Natalie Andersson
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View article: Tracing metastatic spread in pediatric solid tumors using copy number and targeted deep sequencing
Tracing metastatic spread in pediatric solid tumors using copy number and targeted deep sequencing Open
The most common cause of death in pediatric cancer patients is a treatment‐resistant tumor, compounded by metastatic spread, making surgery, radiation therapy, and chemotherapy unfeasible as curative treatment options. However, the mechani…
View article: Molecular subtypes of bladder cancer do not display microenvironment- or metastasis-induced plasticity
Molecular subtypes of bladder cancer do not display microenvironment- or metastasis-induced plasticity Open
Background Transcriptomic and genomic analyses of bladder cancer (BC) reveal a highly diverse disease stratified into molecular subtypes with distinct molecular features and biological behaviors. Intratumor heterogeneity (ITH) and plastici…
View article: Early evolutionary branching across spatial domains predisposes to clonal replacement under chemotherapy in neuroblastoma
Early evolutionary branching across spatial domains predisposes to clonal replacement under chemotherapy in neuroblastoma Open
Neuroblastoma (NB) is one of the most lethal childhood cancers due to its propensity to become treatment resistant. By spatial mapping of subclone geographies before and after chemotherapy across 89 tumor regions from 12 NBs, we find that …
View article: Table S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Table S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Table 1. Overview of the study cohort and the clinical data. This table contains basic clinical information, including age, sex, whether tumors were uni- or bilateral, histology, stage, risk group, treatment to which the rese…
View article: Figure S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Figure S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Figure 1 Geographic overview of histological and genetic features.
View article: Table S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Table S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Table 3. Table. Sample list with TP53 status. All 20 WT cases and their corresponding samples are listed. ‘Sample position’ refers to the individual sample and its position in a certain paraffin block (see Figure 1 for detail…
View article: Table S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Table S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Table 3. Table. Sample list with TP53 status. All 20 WT cases and their corresponding samples are listed. ‘Sample position’ refers to the individual sample and its position in a certain paraffin block (see Figure 1 for detail…
View article: Figure S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Figure S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Figure 1 Geographic overview of histological and genetic features.
View article: Fig S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Fig S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Figure 3. Relationship between anaplasia, copy number aberrations, regression and mitotic rate.
View article: Table S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Table S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Table 2. Representativeness of study participants. Details on how the patients with Wilms tumor in the present study compare to the general population of patients diagnosed with with Wilms tumor.
View article: Fig S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Fig S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Figure 2. Complexity of phylogenetic tree, comparing WT DA to IR and BT WT.
View article: Fig S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Fig S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Figure 2. Complexity of phylogenetic tree, comparing WT DA to IR and BT WT.
View article: Data from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Data from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Purpose: While patients with intermediate-risk Wilms tumors (WT) now have an overall survival rate of almost 90%, those affected by high-stage tumors with diffuse anaplasia (DA) have an overall survival of only around 50%. We here identify…
View article: Table S4 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Table S4 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Table 4. Segmental aberrations. All 20 Wilms tumor (WT) cases and their corresponding samples are listed. ‘Sample position’ refers to the individual sample and its position in a certain paraffin block (see Figure 1 for detail…
View article: Table S4 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Table S4 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Table 4. Segmental aberrations. All 20 Wilms tumor (WT) cases and their corresponding samples are listed. ‘Sample position’ refers to the individual sample and its position in a certain paraffin block (see Figure 1 for detail…
View article: Table S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Table S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Table 1. Overview of the study cohort and the clinical data. This table contains basic clinical information, including age, sex, whether tumors were uni- or bilateral, histology, stage, risk group, treatment to which the rese…
View article: Table S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Table S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Table 2. Representativeness of study participants. Details on how the patients with Wilms tumor in the present study compare to the general population of patients diagnosed with with Wilms tumor.
View article: Fig S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Fig S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution Open
Supplementary Figure 3. Relationship between anaplasia, copy number aberrations, regression and mitotic rate.
View article: Figure S1 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
Figure S1 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution Open
Supplementary Figure 1 Geographic overview of histological and genetic features.
View article: Table S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
Table S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution Open
Supplementary Table 2. Representativeness of study participants. Details on how the patients with Wilms tumor in the present study compare to the general population of patients diagnosed with with Wilms tumor.
View article: Table S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
Table S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution Open
Supplementary Table 2. Representativeness of study participants. Details on how the patients with Wilms tumor in the present study compare to the general population of patients diagnosed with with Wilms tumor.
View article: Table S3 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
Table S3 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution Open
Supplementary Table 3. Table. Sample list with TP53 status. All 20 WT cases and their corresponding samples are listed. ‘Sample position’ refers to the individual sample and its position in a certain paraffin block (see Figure 1 for detail…
View article: Fig S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
Fig S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution Open
Supplementary Figure 2. Complexity of phylogenetic tree, comparing WT DA to IR and BT WT.
View article: Data from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
Data from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution Open
Purpose:While patients with intermediate-risk (IR) Wilms tumors now have an overall survival (OS) rate of almost 90%, those affected by high-stage tumors with diffuse anaplasia have an OS of only around 50%. We here identify key events in …
View article: Fig S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
Fig S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution Open
Supplementary Figure 2. Complexity of phylogenetic tree, comparing WT DA to IR and BT WT.
View article: Table S3 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
Table S3 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution Open
Supplementary Table 3. Table. Sample list with TP53 status. All 20 WT cases and their corresponding samples are listed. ‘Sample position’ refers to the individual sample and its position in a certain paraffin block (see Figure 1 for detail…
View article: Fig S3 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
Fig S3 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution Open
Supplementary Figure 3. Relationship between anaplasia, copy number aberrations, regression and mitotic rate.
View article: Table S4 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
Table S4 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution Open
Supplementary Table 4. Segmental aberrations. All 20 Wilms tumor (WT) cases and their corresponding samples are listed. ‘Sample position’ refers to the individual sample and its position in a certain paraffin block (see Figure 1 for detail…