Ameeta A. Patel
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View article: Supplementary Figure Legends from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Supplementary Figure Legends from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
The Wee-1 inhibitor, MK-1775 Synergizes with cisplatin in vitro in established HNSCC cell lines with known TP53 mutational status; Dual phospho-H3 staining and PI flow cytometric analysis (FACS); The synergy between cisplatin and MK-1775 i…
View article: Supplementary Figure S6 & Supplementary S6 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Figure S6 & Supplementary S6 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Tumor volume growth curves for individual mice in each treatment arm.
View article: Supplementary Figure S4 & Supplementary S4 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Figure S4 & Supplementary S4 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Combined inhibition or Rad51 and Wee1 enhances the DNA damage response in HPV-positive HNSCC cells
View article: Supplementary Materials and Methods from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Materials and Methods from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Supplementary Materials and Methods
View article: Supplementary Figure S1 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Supplementary Figure S1 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
Assessment of the degree of synergy between cisplatin and MK-1775 in HN30 (wild-type TP53) and HN31 (mutant TP53) HNSCC cells respectively using the Chou and Talalay method.
View article: Supplementary Materials and Methods from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Materials and Methods from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Supplementary Materials and Methods
View article: Supplementary Materials and Methods from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Supplementary Materials and Methods from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
Determination of drug synergy by the combination-index and isobologram analyses using the CalcuSyn software.
View article: Data from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Data from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Despite advances in surgery, chemotherapy, and radiation, there are limited treatment options for advanced head and neck squamous cell carcinoma (HNSCC) and survival remains very poor. Therefore, effective therapies are desperately needed.…
View article: Supplementary Figure S7 & Supplementary S7 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Figure S7 & Supplementary S7 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Clustering of HNSCC cell lines by DDR genes.
View article: Supplementary Figure S2 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Supplementary Figure S2 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
Dual phospho-H3 staining for mitotic cells and PI flow cytometric analysis (FACS).
View article: Supplementary Figures S1-S3 & Supplementary S1-S3 Legends from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Figures S1-S3 & Supplementary S1-S3 Legends from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Single agent activity of B02 in HNSCC cell lines, Cell growth assay in HNSCC cells, Cell growth assay in HNSCC cells, and Synergy between B02 and AZD1775 is mediated in part through forced activation of CDK1 and inhibition of Chk1 associat…
View article: Supplementary Figure S6 & Supplementary S6 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Figure S6 & Supplementary S6 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Tumor volume growth curves for individual mice in each treatment arm.
View article: Supplementary Table S1 from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Table S1 from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Supplementary Table S1
View article: Supplementary Table S1 from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Table S1 from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Supplementary Table S1
View article: Supplementary Figure S5 & Supplementary S5 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Figure S5 & Supplementary S5 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Synergy between B02 and AZD1775 is associated with impaired Rad51-mediated homologous recombination repair in HPV-positive HNSCC cells
View article: Supplementary Figures S1-S3 & Supplementary S1-S3 Legends from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Figures S1-S3 & Supplementary S1-S3 Legends from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Single agent activity of B02 in HNSCC cell lines, Cell growth assay in HNSCC cells, Cell growth assay in HNSCC cells, and Synergy between B02 and AZD1775 is mediated in part through forced activation of CDK1 and inhibition of Chk1 associat…
View article: Data from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Data from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Despite advances in surgery, chemotherapy, and radiation, there are limited treatment options for advanced head and neck squamous cell carcinoma (HNSCC) and survival remains very poor. Therefore, effective therapies are desperately needed.…
View article: Supplementary Figure S1 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Supplementary Figure S1 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
Assessment of the degree of synergy between cisplatin and MK-1775 in HN30 (wild-type TP53) and HN31 (mutant TP53) HNSCC cells respectively using the Chou and Talalay method.
View article: Data from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Data from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
Although cisplatin has played a role in “standard-of-care” multimodality therapy for patients with advanced squamous cell carcinoma of the head and neck (HNSCC), the rate of treatment failure remains particularly high for patients receivin…
View article: Supplementary Figure S3 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Supplementary Figure S3 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
The underlying synergy between cisplatin and MK-1775 in HNSCC is not mediated by apoptosis.
View article: Supplementary Figure S4 & Supplementary S4 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Figure S4 & Supplementary S4 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Combined inhibition or Rad51 and Wee1 enhances the DNA damage response in HPV-positive HNSCC cells
View article: Supplementary Figure S2 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Supplementary Figure S2 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
Dual phospho-H3 staining for mitotic cells and PI flow cytometric analysis (FACS).
View article: Supplementary Materials and Methods from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Supplementary Materials and Methods from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
Determination of drug synergy by the combination-index and isobologram analyses using the CalcuSyn software.
View article: Supplementary Figure S3 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Supplementary Figure S3 from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
The underlying synergy between cisplatin and MK-1775 in HNSCC is not mediated by apoptosis.
View article: Supplementary Figure S7 & Supplementary S7 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Figure S7 & Supplementary S7 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Clustering of HNSCC cell lines by DDR genes.
View article: Data from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Data from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
Although cisplatin has played a role in “standard-of-care” multimodality therapy for patients with advanced squamous cell carcinoma of the head and neck (HNSCC), the rate of treatment failure remains particularly high for patients receivin…
View article: Supplementary Figure Legends from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence
Supplementary Figure Legends from Wee-1 Kinase Inhibition Overcomes Cisplatin Resistance Associated with High-Risk <i>TP53</i> Mutations in Head and Neck Cancer through Mitotic Arrest Followed by Senescence Open
The Wee-1 inhibitor, MK-1775 Synergizes with cisplatin in vitro in established HNSCC cell lines with known TP53 mutational status; Dual phospho-H3 staining and PI flow cytometric analysis (FACS); The synergy between cisplatin and MK-1775 i…
View article: Supplementary Figure S5 & Supplementary S5 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
Supplementary Figure S5 & Supplementary S5 Legend from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress Open
Synergy between B02 and AZD1775 is associated with impaired Rad51-mediated homologous recombination repair in HPV-positive HNSCC cells
View article: Supplementary Video S1 from Replication Stress Leading to Apoptosis within the S-phase Contributes to Synergism between Vorinostat and AZD1775 in HNSCC Harboring High-Risk <i>TP53</i> Mutation
Supplementary Video S1 from Replication Stress Leading to Apoptosis within the S-phase Contributes to Synergism between Vorinostat and AZD1775 in HNSCC Harboring High-Risk <i>TP53</i> Mutation Open
Live cell imaging of histone-H2B-RFP expressing PCI13-G245D cells in the presence of AZD1775.
View article: Data from Replication Stress Leading to Apoptosis within the S-phase Contributes to Synergism between Vorinostat and AZD1775 in HNSCC Harboring High-Risk <i>TP53</i> Mutation
Data from Replication Stress Leading to Apoptosis within the S-phase Contributes to Synergism between Vorinostat and AZD1775 in HNSCC Harboring High-Risk <i>TP53</i> Mutation Open
Purpose: The cure rate for patients with advanced head and neck squamous cell carcinoma (HNSCC) remains poor due to resistance to standard therapy primarily consisting of chemoradiation. As mutation of TP53 in HNSCC occurs in…