted by Each Center. Figure S1: Number of putative germline SNPs per sample, before and after unifo…
View article: Table S4 from AACR Project GENIE: Powering Precision Medicine through an International Consortium
Table S4 from AACR Project GENIE: Powering Precision Medicine through an International Consortium Open
Table S4
View article: Data from AACR Project GENIE: Powering Precision Medicine through an International Consortium
Data from AACR Project GENIE: Powering Precision Medicine through an International Consortium Open
The AACR Project GENIE is an international data-sharing consortium focused on generating an evidence base for precision cancer medicine by integrating clinical-grade cancer genomic data with clinical outcome data for tens of thousands of c…
View article: Data from Key Survival Factor, Mcl-1, Correlates with Sensitivity to Combined Bcl-2/Bcl-xL Blockade
Data from Key Survival Factor, Mcl-1, Correlates with Sensitivity to Combined Bcl-2/Bcl-xL Blockade Open
An estimated 40,000 deaths will be attributed to breast cancer in 2016, underscoring the need for improved therapies. Evading cell death is a major hallmark of cancer, driving tumor progression and therapeutic resistance. To evade apoptosi…
View article: Supplementary Figures S3 and S4 from Key Survival Factor, Mcl-1, Correlates with Sensitivity to Combined Bcl-2/Bcl-xL Blockade
Supplementary Figures S3 and S4 from Key Survival Factor, Mcl-1, Correlates with Sensitivity to Combined Bcl-2/Bcl-xL Blockade Open
S3. Representative images of cells grown in 3D Matrigel for 14D and treated with ABT-263 (1.0 uM). S4. Whole cell lysates from cells treated with ABT-263 (1.0uM) for 0=24 hours.