Roosa Kaarijärvi
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View article: DPYSL3B is a regulator of chemoresistance via DNA repair and metabolic reprogramming in prostate cancer
DPYSL3B is a regulator of chemoresistance via DNA repair and metabolic reprogramming in prostate cancer Open
Prostate cancer is among the most common cancers worldwide. Aggressive, treatment-resistant subtypes including androgen receptor (AR) -negative and neuroendocrine prostate cancer, present a significant clinical challenge. Platinum-based ch…
View article: Matrix stiffness modulates androgen response genes and chromatin state in prostate cancer
Matrix stiffness modulates androgen response genes and chromatin state in prostate cancer Open
The interplay between the extracellular matrix (ECM) and prostate cancer has been shown to increase ECM stiffness, correlating with more aggressive disease forms. However, the impact of ECM stiffness on the androgen receptor (AR), a key ta…
View article: SIX2 promotes cell plasticity via Wnt/β-catenin signalling in androgen receptor independent prostate cancer
SIX2 promotes cell plasticity via Wnt/β-catenin signalling in androgen receptor independent prostate cancer Open
The use of androgen receptor (AR) inhibitors in prostate cancer gives rise to increased cellular lineage plasticity resulting in resistance to AR-targeted therapies. In this study, we examined the chromatin landscape of AR-positive prostat…
View article: DPYSL5 is highly expressed in treatment-induced neuroendocrine prostate cancer and promotes lineage plasticity via EZH2/PRC2
DPYSL5 is highly expressed in treatment-induced neuroendocrine prostate cancer and promotes lineage plasticity via EZH2/PRC2 Open
View article: Fanconi anemia pathway regulation by FANCI in prostate cancer
Fanconi anemia pathway regulation by FANCI in prostate cancer Open
Prostate cancer is one of the leading causes of death among men worldwide, and thus, research on the genetic factors enabling the formation of treatment-resistant cancer cells is crucial for improving patient outcomes. Here, we report a ce…
View article: SIX2 promotes cell plasticity via Wnt/ß-catenin signalling in androgen receptor independent prostate cancer
SIX2 promotes cell plasticity via Wnt/ß-catenin signalling in androgen receptor independent prostate cancer Open
View article: Supplementary Table 3 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Table 3 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
qPCR primers used for L1-ORF1, L1-ORF2, FANCI, and GAPDH.
View article: Data from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Data from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
Treatment-eradicated cancer subclones have been reported in leukemia and have recently been detected in solid tumors. Here we introduce Differential Subclone Eradication and Resistance (DSER) analysis, a method developed to identify molecu…
View article: Supplementary Table 5 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Table 5 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
Concordance of L1 insertion calls from the current study with insertion calls reported in Tubio et al.
View article: Supplementary Table 4 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Table 4 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
SNVs and indels in A34 subclones. Eradicated subclones are subclone numbers 12, 13, 14, and 15.
View article: Supplementary Table 1 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Table 1 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
L1 retrotransposition evens identified by TraFiC analysis in A34 in the current study.
View article: Supplementary Table 4 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Table 4 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
SNVs and indels in A34 subclones. Eradicated subclones are subclone numbers 12, 13, 14, and 15.
View article: Supplementary Material-SM1 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Material-SM1 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
Ketola et al Supplementary Material
View article: Supplementary Table 3 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Table 3 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
qPCR primers used for L1-ORF1, L1-ORF2, FANCI, and GAPDH.
View article: Supplementary Material-SM1 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Material-SM1 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
Ketola et al Supplementary Material
View article: Data from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Data from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
Treatment-eradicated cancer subclones have been reported in leukemia and have recently been detected in solid tumors. Here we introduce Differential Subclone Eradication and Resistance (DSER) analysis, a method developed to identify molecu…
View article: Supplementary Table 2 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Table 2 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
FANCI siRNA experimental data depicted in Supp Fig S3
View article: Supplementary Table 1 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Table 1 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
L1 retrotransposition evens identified by TraFiC analysis in A34 in the current study.
View article: Supplementary Table 5 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Table 5 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
Concordance of L1 insertion calls from the current study with insertion calls reported in Tubio et al.
View article: Supplementary Table 2 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Supplementary Table 2 from Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
FANCI siRNA experimental data depicted in Supp Fig S3
View article: Single-cell ATAC and RNA sequencing reveal pre-existing and persistent cells associated with prostate cancer relapse
Single-cell ATAC and RNA sequencing reveal pre-existing and persistent cells associated with prostate cancer relapse Open
View article: Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity
Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity Open
Treatment-eradicated cancer subclones have been reported in leukemia and have recently been detected in solid tumors. Here we introduce Differential Subclone Eradication and Resistance (DSER) analysis, a method developed to identify molecu…
View article: Single-cell ATAC and RNA sequencing reveal pre-existing and persistent subpopulations of cells associated with relapse of prostate cancer
Single-cell ATAC and RNA sequencing reveal pre-existing and persistent subpopulations of cells associated with relapse of prostate cancer Open
View article: Single-cell ATAC and RNA sequencing reveal pre-existing and persistent subpopulations of cells associated with relapse of prostate cancer
Single-cell ATAC and RNA sequencing reveal pre-existing and persistent subpopulations of cells associated with relapse of prostate cancer Open
Prostate cancer is profoundly heterogeneous and patients would benefit from methods that stratify clinically indolent from more aggressive forms of the disease. We employed single-cell assay for transposase-accessible chromatin (ATAC) and …
View article: Molecular and Functional Links between Neurodevelopmental Processes and Treatment-Induced Neuroendocrine Plasticity in Prostate Cancer Progression
Molecular and Functional Links between Neurodevelopmental Processes and Treatment-Induced Neuroendocrine Plasticity in Prostate Cancer Progression Open
Neuroendocrine plasticity and treatment-induced neuroendocrine phenotypes have recently been proposed as important resistance mechanisms underlying prostate cancer progression. Treatment-induced neuroendocrine prostate cancer (t-NEPC) is h…