Selim Misirlioglu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Selim Misirlioglu has a total of 71 co-authors. Here are the top co-authors by number of shared publications:
- Douglas A. Levine
Gynecologic Oncology, Laura and Isaac Perlmutter Cancer Center, NYU Langone Medical Center, New York, New York
50 shared publications - Alireza Khodadadi-Jamayran
Department of Pathology, New York University Grossman School of Medicine, New York, NY 10016, USA
31 shared publications - Luiza Doro Pereira
Division of Gynecologic Oncology, Department of OB/GYN, Laura and Isaac Perlmutter Cancer Center, NYU Langone Health, New York, New York
31 shared publications - Monica Wielgos-Bonvallet
Division of Gynecologic Oncology, Department of OB/GYN, Laura and Isaac Perlmutter Cancer Center, NYU Langone Health, New York, New York
31 shared publications - Petar Jelinic
Division of Gynecologic Oncology, Department of OB/GYN, Laura and Isaac Perlmutter Cancer Center, NYU Langone Health, New York, New York
31 shared publications - Alexander James Roy Bishop
Greehey Children’s Cancer Research Institute, University of Texas Health at San Antonio, San Antonio, USA
18 shared publications
Latest Publications
- Open Access
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Figure S4 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Figure 4 shows IP-10 (CXCL10) expression levels in drug-treated cell lines.
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S4 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Figure 4 shows IP-10 (CXCL10) expression levels in drug-treated cell lines.
- Open Access
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Table S4 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Table 4 shows enriched gene sets upregulated in CAOV3 cells treated with veliparib .
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessTable S4 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Table 4 shows enriched gene sets upregulated in CAOV3 cells treated with veliparib .
- Open Access
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Figure S1 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Figure 1 shows clustering of drug-treated cells compared to controls.
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S1 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Figure 1 shows clustering of drug-treated cells compared to controls.
- Open Access
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Figure S2 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Figure 2 shows Venn diagrams of elevated genes in drug-treated cells.
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S2 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Figure 2 shows Venn diagrams of elevated genes in drug-treated cells.
- Open Access
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Figure S3 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Figure 3 shows CXCL10 gene and protein expression levels in drug-treated cell lines.
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S3 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Figure 3 shows CXCL10 gene and protein expression levels in drug-treated cell lines.
- Open Access
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Table S3 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Table 3 shows enriched gene sets upregulated in OVCAR3 cells treated with veliparib .
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessTable S3 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Table 3 shows enriched gene sets upregulated in OVCAR3 cells treated with veliparib .
- Open Access
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Table S2 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Table 2 shows enriched gene sets upregulated in OVCAR3 cells treated with talazoparib.
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessTable S2 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Table 2 shows enriched gene sets upregulated in OVCAR3 cells treated with talazoparib.
- Open Access
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Table S1 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Table 1 shows enriched gene sets upregulated in CAOV3 cells treated with talazoparib.
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessTable S1 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Supplementary Table 1 shows enriched gene sets upregulated in CAOV3 cells treated with talazoparib.
- Open Access
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Figure 1 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Pro-inflammatory genes are significantly upregulated in CAOV3 and OVCAR3 talazoparib-treated cells compared with control and veliparib-treated cells. Volcano plots highlighting fold change values of a small set of pro-inflammatory genes (FDR < 0.1) in (A and C) talazoparib-treated vs. DMSO-treated cells or (B and D) veliparib-treated vs. DMSO-treated cells. Red circles denote genes that were significantly upregulated, and blue circles represent genes that were significantly downregulated. Results shown are from three independent experiments. E–H, GSEA plots representative of the top upregulated pathway in each of the four comparisons. NES, normalized enrichment score.
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessFigure 1 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
Pro-inflammatory genes are significantly upregulated in CAOV3 and OVCAR3 talazoparib-treated cells compared with control and veliparib-treated cells. Volcano plots highlighting fold change values of a small set of pro-inflammatory genes (FDR < 0.1) in (A and C) talazoparib-treated vs. DMSO-treated cells or (B and D) veliparib-treated vs. DMSO-treated cells. Red circles denote genes that were significantly upregulated, and blue circles represent genes that were significantly downregulated. Results shown are from three independent experiments. E–H, GSEA plots representative of the top upregulated pathway in each of the four comparisons. NES, normalized enrichment score.
- Open Access
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Figure 3 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
IL-8 (CXCL8) is exclusively secreted in BRCA1 methylated or mutated HGSC cells after olaparib treatment but is secreted in all HRD HGSC cells after talazoparib treatment. A, OVCAR3, (B) OVCAR8, and (C) COV362 cells were treated with DMSO, 10 μmol/L veliparib, 10 μmol/L olaparib, or 2 μmol/L talazoparib for 48 hours. The supernatants were then collected, and IL-8 protein expression was analyzed by an ELISA assay. A four-parameter logistic curve fit was used to analyze these results. T tests were performed between DMSO- and the individual PARPi–treated groups. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, not statistically significant.
- 7 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessFigure 3 from PARP Inhibitors Differentially Regulate Immune Responses in Distinct Genetic Backgrounds of High-Grade Serous Tubo-Ovarian Carcinoma
IL-8 (CXCL8) is exclusively secreted in BRCA1 methylated or mutated HGSC cells after olaparib treatment but is secreted in all HRD HGSC cells after talazoparib treatment. A, OVCAR3, (B) OVCAR8, and (C) COV362 cells were treated with DMSO, 10 μmol/L veliparib, 10 μmol/L olaparib, or 2 μmol/L talazoparib for 48 hours. The supernatants were then collected, and IL-8 protein expression was analyzed by an ELISA assay. A four-parameter logistic curve fit was used to analyze these results. T tests were performed between DMSO- and the individual PARPi–treated groups. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, not statistically significant.