A5055420365- Cancer-related Molecular Pathways
- PARP inhibition in cancer therapy
- DNA Repair Mechanisms
- Epigenetics and DNA Methylation
- Ubiquitin and proteasome pathways
- Microtubule and mitosis dynamics
- Cancer Research and Treatments
- interferon and immune responses
- Cancer Genomics and Diagnostics
- RNA modifications and cancer
- Molecular Biology Techniques and Applications
Hunter College
2019-2022
City University of New York
2019-2022
The Graduate Center, CUNY
2019-2022
Abstract Over 80% of triple-negative breast cancers (TNBC) express mutant p53 (mtp53) and some contain oncogenic gain-of-function (GOF) p53. We previously reported that GOF mtp53 R273H upregulates the chromatin association mini chromosome maintenance (MCM) proteins MCM2-7 PARP named this mtp53–PARP–MCM axis. In study, we dissected function between using a number different cell lines, patient-derived xenografts (PDX), tissue microarrays (TMA), The Cancer Genome Atlas (TCGA) database....
Triple negative breast cancer (TNBC) has no targeted detection or treatment method. Mutant p53 (mtp53) is overexpressed in >80% of TNBCs, and the stability mtp53 compared to instability wild-type (wtp53) normal cells makes a promising TNBC target for diagnostic theranostic imaging. We generated Cy5p53Tet, novel nucleus-penetrating mtp53-oligomerization-domain peptide (mtp53ODP) tetramerization domain (TD) mtp53. This mtp53ODP contains TD sequence conjugated Cy5 fluorophore near-infrared...
The TP53 gene is often mutated in cancer, with missense mutations found the central DNA binding domain, and less C-terminal oligomerization domain (OD). These types of are patients rare inherited cancer predisposition disorder called Li-Fraumeni syndrome. We previously that mutant p53 (mtp53) R273H associates replicating promotes chromatin association replication-associated proteins mini-chromosome maintenance 2 (MCM2), poly ADP-ribose polymerase 1(PARP1). Herein, we created dual mutants...
We recently documented that gain-of-function (GOF) mutant p53 (mtp53) R273H in triple negative breast cancer (TNBC) cells interacts with replicating DNA and PARP1. The missense GOF mtp53 has a mutated central binding domain renders it unable to bind specifically DNA, but maintains the capacity interact tightly chromatin. Both C-terminal (CTD) oligomerization (OD) of proteins are intact is unclear whether these regions responsible for chromatin-based replication activities. generated...
Supplementary Figure from The C-terminus of Gain-of-Function Mutant p53 R273H Is Required for Association with PARP1 and Poly-ADP-Ribose
Abstract Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma in children and adolescents. RMS tumors are classified into four subtypes: embryonal, alveolar, spindle cell/sclerosing, pleomorphic. Treatment options for include a combination of surgery, chemotherapy, radiation therapy regimens patients with relapsed metastatic remain limited. However, recent study has reported that pharmacological inhibitors targeting ataxia telangiectasia Rad3-related protein (ATR) currently...
Abstract The TP53 gene is mutated in 80% of triple-negative breast cancers. Cells that harbor the hot-spot p53 mutation R273H produce an oncogenic mutant (mtp53) enhances cell proliferative and metastatic properties. enhanced activities mtp53 are collectively referred to as gain-of-function (GOF), may include transcription-independent chromatin-based shared with wild-type (wtp53) such association replicating DNA replication associated proteins like PARP1. However, how upregulates...
<div>Abstract<p>Over 80% of triple-negative breast cancers (TNBC) express mutant p53 (mtp53) and some contain oncogenic gain-of-function (GOF) p53. We previously reported that GOF mtp53 R273H upregulates the chromatin association mini chromosome maintenance (MCM) proteins MCM2-7 PARP named this mtp53–PARP–MCM axis. In study, we dissected function between using a number different cell lines, patient-derived xenografts (PDX), tissue microarrays (TMA), The Cancer Genome Atlas (TCGA)...
<p>S4 Examples of manually scored p53 and PARP1 staining intensity categories.</p>
<p>S3 Mutant p53/PARP and p53/Edu Complexes in MDA-MB-468 PANC-1 Cells.</p>
<p>S1 Chromatin protein levels of mtp53, H2B and Lamin A were compared by Western blot analysis.</p>
<p>S2 Mutant p53 R273H and Flag-R248W associate with replicating DNA.</p>
<p>S4 Examples of manually scored p53 and PARP1 staining intensity categories.</p>
<p>S3 Mutant p53/PARP and p53/Edu Complexes in MDA-MB-468 PANC-1 Cells.</p>
<p>S2 Mutant p53 R273H and Flag-R248W associate with replicating DNA.</p>
<p>S1 Chromatin protein levels of mtp53, H2B and Lamin A were compared by Western blot analysis.</p>
Supplementary Figure from The C-terminus of Gain-of-Function Mutant p53 R273H Is Required for Association with PARP1 and Poly-ADP-Ribose
Supplementary Figure from The C-terminus of Gain-of-Function Mutant p53 R273H Is Required for Association with PARP1 and Poly-ADP-Ribose
Supplementary Figure from The C-terminus of Gain-of-Function Mutant p53 R273H Is Required for Association with PARP1 and Poly-ADP-Ribose
Supplementary Figure from The C-terminus of Gain-of-Function Mutant p53 R273H Is Required for Association with PARP1 and Poly-ADP-Ribose
Supplementary Figure from The C-terminus of Gain-of-Function Mutant p53 R273H Is Required for Association with PARP1 and Poly-ADP-Ribose
<div>Abstract<p>The TP53 gene is mutated in 80% of triple-negative breast cancers. Cells that harbor the hot-spot p53 mutation R273H produce an oncogenic mutant (mtp53) enhances cell proliferative and metastatic properties. The enhanced activities mtp53 are collectively referred to as gain-of-function (GOF), may include transcription-independent chromatin-based shared with wild-type (wtp53) such association replicating DNA replication associated proteins like PARP1. However, how...
<div>Abstract<p>The TP53 gene is mutated in 80% of triple-negative breast cancers. Cells that harbor the hot-spot p53 mutation R273H produce an oncogenic mutant (mtp53) enhances cell proliferative and metastatic properties. The enhanced activities mtp53 are collectively referred to as gain-of-function (GOF), may include transcription-independent chromatin-based shared with wild-type (wtp53) such association replicating DNA replication associated proteins like PARP1. However, how...
<div>Abstract<p>Over 80% of triple-negative breast cancers (TNBC) express mutant p53 (mtp53) and some contain oncogenic gain-of-function (GOF) p53. We previously reported that GOF mtp53 R273H upregulates the chromatin association mini chromosome maintenance (MCM) proteins MCM2-7 PARP named this mtp53–PARP–MCM axis. In study, we dissected function between using a number different cell lines, patient-derived xenografts (PDX), tissue microarrays (TMA), The Cancer Genome Atlas (TCGA)...
Abstract We recently documented that gain-of-function (GOF) mutant p53 (mtp53) R273H in triple negative breast cancer (TNBC) cells interacts with replicating DNA and PARP1 (Xiao et. al., Cancer Research 2019). The missense GOF mtp53, without a functional central binding domain, has the capacity to interact tightly chromatin but it is unclear what regions of mtp53 are responsible for chromatin-based replication activities. proteins possess an intact C-terminal domain (CTD) oligomerization...