Bastiaan Spanjaard
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View article: Lineage origin and microenvironment shape neuroblastoma transcriptional state and plasticity
Lineage origin and microenvironment shape neuroblastoma transcriptional state and plasticity Open
Neuroblastoma, a neural-crest-derived malignancy of the peripheral nervous system, is a devastating pediatric disease, characterized by high intra- and intertumoral heterogeneity. While expression of several tumor expression modules correl…
View article: Figure S2 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Figure S2 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Figure S2 shows simulation results of clonogenic assays under copy number-dependent and -independent cell fitness
View article: Table S1 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Table S1 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Table S1 contains FISH proteomics datasets
View article: Figure S1 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Figure S1 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Figure S1 characterises the MYCN amplification status, copy number heterogeneity and growth behaviour in neuroblastoma samples
View article: Figure S6 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Figure S6 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Figure S6 shows copy number dynamics in EGFR-amplified glioblastoma samples
View article: Table S2 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Table S2 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Table S2 lists the GDCS compounds used in Supplementary Figure S4L
View article: Figure S4 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Figure S4 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Figure S4 provides computational and experimental models of ecDNA-dependent treatment responses in neuroblastoma
View article: Figure S7 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Figure S7 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Figure S7 demonstrates the impact of MYCN dosage on treatment response in neuroblastoma
View article: Figure S3 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Figure S3 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Figure S3 demonstrates how MYC(N) dosage differences drive phenotypic heterogeneity in ecDNA-containing cancers
View article: Data from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Data from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Extrachromosomal DNA (ecDNA) amplification enhances intercellular oncogene dosage variability and accelerates tumor evolution by violating foundational principles of genetic inheritance through its asymmetric mitotic segregation. Spotlight…
View article: Table S4 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Table S4 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Table S4 contains information about the MYCN status of neuroblastoma patient samples used in Figure 1 and Supplementary Figure 1
View article: Figure S5 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Figure S5 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Figure S5 shows copy number dynamics in ecDNA vs. HSR neuroblastoma cells in response to cytotoxic and targeted therapies
View article: Figure S8 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Figure S8 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Figure S8 illustrates how one-two punch, senolytic therapies can be used to target tumor cells with low MYCN copy numbers
View article: Table S3 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers
Table S3 from Extrachromosomal DNA–Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in <i>MYCN</i>-Amplified Cancers Open
Supplementary Table S3 contains information about the MYCN and TP53 status of cell lines used in Supplementary Figure S4L
View article: Oxidative phosphorylation is required for cardiomyocyte re-differentiation and long-term fish heart regeneration
Oxidative phosphorylation is required for cardiomyocyte re-differentiation and long-term fish heart regeneration Open
In contrast to humans, fish can fully regenerate their hearts after cardiac injury. However, not all fish have the same regenerative potential, allowing comparative inter-species and intra-species analysis to identify the mechanisms contro…
View article: Oncogene Silencing via ecDNA Micronucleation
Oncogene Silencing via ecDNA Micronucleation Open
Extrachromosomal DNA (ecDNA) is a common source of oncogene amplification across many types of cancer. The non-Mendelian inheritance of ecDNA contributes to heterogeneous tumour genomes that rapidly evolve to resist treatment. Here, using …
View article: Mapping lineage-traced cells across time points with moslin
Mapping lineage-traced cells across time points with moslin Open
View article: Supplementary Table S5 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Table S5 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
Metabolite levels in cells with DDX1-MYCN co-amplification compared to cell lines without such co-amplification.
View article: Supplementary Figures S1-S9 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Figures S1-S9 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
Legends for supplementarytables and supplementary figures. Supplementary Figure S1. Passenger genes are frequently co-amplified with oncogenes in cancers. Supplementary Figure S2. DDX1 is highly expressed when co-amplified with MYCN. Suppl…
View article: Supplementary Table S6 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Table S6 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
QC sample reporting for Gas chromatography–mass spectrometry (GS-MS)
View article: Supplementary Table S4 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Table S4 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
Peptides significantly enriched after DDX1 immunoprecipitation as measured using LC-MS/MS.
View article: Supplementary Table S6 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Table S6 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
QC sample reporting for Gas chromatography–mass spectrometry (GS-MS)
View article: Data from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Data from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
DNA amplifications in cancer do not only harbor oncogenes. We sought to determine whether passenger coamplifications could create collateral therapeutic vulnerabilities. Through an analysis of >3,000 cancer genomes followed by the interrog…
View article: Supplementary Table S3 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Table S3 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
Gene sets enriched in in cell lines after ectopic DDX1 expression.
View article: Supplementary Table S7 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Table S7 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
List of antibodies, materials, oligonucleotides, deposited data and software used in this study.
View article: Supplementary Table S1 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Table S1 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
List of gene dependencies associated with DDX1 co-amplification.
View article: Supplementary Table S5 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Table S5 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
Metabolite levels in cells with DDX1-MYCN co-amplification compared to cell lines without such co-amplification.
View article: Supplementary Table S4 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Table S4 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
Peptides significantly enriched after DDX1 immunoprecipitation as measured using LC-MS/MS.
View article: Supplementary Table S7 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Table S7 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
List of antibodies, materials, oligonucleotides, deposited data and software used in this study.
View article: Supplementary Table S1 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer
Supplementary Table S1 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer Open
List of gene dependencies associated with DDX1 co-amplification.