Fen Xia
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View article: GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1
GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1 Open
Resistance to genotoxic therapies remains a major contributor to tumor recurrence and treatment failure, yet the mechanisms by which cancer cells escape these therapies through DNA damage response (DDR) activation are not fully understood.…
View article: 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response Open
View article: Grid Spatially Fractionated Radiation Therapy for Bulky Tumors: A Large Single Institution Experience
Grid Spatially Fractionated Radiation Therapy for Bulky Tumors: A Large Single Institution Experience Open
View article: Producing high quality cranial SRS plans with 4Pi planning technique in a commercial clinical solution
Producing high quality cranial SRS plans with 4Pi planning technique in a commercial clinical solution Open
Purpose To generate high‐quality stereotactic radiosurgery (SRS) plans for single cranial lesions using 4Pi planning technique and compare these to our clinical “status quo” plans. Methods Eighteen vestibular schwannoma (VS) patients previ…
View article: An Innovative Algorithm for Attacking Symmetric Ciphers Using D-Wave Quantum Annealing
An Innovative Algorithm for Attacking Symmetric Ciphers Using D-Wave Quantum Annealing Open
View article: Sirt2 Mitigates Radiation-Induced Oral Mucositis by Promoting Homologous Recombination-Mediated DNA Double-Strand Break Repair in Epithelial Stem Cells
Sirt2 Mitigates Radiation-Induced Oral Mucositis by Promoting Homologous Recombination-Mediated DNA Double-Strand Break Repair in Epithelial Stem Cells Open
View article: 376 Inhibition of GSK3β-mediated 53BP1 T334 phosphorylation in T cells enhances infiltration and cytotoxicity against head and neck squamous cell carcinoma
376 Inhibition of GSK3β-mediated 53BP1 T334 phosphorylation in T cells enhances infiltration and cytotoxicity against head and neck squamous cell carcinoma Open
View article: Supplementary Figure 1 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent
Supplementary Figure 1 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent Open
Supplemental Figure illustrating BRCA1 is excluded from the nuclei following radiation in a p53-dependent manner.
View article: Supplementary Figure 2 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent
Supplementary Figure 2 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent Open
Supplemental figure demonstrating BRCA1 shuttling in response to radiation in vivo requires p53.
View article: Supplementary Figure 3 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent
Supplementary Figure 3 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent Open
Western blots demonstrating knockdown of endogenous p53 and expression of exogenous R273H mutant p53.
View article: Supplementary Figure 3 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent
Supplementary Figure 3 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent Open
Western blots demonstrating knockdown of endogenous p53 and expression of exogenous R273H mutant p53.
View article: Supplementary Figure 2 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent
Supplementary Figure 2 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent Open
Supplemental figure demonstrating BRCA1 shuttling in response to radiation in vivo requires p53.
View article: Data from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent
Data from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent Open
PARP inhibitors (PARPi) are potentially effective therapeutic agents capable of inducing synthetic lethality in tumors with deficiencies in homologous recombination (HR)-mediated DNA repair such as those carrying BRCA1 mutations. However, …
View article: Supplementary Figure 1 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent
Supplementary Figure 1 from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent Open
Supplemental Figure illustrating BRCA1 is excluded from the nuclei following radiation in a p53-dependent manner.
View article: Supplementary Figure Legends Legends from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent
Supplementary Figure Legends Legends from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent Open
Figure legends for Supplemental Figures 1 through 3.
View article: Data from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent
Data from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent Open
PARP inhibitors (PARPi) are potentially effective therapeutic agents capable of inducing synthetic lethality in tumors with deficiencies in homologous recombination (HR)-mediated DNA repair such as those carrying BRCA1 mutations. However, …
View article: Supplementary Figure Legends Legends from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent
Supplementary Figure Legends Legends from Synthetic Lethality of PARP Inhibition and Ionizing Radiation is p53-dependent Open
Figure legends for Supplemental Figures 1 through 3.
View article: Data from Targeting BRCA1 Localization to Augment Breast Tumor Sensitivity to Poly(ADP-Ribose) Polymerase Inhibition
Data from Targeting BRCA1 Localization to Augment Breast Tumor Sensitivity to Poly(ADP-Ribose) Polymerase Inhibition Open
PARP inhibitors have gained recent attention due to their highly selective killing of BRCA1/2-mutated and DNA double-strand break (DSB) repair–deficient tumors. Unfortunately, the majority of sporadic breast cancers carry wild-type BRCA1/2…
View article: Supplementary Methods from Targeting BRCA1 Localization to Augment Breast Tumor Sensitivity to Poly(ADP-Ribose) Polymerase Inhibition
Supplementary Methods from Targeting BRCA1 Localization to Augment Breast Tumor Sensitivity to Poly(ADP-Ribose) Polymerase Inhibition Open
PDF file - 84K
View article: Supplementary Figure 2A from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells
Supplementary Figure 2A from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells Open
Supplementary Figure 2A from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells
View article: Supplementary Methods and Materials, Figure Legends 1-2 from The Ubiquitin-Interacting Motif–Containing Protein RAP80 Interacts with BRCA1 and Functions in DNA Damage Repair Response
Supplementary Methods and Materials, Figure Legends 1-2 from The Ubiquitin-Interacting Motif–Containing Protein RAP80 Interacts with BRCA1 and Functions in DNA Damage Repair Response Open
Supplementary Methods and Materials, Figure Legends 1-2 from The Ubiquitin-Interacting Motif–Containing Protein RAP80 Interacts with BRCA1 and Functions in DNA Damage Repair Response
View article: Supplementary Figure Legends 1-2 from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells
Supplementary Figure Legends 1-2 from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells Open
Supplementary Figure Legends 1-2 from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells
View article: Supplementary Methods and Materials, Figures 1-5 from p53-Dependent BRCA1 Nuclear Export Controls Cellular Susceptibility to DNA Damage
Supplementary Methods and Materials, Figures 1-5 from p53-Dependent BRCA1 Nuclear Export Controls Cellular Susceptibility to DNA Damage Open
PDF file - 883K
View article: Data from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells
Data from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells Open
The epidermal growth factor receptor (EGFR) family has been implicated in several cancers, including breast, and its members have become the target of novel cancer therapies. In this report, we show a novel link between erlotinib, a potent…
View article: Data from The Ubiquitin-Interacting Motif–Containing Protein RAP80 Interacts with BRCA1 and Functions in DNA Damage Repair Response
Data from The Ubiquitin-Interacting Motif–Containing Protein RAP80 Interacts with BRCA1 and Functions in DNA Damage Repair Response Open
In this study, we examine the potential role of receptor-associated protein 80 (RAP80), a nuclear protein containing two ubiquitin-interacting motifs (UIM), in DNA damage response and double-strand break (DSB) repair. We show that followin…
View article: Supplementary Methods from Targeting BRCA1 Localization to Augment Breast Tumor Sensitivity to Poly(ADP-Ribose) Polymerase Inhibition
Supplementary Methods from Targeting BRCA1 Localization to Augment Breast Tumor Sensitivity to Poly(ADP-Ribose) Polymerase Inhibition Open
PDF file - 84K
View article: Supplementary Figure 1 from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells
Supplementary Figure 1 from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells Open
Supplementary Figure 1 from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells
View article: Supplementary Figure 4 from Targeting BRCA1 Localization to Augment Breast Tumor Sensitivity to Poly(ADP-Ribose) Polymerase Inhibition
Supplementary Figure 4 from Targeting BRCA1 Localization to Augment Breast Tumor Sensitivity to Poly(ADP-Ribose) Polymerase Inhibition Open
PDF file - 145K, Representative images of BRCA1 distribution and �H2AX foci in xenograft tissue
View article: Data from The Ubiquitin-Interacting Motif–Containing Protein RAP80 Interacts with BRCA1 and Functions in DNA Damage Repair Response
Data from The Ubiquitin-Interacting Motif–Containing Protein RAP80 Interacts with BRCA1 and Functions in DNA Damage Repair Response Open
In this study, we examine the potential role of receptor-associated protein 80 (RAP80), a nuclear protein containing two ubiquitin-interacting motifs (UIM), in DNA damage response and double-strand break (DSB) repair. We show that followin…
View article: Data from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells
Data from Erlotinib Attenuates Homologous Recombinational Repair of Chromosomal Breaks in Human Breast Cancer Cells Open
The epidermal growth factor receptor (EGFR) family has been implicated in several cancers, including breast, and its members have become the target of novel cancer therapies. In this report, we show a novel link between erlotinib, a potent…