ORCID Profile
0000-0002-1089-7355
Current Organisation
University of Sydney
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Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437834.V1
Abstract: Supplementary Figure 5. Schematic of FST CRISPR KO guides and in vivo experiment. A. Binding of the two commercially available FST CRISPR guides to FST to mediate KO. B. Mice were injected with SKOV3 cells expressing FST sgRNA #2. Mice were then treated 3 times with 10mg/kg Taxol intraperitoneal Paclitaxel at days 7, 14 and 21. C Dissection of control mice presenting with multiple metastases and an FST-KO mice which showed no residual disease. White arrows point to sites of disease.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553437.V1
Abstract: Supplementary Figure 3. The effect of FST or taxol treatment ovarian cancer proliferation and FST secretion, and the ability of a FST neutralization antibody to inhibit FST's effect on proliferation. A. PT340 and PT412 cells were treated with 200 ng/mL FST for 72h before cell counts were performed. B (i) IHC images and (ii) FST+ cell bodies in OVSAHO tumor xenografts treated with or without taxol and stained with both Ki67 (Forangi Blue) and FST (Fast Red). C. Titer of the ability of the anti-FST neutralizing antibody to inhibit the effect of FST on cell growth.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.C.6516069
Abstract: AbstractPurpose: We recently reported that the transcription factor NFATC4, in response to chemotherapy, drives cellular quiescence to increase ovarian cancer chemoresistance. The goal of this work was to better understand the mechanisms of NFATC4-driven ovarian cancer chemoresistance. Experimental Design: We used RNA sequencing to identify NFATC4-mediated differential gene expression. CRISPR-Cas9 and FST (follistatin)-neutralizing antibodies were used to assess impact of loss of FST function on cell proliferation and chemoresistance. ELISA was used to quantify FST induction in patient s les and i in vitro /i in response to chemotherapy. Results: We found that NFATC4 upregulates FST mRNA and protein expression predominantly in quiescent cells and FST is further upregulated following chemotherapy treatment. FST acts in at least a paracrine manner to induce a p-ATF2–dependent quiescent phenotype and chemoresistance in non-quiescent cells. Consistent with this, CRISPR knockout (KO) of i FST /i in ovarian cancer cells or antibody-mediated neutralization of FST sensitizes ovarian cancer cells to chemotherapy treatment. Similarly, CRISPR KO of i FST /i in tumors increased chemotherapy-mediated tumor eradication in an otherwise chemotherapy-resistant tumor model. Suggesting a role for FST in chemoresistance in patients, FST protein in the abdominal fluid of patients with ovarian cancer significantly increases within 24 hours of chemotherapy exposure. FST levels decline to baseline levels in patients no longer receiving chemotherapy with no evidence of disease. Furthermore, elevated FST expression in patient tumors is correlated with poor progression-free, post–progression-free, and overall survival. Conclusions: FST is a novel therapeutic target to improve ovarian cancer response to chemotherapy and potentially reduce recurrence rates. /
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553431
Abstract: Supplementary Figure 5. Schematic of FST CRISPR KO guides and in vivo experiment. A. Binding of the two commercially available FST CRISPR guides to FST to mediate KO. B. Mice were injected with SKOV3 cells expressing FST sgRNA #2. Mice were then treated 3 times with 10mg/kg Taxol intraperitoneal Paclitaxel at days 7, 14 and 21. C Dissection of control mice presenting with multiple metastases and an FST-KO mice which showed no residual disease. White arrows point to sites of disease.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553434
Abstract: Supplementary Figure 4. The effect of ATF2 siRNA on gene expression and PT340 FST induced chemoresistance. A. Schematic detailing the transwell experiments. CellTrace Violet cells were sorted for rapidly iding (Dim) or quiescent cells (Bright) which were then plated in transwell chambers either as Dim:Dim or Bright:Dim. Cells were untreated or treated with taxol alone or in combination with IgG or anti-FST antibody. Cell counts were performed on the dim cells and data was expressed as fold chnage. B. Relative ATF2 gene expression of PT412 and PT340 treated with scrambled siRNA or two independent ATF2 siRNAs (ATF2 siRNA #1 and #2). C. Viable cell number of PT340 cells treated with control scrambled siRNA or knocked down with ATF2 siRNA and treated with cisplatin +/- FST. *P .05, ns = not significant.
Publisher: Public Library of Science (PLoS)
Date: 07-04-2016
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437840.V1
Abstract: Supplementary Figure 3. The effect of FST or taxol treatment ovarian cancer proliferation and FST secretion, and the ability of a FST neutralization antibody to inhibit FST's effect on proliferation. A. PT340 and PT412 cells were treated with 200 ng/mL FST for 72h before cell counts were performed. B (i) IHC images and (ii) FST+ cell bodies in OVSAHO tumor xenografts treated with or without taxol and stained with both Ki67 (Forangi Blue) and FST (Fast Red). C. Titer of the ability of the anti-FST neutralizing antibody to inhibit the effect of FST on cell growth.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553431.V1
Abstract: Supplementary Figure 5. Schematic of FST CRISPR KO guides and in vivo experiment. A. Binding of the two commercially available FST CRISPR guides to FST to mediate KO. B. Mice were injected with SKOV3 cells expressing FST sgRNA #2. Mice were then treated 3 times with 10mg/kg Taxol intraperitoneal Paclitaxel at days 7, 14 and 21. C Dissection of control mice presenting with multiple metastases and an FST-KO mice which showed no residual disease. White arrows point to sites of disease.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820177.V1
Abstract: Supplementary Figure 4. The effect of ATF2 siRNA on gene expression and PT340 FST induced chemoresistance. A. Schematic detailing the transwell experiments. CellTrace Violet cells were sorted for rapidly iding (Dim) or quiescent cells (Bright) which were then plated in transwell chambers either as Dim:Dim or Bright:Dim. Cells were untreated or treated with taxol alone or in combination with IgG or anti-FST antibody. Cell counts were performed on the dim cells and data was expressed as fold chnage. B. Relative ATF2 gene expression of PT412 and PT340 treated with scrambled siRNA or two independent ATF2 siRNAs (ATF2 siRNA #1 and #2). C. Viable cell number of PT340 cells treated with control scrambled siRNA or knocked down with ATF2 siRNA and treated with cisplatin +/- FST. *P .05, ns = not significant.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.C.6516069.V3
Abstract: AbstractPurpose: We recently reported that the transcription factor NFATC4, in response to chemotherapy, drives cellular quiescence to increase ovarian cancer chemoresistance. The goal of this work was to better understand the mechanisms of NFATC4-driven ovarian cancer chemoresistance. Experimental Design: We used RNA sequencing to identify NFATC4-mediated differential gene expression. CRISPR-Cas9 and FST (follistatin)-neutralizing antibodies were used to assess impact of loss of FST function on cell proliferation and chemoresistance. ELISA was used to quantify FST induction in patient s les and i in vitro /i in response to chemotherapy. Results: We found that NFATC4 upregulates FST mRNA and protein expression predominantly in quiescent cells and FST is further upregulated following chemotherapy treatment. FST acts in at least a paracrine manner to induce a p-ATF2–dependent quiescent phenotype and chemoresistance in non-quiescent cells. Consistent with this, CRISPR knockout (KO) of i FST /i in ovarian cancer cells or antibody-mediated neutralization of FST sensitizes ovarian cancer cells to chemotherapy treatment. Similarly, CRISPR KO of i FST /i in tumors increased chemotherapy-mediated tumor eradication in an otherwise chemotherapy-resistant tumor model. Suggesting a role for FST in chemoresistance in patients, FST protein in the abdominal fluid of patients with ovarian cancer significantly increases within 24 hours of chemotherapy exposure. FST levels decline to baseline levels in patients no longer receiving chemotherapy with no evidence of disease. Furthermore, elevated FST expression in patient tumors is correlated with poor progression-free, post–progression-free, and overall survival. Conclusions: FST is a novel therapeutic target to improve ovarian cancer response to chemotherapy and potentially reduce recurrence rates. /
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820171.V1
Abstract: Supplementary Table 1. Primers used in this study.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.C.6516069.V2
Abstract: AbstractPurpose: We recently reported that the transcription factor NFATC4, in response to chemotherapy, drives cellular quiescence to increase ovarian cancer chemoresistance. The goal of this work was to better understand the mechanisms of NFATC4-driven ovarian cancer chemoresistance. Experimental Design: We used RNA sequencing to identify NFATC4-mediated differential gene expression. CRISPR-Cas9 and FST (follistatin)-neutralizing antibodies were used to assess impact of loss of FST function on cell proliferation and chemoresistance. ELISA was used to quantify FST induction in patient s les and i in vitro /i in response to chemotherapy. Results: We found that NFATC4 upregulates FST mRNA and protein expression predominantly in quiescent cells and FST is further upregulated following chemotherapy treatment. FST acts in at least a paracrine manner to induce a p-ATF2–dependent quiescent phenotype and chemoresistance in non-quiescent cells. Consistent with this, CRISPR knockout (KO) of i FST /i in ovarian cancer cells or antibody-mediated neutralization of FST sensitizes ovarian cancer cells to chemotherapy treatment. Similarly, CRISPR KO of i FST /i in tumors increased chemotherapy-mediated tumor eradication in an otherwise chemotherapy-resistant tumor model. Suggesting a role for FST in chemoresistance in patients, FST protein in the abdominal fluid of patients with ovarian cancer significantly increases within 24 hours of chemotherapy exposure. FST levels decline to baseline levels in patients no longer receiving chemotherapy with no evidence of disease. Furthermore, elevated FST expression in patient tumors is correlated with poor progression-free, post–progression-free, and overall survival. Conclusions: FST is a novel therapeutic target to improve ovarian cancer response to chemotherapy and potentially reduce recurrence rates. /
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.C.6516069.V1
Abstract: AbstractPurpose: We recently reported that the transcription factor NFATC4, in response to chemotherapy, drives cellular quiescence to increase ovarian cancer chemoresistance. The goal of this work was to better understand the mechanisms of NFATC4-driven ovarian cancer chemoresistance. Experimental Design: We used RNA sequencing to identify NFATC4-mediated differential gene expression. CRISPR-Cas9 and FST (follistatin)-neutralizing antibodies were used to assess impact of loss of FST function on cell proliferation and chemoresistance. ELISA was used to quantify FST induction in patient s les and i in vitro /i in response to chemotherapy. Results: We found that NFATC4 upregulates FST mRNA and protein expression predominantly in quiescent cells and FST is further upregulated following chemotherapy treatment. FST acts in at least a paracrine manner to induce a p-ATF2–dependent quiescent phenotype and chemoresistance in non-quiescent cells. Consistent with this, CRISPR knockout (KO) of i FST /i in ovarian cancer cells or antibody-mediated neutralization of FST sensitizes ovarian cancer cells to chemotherapy treatment. Similarly, CRISPR KO of i FST /i in tumors increased chemotherapy-mediated tumor eradication in an otherwise chemotherapy-resistant tumor model. Suggesting a role for FST in chemoresistance in patients, FST protein in the abdominal fluid of patients with ovarian cancer significantly increases within 24 hours of chemotherapy exposure. FST levels decline to baseline levels in patients no longer receiving chemotherapy with no evidence of disease. Furthermore, elevated FST expression in patient tumors is correlated with poor progression-free, post–progression-free, and overall survival. Conclusions: FST is a novel therapeutic target to improve ovarian cancer response to chemotherapy and potentially reduce recurrence rates. /
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437846.V1
Abstract: Supplementary Figure 1. Histological analysis of PT340 cell line. PT340 cells were injected into NSG mice, and the resulting tumors were harvested for histological analysis, H& E staining showed features of Clear Cell Ovarian Carcinoma.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437843
Abstract: Supplementary Figure 2. RNA-seq analysis. A. Schematic of the RNA-seq experimental design. B. Waterfall plot of RNA-seq data showing the 141 genes which were DE at all time points compared to luciferase control in HEY1 and SKOV3 cell lines. C. Unsupervised clustering analysis of the 141 DE genes. D. Box plots demonstrating MYC expression following NFATC4 activation. E. STRING analysis of the 141 DE genes.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437846
Abstract: Supplementary Figure 1. Histological analysis of PT340 cell line. PT340 cells were injected into NSG mice, and the resulting tumors were harvested for histological analysis, H& E staining showed features of Clear Cell Ovarian Carcinoma.
Publisher: Springer Science and Business Media LLC
Date: 23-09-2013
DOI: 10.1038/ONC.2013.368
Abstract: The HER2 (ERBB2) and MYC genes are commonly lified in breast cancer, yet little is known about their molecular and clinical interaction. Using a novel chimeric mammary transgenic approach and in vitro models, we demonstrate markedly increased self-renewal and tumour-propagating capability of cells transformed with Her2 and c-Myc. Coexpression of both oncoproteins in cultured cells led to the activation of a c-Myc transcriptional signature and acquisition of a self-renewing phenotype independent of an epithelial-mesenchymal transition programme or regulation of conventional cancer stem cell markers. Instead, Her2 and c-Myc cooperated to induce the expression of lipoprotein lipase, which was required for proliferation and self-renewal in vitro. HER2 and MYC were frequently co lified in breast cancer, associated with aggressive clinical behaviour and poor outcome. Lastly, we show that in HER2(+) breast cancer patients receiving adjuvant chemotherapy (but not targeted anti-Her2 therapy), MYC lification is associated with a poor outcome. These findings demonstrate the importance of molecular and cellular context in oncogenic transformation and acquisition of a malignant stem-like phenotype and have diagnostic and therapeutic consequences for the clinical management of HER2(+) breast cancer.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820174
Abstract: Supplementary Figure 5. Schematic of FST CRISPR KO guides and in vivo experiment. A. Binding of the two commercially available FST CRISPR guides to FST to mediate KO. B. Mice were injected with SKOV3 cells expressing FST sgRNA #2. Mice were then treated 3 times with 10mg/kg Taxol intraperitoneal Paclitaxel at days 7, 14 and 21. C Dissection of control mice presenting with multiple metastases and an FST-KO mice which showed no residual disease. White arrows point to sites of disease.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553428
Abstract: Supplementary Table 1. Primers used in this study.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820171
Abstract: Supplementary Table 1. Primers used in this study.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553428.V1
Abstract: Supplementary Table 1. Primers used in this study.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553443.V1
Abstract: Supplementary Figure 1. Histological analysis of PT340 cell line. PT340 cells were injected into NSG mice, and the resulting tumors were harvested for histological analysis, H& E staining showed features of Clear Cell Ovarian Carcinoma.
Publisher: American Association for Cancer Research (AACR)
Date: 16-02-2023
DOI: 10.1158/1078-0432.CCR-22-2254
Abstract: We recently reported that the transcription factor NFATC4, in response to chemotherapy, drives cellular quiescence to increase ovarian cancer chemoresistance. The goal of this work was to better understand the mechanisms of NFATC4-driven ovarian cancer chemoresistance. We used RNA sequencing to identify NFATC4-mediated differential gene expression. CRISPR-Cas9 and FST (follistatin)-neutralizing antibodies were used to assess impact of loss of FST function on cell proliferation and chemoresistance. ELISA was used to quantify FST induction in patient s les and in vitro in response to chemotherapy. We found that NFATC4 upregulates FST mRNA and protein expression predominantly in quiescent cells and FST is further upregulated following chemotherapy treatment. FST acts in at least a paracrine manner to induce a p-ATF2–dependent quiescent phenotype and chemoresistance in non-quiescent cells. Consistent with this, CRISPR knockout (KO) of FST in ovarian cancer cells or antibody-mediated neutralization of FST sensitizes ovarian cancer cells to chemotherapy treatment. Similarly, CRISPR KO of FST in tumors increased chemotherapy-mediated tumor eradication in an otherwise chemotherapy-resistant tumor model. Suggesting a role for FST in chemoresistance in patients, FST protein in the abdominal fluid of patients with ovarian cancer significantly increases within 24 hours of chemotherapy exposure. FST levels decline to baseline levels in patients no longer receiving chemotherapy with no evidence of disease. Furthermore, elevated FST expression in patient tumors is correlated with poor progression-free, post–progression-free, and overall survival. FST is a novel therapeutic target to improve ovarian cancer response to chemotherapy and potentially reduce recurrence rates.
Publisher: Public Library of Science (PLoS)
Date: 03-08-2010
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820177
Abstract: Supplementary Figure 4. The effect of ATF2 siRNA on gene expression and PT340 FST induced chemoresistance. A. Schematic detailing the transwell experiments. CellTrace Violet cells were sorted for rapidly iding (Dim) or quiescent cells (Bright) which were then plated in transwell chambers either as Dim:Dim or Bright:Dim. Cells were untreated or treated with taxol alone or in combination with IgG or anti-FST antibody. Cell counts were performed on the dim cells and data was expressed as fold chnage. B. Relative ATF2 gene expression of PT412 and PT340 treated with scrambled siRNA or two independent ATF2 siRNAs (ATF2 siRNA #1 and #2). C. Viable cell number of PT340 cells treated with control scrambled siRNA or knocked down with ATF2 siRNA and treated with cisplatin +/- FST. *P .05, ns = not significant.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820186.V1
Abstract: Supplementary Figure 1. Histological analysis of PT340 cell line. PT340 cells were injected into NSG mice, and the resulting tumors were harvested for histological analysis, H& E staining showed features of Clear Cell Ovarian Carcinoma.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820180.V1
Abstract: Supplementary Figure 3. The effect of FST or taxol treatment ovarian cancer proliferation and FST secretion, and the ability of a FST neutralization antibody to inhibit FST's effect on proliferation. A. PT340 and PT412 cells were treated with 200 ng/mL FST for 72h before cell counts were performed. B (i) IHC images and (ii) FST+ cell bodies in OVSAHO tumor xenografts treated with or without taxol and stained with both Ki67 (Forangi Blue) and FST (Fast Red). C. Titer of the ability of the anti-FST neutralizing antibody to inhibit the effect of FST on cell growth.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437840
Abstract: Supplementary Figure 3. The effect of FST or taxol treatment ovarian cancer proliferation and FST secretion, and the ability of a FST neutralization antibody to inhibit FST's effect on proliferation. A. PT340 and PT412 cells were treated with 200 ng/mL FST for 72h before cell counts were performed. B (i) IHC images and (ii) FST+ cell bodies in OVSAHO tumor xenografts treated with or without taxol and stained with both Ki67 (Forangi Blue) and FST (Fast Red). C. Titer of the ability of the anti-FST neutralizing antibody to inhibit the effect of FST on cell growth.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553440
Abstract: Supplementary Figure 2. RNA-seq analysis. A. Schematic of the RNA-seq experimental design. B. Waterfall plot of RNA-seq data showing the 141 genes which were DE at all time points compared to luciferase control in HEY1 and SKOV3 cell lines. C. Unsupervised clustering analysis of the 141 DE genes. D. Box plots demonstrating MYC expression following NFATC4 activation. E. STRING analysis of the 141 DE genes.
Publisher: Frontiers Media SA
Date: 12-06-2014
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553443
Abstract: Supplementary Figure 1. Histological analysis of PT340 cell line. PT340 cells were injected into NSG mice, and the resulting tumors were harvested for histological analysis, H& E staining showed features of Clear Cell Ovarian Carcinoma.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553434.V1
Abstract: Supplementary Figure 4. The effect of ATF2 siRNA on gene expression and PT340 FST induced chemoresistance. A. Schematic detailing the transwell experiments. CellTrace Violet cells were sorted for rapidly iding (Dim) or quiescent cells (Bright) which were then plated in transwell chambers either as Dim:Dim or Bright:Dim. Cells were untreated or treated with taxol alone or in combination with IgG or anti-FST antibody. Cell counts were performed on the dim cells and data was expressed as fold chnage. B. Relative ATF2 gene expression of PT412 and PT340 treated with scrambled siRNA or two independent ATF2 siRNAs (ATF2 siRNA #1 and #2). C. Viable cell number of PT340 cells treated with control scrambled siRNA or knocked down with ATF2 siRNA and treated with cisplatin +/- FST. *P .05, ns = not significant.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553440.V1
Abstract: Supplementary Figure 2. RNA-seq analysis. A. Schematic of the RNA-seq experimental design. B. Waterfall plot of RNA-seq data showing the 141 genes which were DE at all time points compared to luciferase control in HEY1 and SKOV3 cell lines. C. Unsupervised clustering analysis of the 141 DE genes. D. Box plots demonstrating MYC expression following NFATC4 activation. E. STRING analysis of the 141 DE genes.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820180
Abstract: Supplementary Figure 3. The effect of FST or taxol treatment ovarian cancer proliferation and FST secretion, and the ability of a FST neutralization antibody to inhibit FST's effect on proliferation. A. PT340 and PT412 cells were treated with 200 ng/mL FST for 72h before cell counts were performed. B (i) IHC images and (ii) FST+ cell bodies in OVSAHO tumor xenografts treated with or without taxol and stained with both Ki67 (Forangi Blue) and FST (Fast Red). C. Titer of the ability of the anti-FST neutralizing antibody to inhibit the effect of FST on cell growth.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437837.V1
Abstract: Supplementary Figure 4. The effect of ATF2 siRNA on gene expression and PT340 FST induced chemoresistance. A. Schematic detailing the transwell experiments. CellTrace Violet cells were sorted for rapidly iding (Dim) or quiescent cells (Bright) which were then plated in transwell chambers either as Dim:Dim or Bright:Dim. Cells were untreated or treated with taxol alone or in combination with IgG or anti-FST antibody. Cell counts were performed on the dim cells and data was expressed as fold chnage. B. Relative ATF2 gene expression of PT412 and PT340 treated with scrambled siRNA or two independent ATF2 siRNAs (ATF2 siRNA #1 and #2). C. Viable cell number of PT340 cells treated with control scrambled siRNA or knocked down with ATF2 siRNA and treated with cisplatin +/- FST. *P .05, ns = not significant.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820174.V1
Abstract: Supplementary Figure 5. Schematic of FST CRISPR KO guides and in vivo experiment. A. Binding of the two commercially available FST CRISPR guides to FST to mediate KO. B. Mice were injected with SKOV3 cells expressing FST sgRNA #2. Mice were then treated 3 times with 10mg/kg Taxol intraperitoneal Paclitaxel at days 7, 14 and 21. C Dissection of control mice presenting with multiple metastases and an FST-KO mice which showed no residual disease. White arrows point to sites of disease.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437831
Abstract: Supplementary Table 1. Primers used in this study.
Publisher: Elsevier BV
Date: 2018
DOI: 10.1016/J.YGYNO.2017.11.005
Abstract: The most widely used approach for the clinical management of women with high-grade serous ovarian cancer (HGSOC) is surgery, followed by platinum and taxane based chemotherapy. The degree of macroscopic disease remaining at the conclusion of surgery is a key prognostic factor determining progression free and overall survival. We sought to develop a non-invasive test to assist surgeons to determine the likelihood of achieving complete surgical resection. This knowledge could be used to plan surgical approaches for optimal clinical management. We profiled 170 serum microRNAs (miRNAs) using the Serum/Plasma Focus miRNA PCR panel containing locked nucleic acid (LNA) primers (Exiqon) in women with HGSOC (N=56) and age-matched healthy volunteers (N=30). Additionally, we measured serum CA-125 levels in the same s les. The HGSOC cohort was further classified based on the degree of macroscopic disease at the conclusion of surgery. Stepwise logistic regression was used to identify predictive markers. We identified a combination of miR-375 and CA-125 as the strongest discriminator of healthy versus HGSOC serum, with an area under the curve (AUC) of 0.956. The inclusion of miR-210 increased the AUC to 0.984 however, miR-210 was affected by hemolysis. The combination of miR-34a-5p and CA-125 was the strongest predictor of completeness of surgical resection with an AUC of 0.818. A molecular test incorporating circulating miRNA to predict completeness of surgical resection for women with HGSOC has the potential to contribute to planning for optimal patient management, ultimately improving patient outcome.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437843.V1
Abstract: Supplementary Figure 2. RNA-seq analysis. A. Schematic of the RNA-seq experimental design. B. Waterfall plot of RNA-seq data showing the 141 genes which were DE at all time points compared to luciferase control in HEY1 and SKOV3 cell lines. C. Unsupervised clustering analysis of the 141 DE genes. D. Box plots demonstrating MYC expression following NFATC4 activation. E. STRING analysis of the 141 DE genes.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437834
Abstract: Supplementary Figure 5. Schematic of FST CRISPR KO guides and in vivo experiment. A. Binding of the two commercially available FST CRISPR guides to FST to mediate KO. B. Mice were injected with SKOV3 cells expressing FST sgRNA #2. Mice were then treated 3 times with 10mg/kg Taxol intraperitoneal Paclitaxel at days 7, 14 and 21. C Dissection of control mice presenting with multiple metastases and an FST-KO mice which showed no residual disease. White arrows point to sites of disease.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437837
Abstract: Supplementary Figure 4. The effect of ATF2 siRNA on gene expression and PT340 FST induced chemoresistance. A. Schematic detailing the transwell experiments. CellTrace Violet cells were sorted for rapidly iding (Dim) or quiescent cells (Bright) which were then plated in transwell chambers either as Dim:Dim or Bright:Dim. Cells were untreated or treated with taxol alone or in combination with IgG or anti-FST antibody. Cell counts were performed on the dim cells and data was expressed as fold chnage. B. Relative ATF2 gene expression of PT412 and PT340 treated with scrambled siRNA or two independent ATF2 siRNAs (ATF2 siRNA #1 and #2). C. Viable cell number of PT340 cells treated with control scrambled siRNA or knocked down with ATF2 siRNA and treated with cisplatin +/- FST. *P .05, ns = not significant.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/1078-0432.22553437
Abstract: Supplementary Figure 3. The effect of FST or taxol treatment ovarian cancer proliferation and FST secretion, and the ability of a FST neutralization antibody to inhibit FST's effect on proliferation. A. PT340 and PT412 cells were treated with 200 ng/mL FST for 72h before cell counts were performed. B (i) IHC images and (ii) FST+ cell bodies in OVSAHO tumor xenografts treated with or without taxol and stained with both Ki67 (Forangi Blue) and FST (Fast Red). C. Titer of the ability of the anti-FST neutralizing antibody to inhibit the effect of FST on cell growth.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820183
Abstract: Supplementary Figure 2. RNA-seq analysis. A. Schematic of the RNA-seq experimental design. B. Waterfall plot of RNA-seq data showing the 141 genes which were DE at all time points compared to luciferase control in HEY1 and SKOV3 cell lines. C. Unsupervised clustering analysis of the 141 DE genes. D. Box plots demonstrating MYC expression following NFATC4 activation. E. STRING analysis of the 141 DE genes.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/1078-0432.22437831.V1
Abstract: Supplementary Table 1. Primers used in this study.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820183.V1
Abstract: Supplementary Figure 2. RNA-seq analysis. A. Schematic of the RNA-seq experimental design. B. Waterfall plot of RNA-seq data showing the 141 genes which were DE at all time points compared to luciferase control in HEY1 and SKOV3 cell lines. C. Unsupervised clustering analysis of the 141 DE genes. D. Box plots demonstrating MYC expression following NFATC4 activation. E. STRING analysis of the 141 DE genes.
Publisher: American Association for Cancer Research (AACR)
Date: 15-05-2023
DOI: 10.1158/1078-0432.22820186
Abstract: Supplementary Figure 1. Histological analysis of PT340 cell line. PT340 cells were injected into NSG mice, and the resulting tumors were harvested for histological analysis, H& E staining showed features of Clear Cell Ovarian Carcinoma.
No related grants have been discovered for Jaynish Shah.