Mariusz A. Wasik
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View article: Supplementary Figure 5 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Supplementary Figure 5 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells Open
S5. Targeting Polθ + PARP1 and Polθ + RAD52 induced dual synthetic lethality against HR-deficient leukemia cells.
View article: Supplementary Figure 1 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Supplementary Figure 1 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells Open
S1. Genetic aberrations and mRNA expression variabilities of POLQ, PARP1 and RAD52 do not coexist in 519 AML samples from the BEAT-AML cohort.
View article: ADH5/ALDH2 dehydrogenases and DNA polymerase theta protect normal and malignant hematopoietic cells from formaldehyde challenge: therapeutic implications
ADH5/ALDH2 dehydrogenases and DNA polymerase theta protect normal and malignant hematopoietic cells from formaldehyde challenge: therapeutic implications Open
View article: Role of Chromosomal Microarray and RNA Fusion Analysis in Detecting <i>KMT2A</i>-PTD and Stem Cell Transplant Impact on Mortality
Role of Chromosomal Microarray and RNA Fusion Analysis in Detecting <i>KMT2A</i>-PTD and Stem Cell Transplant Impact on Mortality Open
KMT2A partial tandem duplication ( KMT2A -PTD) is a recurrent, high-risk alteration in myeloid neoplasms, yet no gold standard exists for its detection due to complex genomic architecture. We conducted a retrospective study of 97 specimens…
View article: Magnetic resonance spectroscopy–based detection of response to therapy targeting glutaminolysis in lymphoma
Magnetic resonance spectroscopy–based detection of response to therapy targeting glutaminolysis in lymphoma Open
View article: Burnt out? No, it’s not about me
Burnt out? No, it’s not about me Open
View article: Data from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Data from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells Open
DNA polymerase theta (Poltheta, encoded by POLQ gene) plays an essential role in Poltheta-mediated end-joining (TMEJ) of DNA double-strand breaks (DSBs). Inhibition of Poltheta is synthetic lethal in homologous recombination (HR)-deficient…
View article: Supplementary Figure 1 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Supplementary Figure 1 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells Open
S1. Genetic aberrations and mRNA expression variabilities of POLQ, PARP1 and RAD52 do not coexist in 519 AML samples from the BEAT-AML cohort.
View article: Supplementary Figure 4 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Supplementary Figure 4 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells Open
S4. Targeting Polθ + PARP and Polθ + RAD52 induced dual synthetic lethality against HR -deficient MPN cells.
View article: Supplementary Figure 3 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Supplementary Figure 3 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells Open
S3. Simultaneous inhibition of Polθ helicase and DNA polymerase activity exerted synergistic effect against RAD54-/- leukemia cells.
View article: Supplementary Figure 4 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Supplementary Figure 4 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells Open
S4. Targeting Polθ + PARP and Polθ + RAD52 induced dual synthetic lethality against HR -deficient MPN cells.
View article: Supplementary Figure 1 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Supplementary Figure 1 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells Open
S1. Genetic aberrations and mRNA expression variabilities of POLQ, PARP1 and RAD52 do not coexist in 519 AML samples from the BEAT-AML cohort.
View article: Supplementary Figure 3 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Supplementary Figure 3 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells Open
S3. Simultaneous inhibition of Polθ helicase and DNA polymerase activity exerted synergistic effect against RAD54-/- leukemia cells.
View article: Supplementary Figure 5 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Supplementary Figure 5 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells Open
S5. Targeting Polθ + PARP1 and Polθ + RAD52 induced dual synthetic lethality against HR-deficient leukemia cells.
View article: Supplementary Figure 2 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Supplementary Figure 2 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells Open
S2. Phenotype of Polq-/-;Parp1-/- and Polq-/-;Rad52-/- mice.
View article: Supplementary Figure 2 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Supplementary Figure 2 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells Open
S2. Phenotype of Polq-/-;Parp1-/- and Polq-/-;Rad52-/- mice.
View article: Supplementary Figure 5 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Supplementary Figure 5 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells Open
S5. Targeting Polθ + PARP1 and Polθ + RAD52 induced dual synthetic lethality against HR-deficient leukemia cells.
View article: Impact of therapeutic inhibition of oncogenic cell signaling tyrosine kinase on cell metabolism: in vivo-detectable metabolic biomarkers of inhibition
Impact of therapeutic inhibition of oncogenic cell signaling tyrosine kinase on cell metabolism: in vivo-detectable metabolic biomarkers of inhibition Open
View article: Diverse and reprogrammable mechanisms of malignant cell transformation in lymphocytes: pathogenetic insights and translational implications
Diverse and reprogrammable mechanisms of malignant cell transformation in lymphocytes: pathogenetic insights and translational implications Open
While normal B- and T-lymphocytes require antigenic ligands to become activated via their B- and T-cell receptors (BCR and TCR, respectively), B- and T-cell lymphomas show the broad spectrum of cell activation mechanisms regarding their de…
View article: P087: Retrospective analysis of comprehensive cancer panel sequencing at Fox Chase Cancer Center to evaluate the QIAGEN Clinical Insight Interpret database
P087: Retrospective analysis of comprehensive cancer panel sequencing at Fox Chase Cancer Center to evaluate the QIAGEN Clinical Insight Interpret database Open
As the utilization of next-generation sequencing panels for tumor genomic profiling expands, there is an increasing volume of somatic variants identified, but interpretation of these variants poses a challenge for clinical molecular oncolo…
View article: Validation of a Molecular Diagnostic Test for Circulating Tumor DNA by Next-Gen Sequencing
Validation of a Molecular Diagnostic Test for Circulating Tumor DNA by Next-Gen Sequencing Open
A modified version of the PGDx elioTM Plasma Resolve assay was validated as a laboratory-developed test (LDT) for clinical use in the Molecular Diagnostics Laboratory at Fox Chase Cancer Center. The test detects single nucleotide variants …
View article: Supplementary Figure 4 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Supplementary Figure 4 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells Open
S4. Targeting Polθ + PARP and Polθ + RAD52 induced dual synthetic lethality against HR -deficient MPN cells.
View article: Data from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Data from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells Open
DNA polymerase theta (Polθ, encoded by POLQ gene) plays an essential role in Polθ-mediated end-joining (TMEJ) of DNA double-strand breaks (DSB). Inhibition of Polθ is synthetic lethal in homologous recombination (HR)-deficient tumor…
View article: Supplementary Figure 4 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Supplementary Figure 4 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells Open
S4. Targeting Polθ + PARP and Polθ + RAD52 induced dual synthetic lethality against HR -deficient MPN cells.
View article: Supplementary Figure 1 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Supplementary Figure 1 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells Open
S1. Genetic aberrations and mRNA expression variabilities of POLQ, PARP1 and RAD52 do not coexist in 519 AML samples from the BEAT-AML cohort.
View article: Supplementary Figure 1 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Supplementary Figure 1 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells Open
S1. Genetic aberrations and mRNA expression variabilities of POLQ, PARP1 and RAD52 do not coexist in 519 AML samples from the BEAT-AML cohort.
View article: Supplementary Figure 5 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Supplementary Figure 5 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells Open
S5. Targeting Polθ + PARP1 and Polθ + RAD52 induced dual synthetic lethality against HR-deficient leukemia cells.
View article: Supplementary Figure 2 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Supplementary Figure 2 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells Open
S2. Phenotype of Polq-/-;Parp1-/- and Polq-/-;Rad52-/- mice.
View article: Supplementary Figure 5 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Supplementary Figure 5 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells Open
S5. Targeting Polθ + PARP1 and Polθ + RAD52 induced dual synthetic lethality against HR-deficient leukemia cells.
View article: Supplementary Figure 3 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells
Supplementary Figure 3 from Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination–Deficient Leukemia Cells Open
S3. Simultaneous inhibition of Polθ helicase and DNA polymerase activity exerted synergistic effect against RAD54-/- leukemia cells.