ORCID Profile
0000-0002-7968-4032
Current Organisations
International Centre for Theoretical Sciences
,
University of Adelaide
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Publisher: American Association for Cancer Research (AACR)
Date: 12-2020
DOI: 10.1158/1940-6207.CAPR-20-0186
Abstract: Chemoprevention trials for prostate cancer by androgen receptor or androgen synthesis inhibition have proven ineffective. Recently, it has been demonstrated that the histone methlytransferase, EZH2 is deregulated in mouse and human high-grade prostatic intraepithelial neoplasia (HG-PIN). Using preclinical mouse and human models of prostate cancer, we demonstrate that genetic and chemical disruption of EZH2 expression and catalytic activity reversed the HG-PIN phenotype. Furthermore, inhibition of EZH2 function was associated with loss of cellular proliferation and induction of Tp53-dependent senescence. Together, these data provide provocative evidence for EZH2 as an actionable therapeutic target toward prevention of prostate cancer.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.C.6544955.V1
Abstract: Abstract NF-κB activation has been linked to prostate cancer progression and is commonly observed in castrate-resistant disease. It has been suggested that NF-κB–driven resistance to androgen-deprivation therapy (ADT) in prostate cancer cells may be mediated by aberrant androgen receptor (AR) activation and AR splice variant production. Preventing resistance to ADT may therefore be achieved by using NF-κB inhibitors. However, low oral bioavailability and high toxicity of NF-κB inhibitors is a major challenge for clinical translation. Dimethylaminoparthenolide (DMAPT) is an oral NF-κB inhibitor in clinical development and has already shown favorable pharmacokinetic and pharmacodyanamic data in patients with heme malignancies, including decrease of NF-κB in circulating leuchemic blasts. Here, we report that activation of NF-κB 65 by castration in mouse and human prostate cancer models resulted in a significant increase in AR variant-7 (AR-V7) expression and modest upregulation of AR. i In vivo /i castration of VCaP-CR tumors resulted in significant upregulation of phosphorylated-p65 and AR-V7, which was attenuated by combination with DMAPT and DMAPT increased the efficacy of AR inhibition. We further demonstrate that the effects of DMAPT-sensitizing prostate cancer cells to castration were dependent on the ability of DMAPT to inhibit phosphorylated-p65 function. Implications: Our study shows that DMAPT, an oral NF-κB inhibitor in clinical development, inhibits phosphorylated-p65 upregulation of AR-V7 and delays prostate cancer castration resistance. This provides rationale for the development of DMAPT as a novel therapeutic strategy to increase durable response in patients receiving AR-targeted therapy. /
Publisher: Cold Spring Harbor Laboratory
Date: 05-08-2022
DOI: 10.1101/2022.08.05.500896
Abstract: Phenotypic plasticity is a hallmark of cancer and increasingly realized as a mechanism of resistance in androgen indifferent prostate tumors. It is critical to identify mechanisms and actionable targets driving phenotypic plasticity. Here, we report that loss of tristetraprolin (TTP, gene ZFP36 ), an RNA binding protein that regulates mRNA stability increases NF-κB activation and is associated with higher rates of aggressive disease and early recurrence in primary prostate cancer (PCa). We examined the clinical and biological impact of ZFP36 loss combined with PTEN loss, a known driver of PCa. Combined loss of PTEN and ZFP36 expression was associated with increased risk of recurrence in multiple independent primary PCa cohorts, and significantly reduced overall survival and time to progression following castration in genetically engineered mouse models. ZFP36 loss alters the cell state that is driven by PTEN loss, demonstrated by positive enrichment of gene sets including EMT, inflammation, TNFα/NF-κB, IL6-JAK/STAT3. ZFP36 loss also induces enrichment of multiple gene sets involved in cell migration, chemotaxis, and proliferation. Use of the NF-κB inhibitor dimethylaminoparthenolide induced significant therapeutic responses in tumors with PTEN and ZFP36 co-loss and reversed castration resistance. This work identifies a novel molecular mechanism driving phenotypic plasticity and castration resistance through loss of ZFP36 expression, that can be reversed by inhibition of NF-κB activity.
Publisher: Radiation Research Society
Date: 05-01-2014
DOI: 10.1667/RR13460.1
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.C.6541423.V1
Abstract: Abstract The increased treatment of metastatic castration-resistant prostate cancer (mCRPC) with second-generation antiandrogen therapies (ADT) has coincided with a greater incidence of lethal, aggressive variant prostate cancer (AVPC) tumors that have lost dependence on androgen receptor (AR) signaling. These AR-independent tumors may also transdifferentiate to express neuroendocrine lineage markers and are termed neuroendocrine prostate cancer (NEPC). Recent evidence suggests kinase signaling may be an important driver of NEPC. To identify targetable kinases in NEPC, we performed global phosphoproteomics comparing several AR-independent to AR-dependent prostate cancer cell lines and identified multiple altered signaling pathways, including enrichment of RET kinase activity in the AR-independent cell lines. Clinical NEPC patient s les and NEPC patient-derived xenografts displayed upregulated RET transcript and RET pathway activity. Genetic knockdown or pharmacologic inhibition of RET kinase in multiple mouse and human models of NEPC dramatically reduced tumor growth and decreased cell viability. Our results suggest that targeting RET in NEPC tumors with high RET expression could be an effective treatment option. Currently, there are limited treatment options for patients with aggressive neuroendocrine prostate cancer and none are curative. Implications: Identification of aberrantly expressed RET kinase as a driver of tumor growth in multiple models of NEPC provides a significant rationale for testing the clinical application of RET inhibitors in patients with AVPC. /
Publisher: Public Library of Science (PLoS)
Date: 27-03-2014
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1940-6207.22534898.V1
Abstract: Supplementary Data
Publisher: Springer International Publishing
Date: 2019
DOI: 10.1007/978-3-030-32656-2_13
Abstract: The RB tumor suppressor is one of the most commonly deleted/mutated genes in human cancers. In prostate cancer specifically, mutation of RB is most frequently observed in aggressive, metastatic disease. As one of the earliest tumor suppressors to be identified, the molecular functions of RB that are lost in tumor development have been studied for decades. Earlier work focused on the canonical RB pathway connecting mitogenic signaling to the cell cycle via Cyclin/CDK inactivation of RB, thereby releasing the E2F transcription factors. More in-depth analysis revealed that RB-E2F complexes regulate cellular processes beyond proliferation. Most recently, "non-canonical" roles for RB function have been expanded beyond its E2F interactions, which may play a particular role in advanced prostate cancer. For ex le, in mouse models of prostate cancer, loss of RB has been shown to induce lineage plasticity, which enables resistance to androgen deprivation therapy. This increased understanding of the potential downstream functions of RB in prostate cancer may lead the way to identifying therapeutic vulnerabilities in cells following RB loss.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525904.V1
Abstract: List of qPCR primers.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525910.V1
Abstract: Comparison of AR-v7 and AR-FL mRNA expression in parental vs empty vector control cell lines.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525901
Abstract: List of antibodies.
Publisher: American Association for Cancer Research (AACR)
Date: 08-2020
DOI: 10.1158/1541-7786.MCR-19-1245
Abstract: Identification of aberrantly expressed RET kinase as a driver of tumor growth in multiple models of NEPC provides a significant rationale for testing the clinical application of RET inhibitors in patients with AVPC.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525904
Abstract: List of qPCR primers.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1940-6207.22534898
Abstract: Supplementary Data
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525916.V1
Abstract: In idual VCaP-CR tumor growth curves in mice treated with vehicle, DMAPT, castration or DMAPT plus castration.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22516600
Abstract: Supplemental Table 1: Known genetic mutations of genes commonly mutated in mCRPC in cell lines used in phosphoproteome analysis Supplemental Table 2: Phospho-Serine/Threonine proteome of Prostate Cancer Adenocarcinoma and Aggressive Variant Prostate Cancer Cell Lines Supplemental Table 3: Phospho-Tyrosine proteome of Prostate Cancer Adenocarcinoma and Aggressive Variant Prostate Cancer Cell Lines Supplemental Table 4: Kinase Substrate Enrichment Analysis results from phospho-serine/threonine proteome dataset Supplemental Table 5: Kinase Substrate Enrichment Analysis results from phospho-tyrosine proteome dataset Supplemental Table 6: Phospho-Serine/Threonine proteome of Adenocarcinoma or Small cell/Mixed phenotype mCRPC patient s les Supplemental Table 7. Spearman's Correlation Between the Dependency Ranks of RET and Other Genes in Prostate Cancer Cell Lines Supplemental Table 8. RET Dependency Scores of Cancer Cell Lines
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525907
Abstract: Representative images of cell death staining in 22Rv1 empty vector control and p65 overexpressing tumoroids treated +/- DMAPT and/or enzalutamide.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.C.6544955
Abstract: Abstract NF-κB activation has been linked to prostate cancer progression and is commonly observed in castrate-resistant disease. It has been suggested that NF-κB–driven resistance to androgen-deprivation therapy (ADT) in prostate cancer cells may be mediated by aberrant androgen receptor (AR) activation and AR splice variant production. Preventing resistance to ADT may therefore be achieved by using NF-κB inhibitors. However, low oral bioavailability and high toxicity of NF-κB inhibitors is a major challenge for clinical translation. Dimethylaminoparthenolide (DMAPT) is an oral NF-κB inhibitor in clinical development and has already shown favorable pharmacokinetic and pharmacodyanamic data in patients with heme malignancies, including decrease of NF-κB in circulating leuchemic blasts. Here, we report that activation of NF-κB 65 by castration in mouse and human prostate cancer models resulted in a significant increase in AR variant-7 (AR-V7) expression and modest upregulation of AR. i In vivo /i castration of VCaP-CR tumors resulted in significant upregulation of phosphorylated-p65 and AR-V7, which was attenuated by combination with DMAPT and DMAPT increased the efficacy of AR inhibition. We further demonstrate that the effects of DMAPT-sensitizing prostate cancer cells to castration were dependent on the ability of DMAPT to inhibit phosphorylated-p65 function. Implications: Our study shows that DMAPT, an oral NF-κB inhibitor in clinical development, inhibits phosphorylated-p65 upregulation of AR-V7 and delays prostate cancer castration resistance. This provides rationale for the development of DMAPT as a novel therapeutic strategy to increase durable response in patients receiving AR-targeted therapy. /
Publisher: American Association for Cancer Research (AACR)
Date: 12-2017
DOI: 10.1158/1535-7163.MCT-17-0074
Abstract: We investigated the potential of combining the hypoglycemic drug metformin (MET) and the antiepileptic drug valproic acid (VPA), which act via different biochemical pathways, to provide enhanced antitumor responses in prostate cancer. Prostate cancer cell lines (LNCaP and PC-3), normal prostate epithelial cells (PrEC), and patient-derived prostate tumor explants were treated with MET and/or VPA. Proliferation and apoptosis were assessed. The role of p53 in response to MET + VPA was assessed in cell lines using RNAi in LNCaP (p53+) and ectopic expression of p53 in PC-3 (p53−). The role of the androgen receptor (AR) was investigated using the AR antagonist enzalutamide. The combination of MET and VPA synergistically inhibited proliferation in LNCaP and PC-3, with no significant effect in PrEC. LNCaP, but not PC-3, demonstrated synergistic intrinsic apoptosis in response to MET + VPA. Knockdown of p53 in LNCaP (p53+, AR+) reduced the synergistic apoptotic response as did inhibition of AR. Ectopic expression of p53 in PC-3 (p53−, AR−) increased apoptosis in response to MET + VPA. In patient-derived prostate tumor explants, MET + VPA also induced a significant decrease in proliferation and an increase in apoptosis in tumor cells. In conclusion, we demonstrate that MET + VPA can synergistically kill more prostate cancer cells than either drug alone. The response is dependent on the presence of p53 and AR signaling, which have critical roles in prostate carcinogenesis. Further in vivo/ex vivo preclinical studies are required to determine the relative efficacy of MET + VPA as a potential treatment for prostate cancer. Mol Cancer Ther 16(12) 2689–700. ©2017 AACR.
Publisher: American Association for Cancer Research (AACR)
Date: 16-04-2021
DOI: 10.1158/1541-7786.MCR-21-0099
Abstract: Our study shows that DMAPT, an oral NF-κB inhibitor in clinical development, inhibits phosphorylated-p65 upregulation of AR-V7 and delays prostate cancer castration resistance. This provides rationale for the development of DMAPT as a novel therapeutic strategy to increase durable response in patients receiving AR-targeted therapy.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.C.6541423
Abstract: Abstract The increased treatment of metastatic castration-resistant prostate cancer (mCRPC) with second-generation antiandrogen therapies (ADT) has coincided with a greater incidence of lethal, aggressive variant prostate cancer (AVPC) tumors that have lost dependence on androgen receptor (AR) signaling. These AR-independent tumors may also transdifferentiate to express neuroendocrine lineage markers and are termed neuroendocrine prostate cancer (NEPC). Recent evidence suggests kinase signaling may be an important driver of NEPC. To identify targetable kinases in NEPC, we performed global phosphoproteomics comparing several AR-independent to AR-dependent prostate cancer cell lines and identified multiple altered signaling pathways, including enrichment of RET kinase activity in the AR-independent cell lines. Clinical NEPC patient s les and NEPC patient-derived xenografts displayed upregulated RET transcript and RET pathway activity. Genetic knockdown or pharmacologic inhibition of RET kinase in multiple mouse and human models of NEPC dramatically reduced tumor growth and decreased cell viability. Our results suggest that targeting RET in NEPC tumors with high RET expression could be an effective treatment option. Currently, there are limited treatment options for patients with aggressive neuroendocrine prostate cancer and none are curative. Implications: Identification of aberrantly expressed RET kinase as a driver of tumor growth in multiple models of NEPC provides a significant rationale for testing the clinical application of RET inhibitors in patients with AVPC. /
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1940-6207.C.6547697.V1
Abstract: Abstract Chemoprevention trials for prostate cancer by androgen receptor or androgen synthesis inhibition have proven ineffective. Recently, it has been demonstrated that the histone methlytransferase, EZH2 is deregulated in mouse and human high-grade prostatic intraepithelial neoplasia (HG-PIN). Using preclinical mouse and human models of prostate cancer, we demonstrate that genetic and chemical disruption of EZH2 expression and catalytic activity reversed the HG-PIN phenotype. Furthermore, inhibition of EZH2 function was associated with loss of cellular proliferation and induction of Tp53-dependent senescence. Together, these data provide provocative evidence for EZH2 as an actionable therapeutic target toward prevention of prostate cancer. /
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 04-2017
Publisher: Radiation Research Society
Date: 16-05-2019
DOI: 10.1667/RR15404.1
Publisher: Springer Science and Business Media LLC
Date: 23-06-2018
DOI: 10.1007/S10585-018-9915-9
Abstract: Despite advances in prostate cancer therapy, dissemination and growth of metastases results in shortened survival. Here we examined the potential anti-cancer effect of the NF-κB inhibitor parthenolide (PTL) and its water soluble analogue dimethylaminoparthenolide (DMAPT) on tumour progression and metastasis in the TRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model of prostate cancer. Six-week-old male TRAMP mice received PTL (40 mg/kg in 10% ethanol/saline), DMAPT (100 mg/kg in sterile water), or vehicle controls by oral gavage thrice weekly until palpable tumour formation. DMAPT treatment slowed normal tumour development in TRAMP mice, extending the time-to-palpable prostate tumour by 20%. PTL did not slow overall tumour development, while the ethanol/saline vehicle used to administer PTL unexpectedly induced an aggressive metastatic tumour phenotype. Chronic ethanol/saline vehicle upregulated expression of NF-κB, MMP2, integrin β1, collagen IV, and laminin, and induced vascular basement membrane degradation in primary prostate tumours, as well as increased metastatic spread to the lung and liver. All of these changes were largely prevented by co-administration with PTL. DMAPT (in water) reduced metastasis to below that of water-control. These data suggest that DMAPT has the potential to be used as a cancer preventive and anti-metastatic therapy for prostate cancer. Although low levels of ethanol consumption have not been shown to strongly correlate with prostate cancer epidemiology, these results would support a potential effect of chronic low dose ethanol on metastasis and the TRAMP model provides a useful system in which to further explore the mechanisms involved.
Publisher: Cold Spring Harbor Laboratory
Date: 08-08-2019
DOI: 10.1101/730135
Abstract: Prostate cancers are considered immunologically ‘cold’ tumors given the very few patients who respond to checkpoint inhibitor therapy (CPI). Recently, enrichment of interferon (IFN) response genes predicts a favorable response to CPI across various disease sites. The enhancer of zeste homolog-2 (EZH2) is over-expressed in prostate cancer and is known to negatively regulate IFN response genes. Here, we demonstrate that inhibition of EZH2 catalytic activity in prostate cancer models derepresses expression of double-strand RNA (dsRNA), associated with upregulation of genes involved in antigen presentation, Th-1 chemokine signaling, and interferon (IFN) response, including PD-L1. Similarly, application of a novel EZH2 derived gene signature to human prostate s le analysis indicated an inverse correlation between tumor EZH2 activity/expression with T-cell inflamed and IFN gene signatures and PD-L1 expression. EZH2 inhibition combined with PD-1 CPI significantly enhances antitumor response that is dependent on up-regulation of tumor PD-L1 expression. Further, combination therapy significantly increases intratumoral trafficking of activated CD8+ T-cells and M1 tumor associated macrophages (TAMs) with concurrent loss of M2 TAMs. Our study identifies EZH2 as a potent inhibitor of antitumor immunity and responsiveness to CPI. This data suggests EZH2 inhibition as a novel therapeutic direction to enhance prostate cancer response to PD-1 CPI.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22516606
Abstract: Supplemental Figure 1. RET expression is higher in prostate cancer lines that have lost androgen receptor signaling Supplemental Figure 2. RET gene expression is higher in patient s les with pure/mixed small cell phenotype or primary NEPC and correlates with other neuroendocrine markers. Supplemental Figure 3. Knockdown of RET kinase in PC3 cells shows a modest reduction in cellular proliferation. Supplemental Figure 4. Prostate cancer cell lines show variable sensitivity to RET inhibitor treatment. Supplemental Figure 5. Organoids derived from PTEN-/- and Rb-/- prostate cells model multiple aspects of NEPC including resistance to enzalutamide treatment. Supplemental Figure 6. A higher dose replicate of AD80 treatment of NCI-H660 xenograft tumors shows a similar effect of restricting tumor growth.
Publisher: Springer Science and Business Media LLC
Date: 22-03-2021
DOI: 10.1038/S43018-021-00185-W
Abstract: Prostate cancers are considered to be immunologically 'cold' tumors given the very few patients who respond to checkpoint inhibitor (CPI) therapy. Recently, enrichment of interferon-stimulated genes (ISGs) predicted a favorable response to CPI across various disease sites. The enhancer of zeste homolog-2 (EZH2) is overexpressed in prostate cancer and known to negatively regulate ISGs. In the present study, we demonstrate that EZH2 inhibition in prostate cancer models activates a double-stranded RNA-STING-ISG stress response upregulating genes involved in antigen presentation, Th1 chemokine signaling and interferon response, including programmed cell death protein 1 (PD-L1) that is dependent on STING activation. EZH2 inhibition substantially increased intratumoral trafficking of activated CD8
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525901.V1
Abstract: List of antibodies.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525907.V1
Abstract: Representative images of cell death staining in 22Rv1 empty vector control and p65 overexpressing tumoroids treated +/- DMAPT and/or enzalutamide.
Publisher: Cold Spring Harbor Laboratory
Date: 05-04-2021
DOI: 10.1101/2021.04.05.438428
Abstract: Cytoplasmic dynein 1 (dynein) is the primary minus end-directed motor protein in most eukaryotic cells. Dynein remains in an inactive conformation until the formation of a tripartite complex comprising dynein, its regulator dynactin and a cargo adaptor. How this process of dynein activation occurs is unclear, since it entails the formation of a three-protein complex inside the crowded environs of a cell. Here, we employed live-cell, single-molecule imaging to visualise and track fluorescently tagged dynein. First, we observed that only ~30% of dynein molecules that bound to the microtubule (MT) engaged in minus end-directed movement, and that too for a short duration of ~0.6 s. Next, using high-resolution imaging in live and fixed cells, and using correlative light and electron microscopy, we discovered that dynactin and endosomal cargo remained in proximity to each other and to MTs. We then employed two-colour imaging to visualise cargo movement effected by single motor binding. Finally, we performed long-term imaging to show short movements are sufficient to drive cargo to the perinuclear region of the cell. We then used these discoveries as the basis for a stochastic model incorporating dynamic motors binding to cargo located along MTs, and also developed a coarse-grained 3-state run- and-tumble particle (RTP) model for the cargo that quantitatively recapitulates the emergent statistics of cargo movement. Taken together, we discovered a search mechanism that is facilitated by dynein’s frequent MT binding-unbinding kinetics: (1) in a futile event when dynein does not encounter cargo anchored in proximity to the MT, dynein dissociates and diffuses into the cytoplasm, (2) when dynein encounters cargo and dynactin upon MT-binding, it moves cargo in a short run. Several of these short runs are undertaken in succession for long-range directed movement. In conclusion, we demonstrate that dynein activation and cargo capture are coupled in a step that relies on the reduction of dimensionality to enable minus end-directed transport in cellulo , and that complex cargo behaviour emerges from stochastic motor-cargo interactions.
Publisher: Radiation Research Society
Date: 05-2017
DOI: 10.1667/RR14710.1
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525910
Abstract: Comparison of AR-v7 and AR-FL mRNA expression in parental vs empty vector control cell lines.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22516606.V1
Abstract: Supplemental Figure 1. RET expression is higher in prostate cancer lines that have lost androgen receptor signaling Supplemental Figure 2. RET gene expression is higher in patient s les with pure/mixed small cell phenotype or primary NEPC and correlates with other neuroendocrine markers. Supplemental Figure 3. Knockdown of RET kinase in PC3 cells shows a modest reduction in cellular proliferation. Supplemental Figure 4. Prostate cancer cell lines show variable sensitivity to RET inhibitor treatment. Supplemental Figure 5. Organoids derived from PTEN-/- and Rb-/- prostate cells model multiple aspects of NEPC including resistance to enzalutamide treatment. Supplemental Figure 6. A higher dose replicate of AD80 treatment of NCI-H660 xenograft tumors shows a similar effect of restricting tumor growth.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525916
Abstract: In idual VCaP-CR tumor growth curves in mice treated with vehicle, DMAPT, castration or DMAPT plus castration.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525913
Abstract: Cleaved caspase-3 IHC staining and quantification in VCaP-CR tumors.
Publisher: American Chemical Society (ACS)
Date: 03-2008
DOI: 10.1021/NP700738K
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22516600.V1
Abstract: Supplemental Table 1: Known genetic mutations of genes commonly mutated in mCRPC in cell lines used in phosphoproteome analysis Supplemental Table 2: Phospho-Serine/Threonine proteome of Prostate Cancer Adenocarcinoma and Aggressive Variant Prostate Cancer Cell Lines Supplemental Table 3: Phospho-Tyrosine proteome of Prostate Cancer Adenocarcinoma and Aggressive Variant Prostate Cancer Cell Lines Supplemental Table 4: Kinase Substrate Enrichment Analysis results from phospho-serine/threonine proteome dataset Supplemental Table 5: Kinase Substrate Enrichment Analysis results from phospho-tyrosine proteome dataset Supplemental Table 6: Phospho-Serine/Threonine proteome of Adenocarcinoma or Small cell/Mixed phenotype mCRPC patient s les Supplemental Table 7. Spearman's Correlation Between the Dependency Ranks of RET and Other Genes in Prostate Cancer Cell Lines Supplemental Table 8. RET Dependency Scores of Cancer Cell Lines
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1541-7786.22525913.V1
Abstract: Cleaved caspase-3 IHC staining and quantification in VCaP-CR tumors.
Location: Germany
No related grants have been discovered for Katherine Morel.