ORCID Profile
0000-0001-5093-5945
Current Organisations
Universiteit Utrecht
,
Nederlands Kanker Instituut - Antoni van Leeuwenhoek Ziekenhuis
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Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.C.6489283.V2
Abstract: Abstract The response rates upon neoadjuvant immune checkpoint blockade (ICB) in stage III melanoma are higher as compared to stage IV disease. Given that successful ICB depends on systemic immune response, we hypothesized that systemic immune suppression might be a mechanism responsible for lower response rates in late-stage disease, and also potentially with disease recurrence in early-stage disease. Plasma and serum s les of cohorts of melanoma patients were analyzed for circulating proteins using mass spectrometry proteomic profiling and Olink proteomic assay. A cohort of paired s les of patients with stage III that progressed to stage IV disease (n=64) was used to identify markers associated with higher tumor burden. Baseline patient s les from the OpACIN-neo study (n=83) and PRADO study (n=49 NCT02977052) were used as two independent cohorts to analyze whether the potential identified markers are also associated with disease recurrence after neoadjuvant ICB therapy. When comparing baseline proteins overlapping between patients with progressive disease and patients with recurrent disease, we found leucine-rich alpha-2-glycoprotein 1 (LRG1) to be associated with worse prognosis. Especially non-responder patients to neoadjuvant ICB (OpACIN-neo) with high LRG1 expression had a poor outcome with an estimated 36-month event-free survival of 14% as compared to 83% for non-responders with a low LRG1 expression (P = 0.014). This finding was validated in an independent cohort (P = 0.0021). LRG1 can be used as a biomarker to identify patients with high risk for disease progression and recurrence, and might be a target to be combined with neoadjuvant ICB. /
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665684.V1
Abstract: Table S3 shows the patient characteristics PRADO
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.C.6489283.V1
Abstract: Abstract The response rates upon neoadjuvant immune checkpoint blockade (ICB) in stage III melanoma are higher as compared to stage IV disease. Given that successful ICB depends on systemic immune response, we hypothesized that systemic immune suppression might be a mechanism responsible for lower response rates in late-stage disease, and also potentially with disease recurrence in early-stage disease. Plasma and serum s les of cohorts of melanoma patients were analyzed for circulating proteins using mass spectrometry proteomic profiling and Olink proteomic assay. A cohort of paired s les of patients with stage III that progressed to stage IV disease (n=64) was used to identify markers associated with higher tumor burden. Baseline patient s les from the OpACIN-neo study (n=83) and PRADO study (n=49 NCT02977052) were used as two independent cohorts to analyze whether the potential identified markers are also associated with disease recurrence after neoadjuvant ICB therapy. When comparing baseline proteins overlapping between patients with progressive disease and patients with recurrent disease, we found leucine-rich alpha-2-glycoprotein 1 (LRG1) to be associated with worse prognosis. Especially non-responder patients to neoadjuvant ICB (OpACIN-neo) with high LRG1 expression had a poor outcome with an estimated 36-month event-free survival of 14% as compared to 83% for non-responders with a low LRG1 expression (P = 0.014). This finding was validated in an independent cohort (P = 0.0021). LRG1 can be used as a biomarker to identify patients with high risk for disease progression and recurrence, and might be a target to be combined with neoadjuvant ICB. /
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665708
Abstract: Figure S1 shows a flowchart of patients OpACIN-neo study
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348738.V1
Abstract: Figure S4 shows the serum analysis using Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348744.V1
Abstract: Figure S2 shows a flowchart of patients PRADO study
Publisher: American Chemical Society (ACS)
Date: 02-12-2016
DOI: 10.1021/ACS.JPROTEOME.6B00825
Abstract: A key step in shotgun proteomics is the digestion of proteins into peptides amenable for mass spectrometry. Tryptic peptides can be readily sequenced and identified by collision-induced dissociation (CID) or higher-energy collisional dissociation (HCD) because the fragmentation rules are well-understood. Here, we investigate LysargiNase, a perfect trypsin mirror protease, because it cleaves equally specific at arginine and lysine residues, albeit at the N-terminal end. LysargiNase peptides are therefore practically tryptic-like in length and sequence except that following ESI, the two protons are now both positioned at the N-terminus. Here, we compare side-by-side the chromatographic separation properties, gas-phase fragmentation characteristics, and (phospho)proteome sequence coverage of tryptic (i.e., (X)
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546867
Abstract: Table S3 shows the patient characteristics PRADO
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546888.V1
Abstract: Figure S2 shows a flowchart of patients PRADO study
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665702.V1
Abstract: Figure S3 shows that SAA1, CRP and LDHB are associated with melanoma disease progression.
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348744
Abstract: Figure S2 shows a flowchart of patients PRADO study
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2159-8290.C.6549566.V1
Abstract: Abstract In prostate cancer, androgen receptor (AR)–targeting agents are very effective in various disease stages. However, therapy resistance inevitably occurs, and little is known about how tumor cells adapt to bypass AR suppression. Here, we performed integrative multiomics analyses on tissues isolated before and after 3 months of AR-targeting enzalutamide monotherapy from patients with high-risk prostate cancer enrolled in a neoadjuvant clinical trial. Transcriptomic analyses demonstrated that AR inhibition drove tumors toward a neuroendocrine-like disease state. Additionally, epigenomic profiling revealed massive enzalutamide-induced reprogramming of pioneer factor FOXA1 from inactive chromatin sites toward active i cis /i -regulatory elements that dictate prosurvival signals. Notably, treatment-induced FOXA1 sites were enriched for the circadian clock component ARNTL. Posttreatment ARNTL levels were associated with patients’ clinical outcomes, and ARNTL knockout strongly decreased prostate cancer cell growth. Our data highlight a remarkable cistromic plasticity of FOXA1 following AR-targeted therapy and revealed an acquired dependency on the circadian regulator ARNTL, a novel candidate therapeutic target. Significance: Understanding how prostate cancers adapt to AR-targeted interventions is critical for identifying novel drug targets to improve the clinical management of treatment-resistant disease. Our study revealed an enzalutamide-induced epigenomic plasticity toward prosurvival signaling and uncovered the circadian regulator ARNTL as an acquired vulnerability after AR inhibition, presenting a novel lead for therapeutic development. i a href="ancerdiscovery/article/doi/10.1158/2159-8290.CD-22-0702" target="_blank" See related commentary by Zhang et al., p. 2017 /a . /i i a href="ancerdiscovery/article/doi/10.1158/2159-8290.CD-12-9-ITI" target="_blank" This article is highlighted in the In This Issue feature, p. 2007 /a /i /
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348747
Abstract: Figure S1 shows a flowchart of patients OpACIN-neo study
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665705
Abstract: Figure S2 shows a flowchart of patients PRADO study
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348741
Abstract: Figure S3 shows that SAA1, CRP and LDHB are associated with melanoma disease progression.
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348747.V1
Abstract: Figure S1 shows a flowchart of patients OpACIN-neo study
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665702
Abstract: Figure S3 shows that SAA1, CRP and LDHB are associated with melanoma disease progression.
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665690.V1
Abstract: Table S1 shows an overview evaluated immuno-oncology markers by Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.C.6489283.V3
Abstract: The response rates upon neoadjuvant immune checkpoint blockade (ICB) in stage III melanoma are higher as compared with stage IV disease. Given that successful ICB depends on systemic immune response, we hypothesized that systemic immune suppression might be a mechanism responsible for lower response rates in late-stage disease, and also potentially with disease recurrence in early-stage disease. Plasma and serum s les of cohorts of patients with melanoma were analyzed for circulating proteins using mass spectrometry proteomic profiling and Olink proteomic assay. A cohort of paired s les of patients with stage III that progressed to stage IV disease ( i n /i = 64) was used to identify markers associated with higher tumor burden. Baseline patient s les from the OpACIN-neo study ( i n /i = 83) and PRADO study ( i n /i = 49 NCT02977052) were used as two independent cohorts to analyze whether the potential identified markers are also associated with disease recurrence after neoadjuvant ICB therapy. When comparing baseline proteins overlapping between patients with progressive disease and patients with recurrent disease, we found leucine-rich alpha-2-glycoprotein 1 (LRG1) to be associated with worse prognosis. Especially nonresponder patients to neoadjuvant ICB (OpACIN-neo) with high LRG1 expression had a poor outcome with an estimated 36-month event-free survival of 14% as compared with 83% for nonresponders with a low LRG1 expression ( i P /i = 0.014). This finding was validated in an independent cohort ( i P /i = 0.0021). LRG1 can be used as a biomarker to identify patients with high risk for disease progression and recurrence, and might be a target to be combined with neoadjuvant ICB. Significance: LRG1 could serve as a potential target and as a biomarker to identify patients with high risk for disease recurrence, and consequently benefit from additional therapies and intensive follow-up. /
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348741.V1
Abstract: Figure S3 shows that SAA1, CRP and LDHB are associated with melanoma disease progression.
Publisher: Springer Science and Business Media LLC
Date: 28-08-2015
DOI: 10.1038/SREP13592
Abstract: Degradation of plant biomass to fermentable sugars is of critical importance for the use of plant materials for biofuels. Filamentous fungi are ubiquitous organisms and major plant biomass degraders. Single colonies of some fungal species can colonize massive areas as large as five soccer stadia. During growth, the mycelium encounters heterogeneous carbon sources. Here we assessed whether substrate heterogeneity is a major determinant of spatial gene expression in colonies of Aspergillus niger . We analyzed whole-genome gene expression in five concentric zones of 5-day-old colonies utilizing sugar beet pulp as a complex carbon source. Growth, protein production and secretion occurred throughout the colony. Genes involved in carbon catabolism were expressed uniformly from the centre to the periphery whereas genes encoding plant biomass degrading enzymes and nitrate utilization were expressed differentially across the colony. A combined adaptive response of carbon-catabolism and enzyme production to locally available monosaccharides was observed. Finally, our results demonstrate that A. niger employs different enzymatic tools to adapt its metabolism as it colonizes complex environments.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546873.V1
Abstract: Table S1 shows an overview evaluated immuno-oncology markers by Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665687.V1
Abstract: Table S2 shows the patient characteristics OpACIN-neo
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546891
Abstract: Figure S1 shows a flowchart of patients OpACIN-neo study
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.C.6489283
Abstract: The response rates upon neoadjuvant immune checkpoint blockade (ICB) in stage III melanoma are higher as compared with stage IV disease. Given that successful ICB depends on systemic immune response, we hypothesized that systemic immune suppression might be a mechanism responsible for lower response rates in late-stage disease, and also potentially with disease recurrence in early-stage disease. Plasma and serum s les of cohorts of patients with melanoma were analyzed for circulating proteins using mass spectrometry proteomic profiling and Olink proteomic assay. A cohort of paired s les of patients with stage III that progressed to stage IV disease ( i n /i = 64) was used to identify markers associated with higher tumor burden. Baseline patient s les from the OpACIN-neo study ( i n /i = 83) and PRADO study ( i n /i = 49 NCT02977052) were used as two independent cohorts to analyze whether the potential identified markers are also associated with disease recurrence after neoadjuvant ICB therapy. When comparing baseline proteins overlapping between patients with progressive disease and patients with recurrent disease, we found leucine-rich alpha-2-glycoprotein 1 (LRG1) to be associated with worse prognosis. Especially nonresponder patients to neoadjuvant ICB (OpACIN-neo) with high LRG1 expression had a poor outcome with an estimated 36-month event-free survival of 14% as compared with 83% for nonresponders with a low LRG1 expression ( i P /i = 0.014). This finding was validated in an independent cohort ( i P /i = 0.0021). LRG1 can be used as a biomarker to identify patients with high risk for disease progression and recurrence, and might be a target to be combined with neoadjuvant ICB. Significance: LRG1 could serve as a potential target and as a biomarker to identify patients with high risk for disease recurrence, and consequently benefit from additional therapies and intensive follow-up. /
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2159-8290.22541192.V1
Abstract: Supplementary Figure from Drug-Induced Epigenomic Plasticity Reprograms Circadian Rhythm Regulation to Drive Prostate Cancer toward Androgen Independence
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2159-8290.22541195
Abstract: Supplementary Data from Drug-Induced Epigenomic Plasticity Reprograms Circadian Rhythm Regulation to Drive Prostate Cancer toward Androgen Independence
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348738
Abstract: Figure S4 shows the serum analysis using Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665696
Abstract: Figure S5 shows that complement factor B (CFB), component 7 (C7) and alpha-1B-glycoportein (A1BG) expression are increased upon melanoma progression and recurrence.
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665705.V1
Abstract: Figure S2 shows a flowchart of patients PRADO study
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665693.V1
Abstract: Figure S6 shows that neutrophil count and neutrophil-to-lymphocyte ratio (NLR) are not associated with recurrence in non-responding patients
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2159-8290.22541192
Abstract: Supplementary Figure from Drug-Induced Epigenomic Plasticity Reprograms Circadian Rhythm Regulation to Drive Prostate Cancer toward Androgen Independence
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2159-8290.22541195.V1
Abstract: Supplementary Data from Drug-Induced Epigenomic Plasticity Reprograms Circadian Rhythm Regulation to Drive Prostate Cancer toward Androgen Independence
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665693
Abstract: Figure S6 shows that neutrophil count and neutrophil-to-lymphocyte ratio (NLR) are not associated with recurrence in non-responding patients
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348735
Abstract: Figure S5 shows that complement factor B (CFB), component 7 (C7) and alpha-1B-glycoportein (A1BG) expression are increased upon melanoma progression and recurrence.
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665690
Abstract: Table S1 shows an overview evaluated immuno-oncology markers by Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348732
Abstract: Figure S6 shows that neutrophil count and neutrophil-to-lymphocyte ratio (NLR) are not associated with recurrence in non-responding patients
Publisher: EMBO
Date: 30-10-2023
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665699
Abstract: Figure S4 shows the serum analysis using Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546885
Abstract: Figure S3 shows that SAA1, CRP and LDHB are associated with melanoma disease progression.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546876.V1
Abstract: Figure S6 shows that neutrophil count and neutrophil-to-lymphocyte ratio (NLR) are not associated with recurrence in non-responding patients
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546882
Abstract: Figure S4 shows the serum analysis using Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546882.V1
Abstract: Figure S4 shows the serum analysis using Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348723.V1
Abstract: Table S3 shows the patient characteristics PRADO
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.CRC-23-0015
Abstract: The response rates upon neoadjuvant immune checkpoint blockade (ICB) in stage III melanoma are higher as compared with stage IV disease. Given that successful ICB depends on systemic immune response, we hypothesized that systemic immune suppression might be a mechanism responsible for lower response rates in late-stage disease, and also potentially with disease recurrence in early-stage disease. Plasma and serum s les of cohorts of patients with melanoma were analyzed for circulating proteins using mass spectrometry proteomic profiling and Olink proteomic assay. A cohort of paired s les of patients with stage III that progressed to stage IV disease (n = 64) was used to identify markers associated with higher tumor burden. Baseline patient s les from the OpACIN-neo study (n = 83) and PRADO study (n = 49 NCT02977052) were used as two independent cohorts to analyze whether the potential identified markers are also associated with disease recurrence after neoadjuvant ICB therapy. When comparing baseline proteins overlapping between patients with progressive disease and patients with recurrent disease, we found leucine-rich alpha-2-glycoprotein 1 (LRG1) to be associated with worse prognosis. Especially nonresponder patients to neoadjuvant ICB (OpACIN-neo) with high LRG1 expression had a poor outcome with an estimated 36-month event-free survival of 14% as compared with 83% for nonresponders with a low LRG1 expression (P = 0.014). This finding was validated in an independent cohort (P = 0.0021). LRG1 can be used as a biomarker to identify patients with high risk for disease progression and recurrence, and might be a target to be combined with neoadjuvant ICB. LRG1 could serve as a potential target and as a biomarker to identify patients with high risk for disease recurrence, and consequently benefit from additional therapies and intensive follow-up.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546888
Abstract: Figure S2 shows a flowchart of patients PRADO study
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348726
Abstract: Table S2 shows the patient characteristics OpACIN-neo
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665684
Abstract: Table S3 shows the patient characteristics PRADO
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348729
Abstract: Table S1 shows an overview evaluated immuno-oncology markers by Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348723
Abstract: Table S3 shows the patient characteristics PRADO
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665696.V1
Abstract: Figure S5 shows that complement factor B (CFB), component 7 (C7) and alpha-1B-glycoportein (A1BG) expression are increased upon melanoma progression and recurrence.
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348726.V1
Abstract: Table S2 shows the patient characteristics OpACIN-neo
Publisher: American Association for Cancer Research (AACR)
Date: 27-06-2022
DOI: 10.1158/2159-8290.CD-21-0576
Abstract: Understanding how prostate cancers adapt to AR-targeted interventions is critical for identifying novel drug targets to improve the clinical management of treatment-resistant disease. Our study revealed an enzalutamide-induced epigenomic plasticity toward prosurvival signaling and uncovered the circadian regulator ARNTL as an acquired vulnerability after AR inhibition, presenting a novel lead for therapeutic development. See related commentary by Zhang et al., p. 2017. This article is highlighted in the In This Issue feature, p. 2007
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665708.V1
Abstract: Figure S1 shows a flowchart of patients OpACIN-neo study
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546879.V1
Abstract: Figure S5 shows that complement factor B (CFB), component 7 (C7) and alpha-1B-glycoportein (A1BG) expression are increased upon melanoma progression and recurrence.
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665687
Abstract: Table S2 shows the patient characteristics OpACIN-neo
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2159-8290.C.6549566
Abstract: Abstract In prostate cancer, androgen receptor (AR)–targeting agents are very effective in various disease stages. However, therapy resistance inevitably occurs, and little is known about how tumor cells adapt to bypass AR suppression. Here, we performed integrative multiomics analyses on tissues isolated before and after 3 months of AR-targeting enzalutamide monotherapy from patients with high-risk prostate cancer enrolled in a neoadjuvant clinical trial. Transcriptomic analyses demonstrated that AR inhibition drove tumors toward a neuroendocrine-like disease state. Additionally, epigenomic profiling revealed massive enzalutamide-induced reprogramming of pioneer factor FOXA1 from inactive chromatin sites toward active i cis /i -regulatory elements that dictate prosurvival signals. Notably, treatment-induced FOXA1 sites were enriched for the circadian clock component ARNTL. Posttreatment ARNTL levels were associated with patients’ clinical outcomes, and ARNTL knockout strongly decreased prostate cancer cell growth. Our data highlight a remarkable cistromic plasticity of FOXA1 following AR-targeted therapy and revealed an acquired dependency on the circadian regulator ARNTL, a novel candidate therapeutic target. Significance: Understanding how prostate cancers adapt to AR-targeted interventions is critical for identifying novel drug targets to improve the clinical management of treatment-resistant disease. Our study revealed an enzalutamide-induced epigenomic plasticity toward prosurvival signaling and uncovered the circadian regulator ARNTL as an acquired vulnerability after AR inhibition, presenting a novel lead for therapeutic development. i a href="ancerdiscovery/article/doi/10.1158/2159-8290.CD-22-0702" target="_blank" See related commentary by Zhang et al., p. 2017 /a . /i i a href="ancerdiscovery/article/doi/10.1158/2159-8290.CD-12-9-ITI" target="_blank" This article is highlighted in the In This Issue feature, p. 2007 /a /i /
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546873
Abstract: Table S1 shows an overview evaluated immuno-oncology markers by Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546870
Abstract: Table S2 shows the patient characteristics OpACIN-neo
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348735.V1
Abstract: Figure S5 shows that complement factor B (CFB), component 7 (C7) and alpha-1B-glycoportein (A1BG) expression are increased upon melanoma progression and recurrence.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546867.V1
Abstract: Table S3 shows the patient characteristics PRADO
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546879
Abstract: Figure S5 shows that complement factor B (CFB), component 7 (C7) and alpha-1B-glycoportein (A1BG) expression are increased upon melanoma progression and recurrence.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546876
Abstract: Figure S6 shows that neutrophil count and neutrophil-to-lymphocyte ratio (NLR) are not associated with recurrence in non-responding patients
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546885.V1
Abstract: Figure S3 shows that SAA1, CRP and LDHB are associated with melanoma disease progression.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546891.V1
Abstract: Figure S1 shows a flowchart of patients OpACIN-neo study
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348732.V1
Abstract: Figure S6 shows that neutrophil count and neutrophil-to-lymphocyte ratio (NLR) are not associated with recurrence in non-responding patients
Publisher: American Association for Cancer Research (AACR)
Date: 20-04-2023
DOI: 10.1158/2767-9764.22665699.V1
Abstract: Figure S4 shows the serum analysis using Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 28-03-2023
DOI: 10.1158/2767-9764.22348729.V1
Abstract: Table S1 shows an overview evaluated immuno-oncology markers by Olink proteomic assay
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2767-9764.22546870.V1
Abstract: Table S2 shows the patient characteristics OpACIN-neo
Publisher: Wiley
Date: 2015
DOI: 10.3402/JEV.V4.27783
Location: Netherlands
No related grants have been discovered for Maarten Altelaar.