- DNA Repair Mechanisms
- PARP inhibition in cancer therapy
- DNA and Nucleic Acid Chemistry
- Acute Myeloid Leukemia Research
- Epigenetics and DNA Methylation
- Prostate Cancer Treatment and Research
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Ferroptosis and cancer prognosis
- Genomics, phytochemicals, and oxidative stress
- CRISPR and Genetic Engineering
- Cancer therapeutics and mechanisms
- Cancer Genomics and Diagnostics
- Insect Resistance and Genetics
- Cell death mechanisms and regulation
- Cancer-related gene regulation
Temple University
2023-2024
Center for Personalized Cancer Treatment
2024
DNA polymerase theta (Polθ, encoded by POLQ gene) plays an essential role in Polθ-mediated end-joining (TMEJ) of double-strand breaks (DSB). Inhibition Polθ is synthetic lethal homologous recombination (HR)-deficient tumor cells. However, DSBs can be also repaired PARP1 and RAD52-mediated mechanisms. Because leukemia cells accumulate spontaneous DSBs, we tested if simultaneous targeting or RAD52 enhance the effect HR-deficient Transformation potential oncogenes inducing BRCA1/2-deficiency...
<title>Abstract</title> Prostate cancer (PCa) is the most common diagnosed in men worldwide and second leading cause of cancer-related deaths US males 2022. also represents highest mortality disparity between non-Hispanic blacks whites. However, there a relatively small number prostate normal cell lines compared to other cancers. To identify molecular basis PCa progression, it important have epithelial (PrEC) as karyotypically possible. Our lab recently developed novel methodology for rapid...
Prostate cancer (PCa) is the most common diagnosed in men worldwide and was second leading cause of cancer-related deaths US males 2022. also represents highest mortality disparity between non-Hispanic blacks whites. However, there a relatively small number prostate normal cell lines compared to other cancers. To identify molecular basis PCa progression, it important have epithelial (PrEC) as karyotypically possible. Our lab recently developed novel methodology for rapid efficient...
<p>S2. Phenotype of Polq-/-;Parp1-/- and Polq-/-;Rad52-/- mice.</p>
<p>S1. Genetic aberrations and mRNA expression variabilities of POLQ, PARP1 RAD52 do not coexist in 519 AML samples from the BEAT-AML cohort.</p>
<p>S5. Targeting Polθ + PARP1 and RAD52 induced dual synthetic lethality against HR-deficient leukemia cells.</p>
<p>S4. Targeting Polθ + PARP and RAD52 induced dual synthetic lethality against HR -deficient MPN cells.</p>
<p>S3. Simultaneous inhibition of Polθ helicase and DNA polymerase activity exerted synergistic effect against RAD54-/- leukemia cells.</p>
<div>Abstract<p>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 Poltheta is synthetic lethal homologous recombination (HR)-deficient tumor cells. However, DSBs can be also repaired PARP1 and RAD52 -mediated mechanisms. Since leukemia cells accumulate spontaneous DSBs, we tested if simultaneous targeting Pol or enhance the effect HR-deficient Transformation...
<p>S4. Targeting Polθ + PARP and RAD52 induced dual synthetic lethality against HR -deficient MPN cells.</p>
<p>S3. Simultaneous inhibition of Polθ helicase and DNA polymerase activity exerted synergistic effect against RAD54-/- leukemia cells.</p>
<p>S1. Genetic aberrations and mRNA expression variabilities of POLQ, PARP1 RAD52 do not coexist in 519 AML samples from the BEAT-AML cohort.</p>
<p>S5. Targeting Polθ + PARP1 and RAD52 induced dual synthetic lethality against HR-deficient leukemia cells.</p>
<p>S2. Phenotype of Polq-/-;Parp1-/- and Polq-/-;Rad52-/- mice.</p>
<p>S2. Phenotype of Polq-/-;Parp1-/- and Polq-/-;Rad52-/- mice.</p>
<p>S3. Simultaneous inhibition of Polθ helicase and DNA polymerase activity exerted synergistic effect against RAD54-/- leukemia cells.</p>
<p>S1. Genetic aberrations and mRNA expression variabilities of POLQ, PARP1 RAD52 do not coexist in 519 AML samples from the BEAT-AML cohort.</p>
<p>S5. Targeting Polθ + PARP1 and RAD52 induced dual synthetic lethality against HR-deficient leukemia cells.</p>
<p>S5. Targeting Polθ + PARP1 and RAD52 induced dual synthetic lethality against HR-deficient leukemia cells.</p>
<p>S1. Genetic aberrations and mRNA expression variabilities of POLQ, PARP1 RAD52 do not coexist in 519 AML samples from the BEAT-AML cohort.</p>
<p>S2. Phenotype of Polq-/-;Parp1-/- and Polq-/-;Rad52-/- mice.</p>