Arun Kanakkanthara
YOU?
Author Swipe
View article: Mitotic MTH1 inhibitor karonudib kills epithelial ovarian cancer independent of platinum sensitivity
Mitotic MTH1 inhibitor karonudib kills epithelial ovarian cancer independent of platinum sensitivity Open
View article: An ATM D-compartmentalization in DNA damage response
An ATM D-compartmentalization in DNA damage response Open
View article: Supplementary Table S2 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Supplementary Table S2 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
Supplementary Table S2. PDX models minimal information standard (PDX-MI).
View article: Data from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Data from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
PARP inhibitors (PARPi) have activity in homologous recombination (HR) repair-deficient, high-grade serous ovarian cancers (HGSOC). However, even responsive tumors develop PARPi resistance, highlighting the need to delay or prevent the app…
View article: Supplementary Figures 1-8 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Supplementary Figures 1-8 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
Supplementary Figures 1-8 with legends
View article: Supplementary Materials and Methods from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Supplementary Materials and Methods from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
Supplementary Materials and Methods
View article: Supplementary Table S2 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Supplementary Table S2 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
Supplementary Table S2. PDX models minimal information standard (PDX-MI).
View article: Supplementary Table S3 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Supplementary Table S3 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
Supplementary Table S3. P-values for indicated PDX tumor growth comparisons
View article: Supplementary Table S1 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Supplementary Table S1 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
Supplementary Table 1 showing qRT-PCR primer sequences
View article: Supplementary Table S1 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Supplementary Table S1 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
Supplementary Table 1 showing qRT-PCR primer sequences
View article: Data from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Data from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
PARP inhibitors (PARPi) have activity in homologous recombination (HR) repair-deficient, high-grade serous ovarian cancers (HGSOC). However, even responsive tumors develop PARPi resistance, highlighting the need to delay or prevent the app…
View article: Supplementary Materials and Methods from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Supplementary Materials and Methods from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
Supplementary Materials and Methods
View article: Supplementary Table S3 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Supplementary Table S3 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
Supplementary Table S3. P-values for indicated PDX tumor growth comparisons
View article: Supplementary Figures 1-8 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma
Supplementary Figures 1-8 from Repurposing Ceritinib Induces DNA Damage and Enhances PARP Inhibitor Responses in High-Grade Serous Ovarian Carcinoma Open
Supplementary Figures 1-8 with legends
View article: Data from Peloruside- and Laulimalide-Resistant Human Ovarian Carcinoma Cells Have βI-Tubulin Mutations and Altered Expression of βII- and βIII-Tubulin Isotypes
Data from Peloruside- and Laulimalide-Resistant Human Ovarian Carcinoma Cells Have βI-Tubulin Mutations and Altered Expression of βII- and βIII-Tubulin Isotypes Open
Peloruside A and laulimalide are potent microtubule-stabilizing natural products with a mechanism of action similar to that of paclitaxel. However, the binding site of peloruside A and laulimalide on tubulin remains poorly understood. Drug…
View article: Supplementary Data from VLX600 Disrupts Homologous Recombination and Synergizes with PARP Inhibitors and Cisplatin by Inhibiting Histone Lysine Demethylases
Supplementary Data from VLX600 Disrupts Homologous Recombination and Synergizes with PARP Inhibitors and Cisplatin by Inhibiting Histone Lysine Demethylases Open
Supplementary Figures S1-S7, figure legends, and Tables S1 and S2.
View article: Data from βII-Tubulin and βIII-Tubulin Mediate Sensitivity to Peloruside A and Laulimalide, but not Paclitaxel or Vinblastine, in Human Ovarian Carcinoma Cells
Data from βII-Tubulin and βIII-Tubulin Mediate Sensitivity to Peloruside A and Laulimalide, but not Paclitaxel or Vinblastine, in Human Ovarian Carcinoma Cells Open
Increased abundance of βII- and βIII-tubulin isotypes in cancer cells confers resistance to vinca and taxoid site drugs; however, the role of these isotypes in the acquired resistance of cancer cells to non-vinca or non-taxoid site binding…
View article: Supplementary Figures 1-2, Tables 1-3 from βII-Tubulin and βIII-Tubulin Mediate Sensitivity to Peloruside A and Laulimalide, but not Paclitaxel or Vinblastine, in Human Ovarian Carcinoma Cells
Supplementary Figures 1-2, Tables 1-3 from βII-Tubulin and βIII-Tubulin Mediate Sensitivity to Peloruside A and Laulimalide, but not Paclitaxel or Vinblastine, in Human Ovarian Carcinoma Cells Open
PDF file - 1.6MB
View article: Supplementary Figures 1-2, Tables 1-3 from βII-Tubulin and βIII-Tubulin Mediate Sensitivity to Peloruside A and Laulimalide, but not Paclitaxel or Vinblastine, in Human Ovarian Carcinoma Cells
Supplementary Figures 1-2, Tables 1-3 from βII-Tubulin and βIII-Tubulin Mediate Sensitivity to Peloruside A and Laulimalide, but not Paclitaxel or Vinblastine, in Human Ovarian Carcinoma Cells Open
PDF file - 1.6MB
View article: Data from VLX600 Disrupts Homologous Recombination and Synergizes with PARP Inhibitors and Cisplatin by Inhibiting Histone Lysine Demethylases
Data from VLX600 Disrupts Homologous Recombination and Synergizes with PARP Inhibitors and Cisplatin by Inhibiting Histone Lysine Demethylases Open
Tumors with defective homologous recombination (HR) DNA repair are more sensitive to chemotherapies that induce lesions repaired by HR as well as PARP inhibitors (PARPis). However, these therapies have limited activity in HR-proficient cel…
View article: Data from Peloruside- and Laulimalide-Resistant Human Ovarian Carcinoma Cells Have βI-Tubulin Mutations and Altered Expression of βII- and βIII-Tubulin Isotypes
Data from Peloruside- and Laulimalide-Resistant Human Ovarian Carcinoma Cells Have βI-Tubulin Mutations and Altered Expression of βII- and βIII-Tubulin Isotypes Open
Peloruside A and laulimalide are potent microtubule-stabilizing natural products with a mechanism of action similar to that of paclitaxel. However, the binding site of peloruside A and laulimalide on tubulin remains poorly understood. Drug…
View article: Supplementary Tables 1-4, Figures 1-4 from Peloruside- and Laulimalide-Resistant Human Ovarian Carcinoma Cells Have βI-Tubulin Mutations and Altered Expression of βII- and βIII-Tubulin Isotypes
Supplementary Tables 1-4, Figures 1-4 from Peloruside- and Laulimalide-Resistant Human Ovarian Carcinoma Cells Have βI-Tubulin Mutations and Altered Expression of βII- and βIII-Tubulin Isotypes Open
Supplementary Tables 1-4, Figures 1-4 from Peloruside- and Laulimalide-Resistant Human Ovarian Carcinoma Cells Have βI-Tubulin Mutations and Altered Expression of βII- and βIII-Tubulin Isotypes
View article: Data from VLX600 Disrupts Homologous Recombination and Synergizes with PARP Inhibitors and Cisplatin by Inhibiting Histone Lysine Demethylases
Data from VLX600 Disrupts Homologous Recombination and Synergizes with PARP Inhibitors and Cisplatin by Inhibiting Histone Lysine Demethylases Open
Tumors with defective homologous recombination (HR) DNA repair are more sensitive to chemotherapies that induce lesions repaired by HR as well as PARP inhibitors (PARPis). However, these therapies have limited activity in HR-proficient cel…
View article: Data from βII-Tubulin and βIII-Tubulin Mediate Sensitivity to Peloruside A and Laulimalide, but not Paclitaxel or Vinblastine, in Human Ovarian Carcinoma Cells
Data from βII-Tubulin and βIII-Tubulin Mediate Sensitivity to Peloruside A and Laulimalide, but not Paclitaxel or Vinblastine, in Human Ovarian Carcinoma Cells Open
Increased abundance of βII- and βIII-tubulin isotypes in cancer cells confers resistance to vinca and taxoid site drugs; however, the role of these isotypes in the acquired resistance of cancer cells to non-vinca or non-taxoid site binding…
View article: Supplementary Data from VLX600 Disrupts Homologous Recombination and Synergizes with PARP Inhibitors and Cisplatin by Inhibiting Histone Lysine Demethylases
Supplementary Data from VLX600 Disrupts Homologous Recombination and Synergizes with PARP Inhibitors and Cisplatin by Inhibiting Histone Lysine Demethylases Open
Supplementary Figures S1-S7, figure legends, and Tables S1 and S2.
View article: Supplementary Tables 1-4, Figures 1-4 from Peloruside- and Laulimalide-Resistant Human Ovarian Carcinoma Cells Have βI-Tubulin Mutations and Altered Expression of βII- and βIII-Tubulin Isotypes
Supplementary Tables 1-4, Figures 1-4 from Peloruside- and Laulimalide-Resistant Human Ovarian Carcinoma Cells Have βI-Tubulin Mutations and Altered Expression of βII- and βIII-Tubulin Isotypes Open
Supplementary Tables 1-4, Figures 1-4 from Peloruside- and Laulimalide-Resistant Human Ovarian Carcinoma Cells Have βI-Tubulin Mutations and Altered Expression of βII- and βIII-Tubulin Isotypes
View article: Supplementary Table S1 from BRCA1 Deficiency Upregulates NNMT, Which Reprograms Metabolism and Sensitizes Ovarian Cancer Cells to Mitochondrial Metabolic Targeting Agents
Supplementary Table S1 from BRCA1 Deficiency Upregulates NNMT, Which Reprograms Metabolism and Sensitizes Ovarian Cancer Cells to Mitochondrial Metabolic Targeting Agents Open
Excel data file of RNA-seq from OVCAR-8 cells transfected with luciferase vs CDK12 siRNAs.
View article: Supplementary Table S2 from BRCA1 Deficiency Upregulates NNMT, Which Reprograms Metabolism and Sensitizes Ovarian Cancer Cells to Mitochondrial Metabolic Targeting Agents
Supplementary Table S2 from BRCA1 Deficiency Upregulates NNMT, Which Reprograms Metabolism and Sensitizes Ovarian Cancer Cells to Mitochondrial Metabolic Targeting Agents Open
Excel data file of NNMT and CDK12 protein levels in HGSOC tumors from patients.
View article: Data from BRCA1 Deficiency Upregulates NNMT, Which Reprograms Metabolism and Sensitizes Ovarian Cancer Cells to Mitochondrial Metabolic Targeting Agents
Data from BRCA1 Deficiency Upregulates NNMT, Which Reprograms Metabolism and Sensitizes Ovarian Cancer Cells to Mitochondrial Metabolic Targeting Agents Open
BRCA1 plays a key role in homologous recombination (HR) DNA repair. Accordingly, changes that downregulate BRCA1, including BRCA1 mutations and reduced BRCA1 transcription, due to promoter hypermethylation or loss of the BRCA…
View article: Supplementary Methods and oligonucleotide sequences from BRCA1 Deficiency Upregulates NNMT, Which Reprograms Metabolism and Sensitizes Ovarian Cancer Cells to Mitochondrial Metabolic Targeting Agents
Supplementary Methods and oligonucleotide sequences from BRCA1 Deficiency Upregulates NNMT, Which Reprograms Metabolism and Sensitizes Ovarian Cancer Cells to Mitochondrial Metabolic Targeting Agents Open
Supplementary Methods file that includes oligonucleotide sequences used in the study.