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Article: Saracatinib synergizes with enzalutamide to downregulate androgen receptor activity in castration resistant prostate cancer.

White, Ralph E / Bannister, Maxwell / Day, Abderrahman / Bergom, Hannah E / Tan, Victor M / Hwang, Justin / Nguyen, Hai Dang / Drake, Justin M

bioRxiv : the preprint server for biology

2023

Abstract: Prostate cancer (PCa) remains the most diagnosed non-skin cancer amongst the American male population. Treatment for localized prostate cancer consists of androgen deprivation therapies (ADTs), which typically inhibit androgen production and the androgen ...

Abstract	Prostate cancer (PCa) remains the most diagnosed non-skin cancer amongst the American male population. Treatment for localized prostate cancer consists of androgen deprivation therapies (ADTs), which typically inhibit androgen production and the androgen receptor (AR). Though initially effective, a subset of patients will develop resistance to ADTs and the tumors will transition to castration-resistant prostate cancer (CRPC). Second generation hormonal therapies such as abiraterone acetate and enzalutamide are typically given to men with CRPC. However, these treatments are not curative and typically prolong survival only by a few months. Several resistance mechanisms contribute to this lack of efficacy such as the emergence of AR mutations, AR amplification, lineage plasticity, AR splice variants (AR-Vs) and increased kinase signaling. Having identified SRC kinase as a key tyrosine kinase enriched in CRPC patient tumors from our previous work, we evaluated whether inhibition of SRC kinase synergizes with enzalutamide or chemotherapy in several prostate cancer cell lines expressing variable AR isoforms. We observed robust synergy between the SRC kinase inhibitor, saracatinib, and enzalutamide, in the AR-FL+/AR-V+ CRPC cell lines, LNCaP95 and 22Rv1. We also observed that saracatinib significantly decreases AR Y
Language	English
Publishing date	2023-04-25
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.22.537922
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Article: Saracatinib synergizes with enzalutamide to downregulate AR activity in CRPC.

White, Ralph E / Bannister, Maxwell / Day, Abderrahman / Bergom, Hannah E / Tan, Victor M / Hwang, Justin / Dang Nguyen, Hai / Drake, Justin M

Frontiers in oncology

2023 Volume 13, Page(s) 1210487

Abstract	Prostate cancer (PCa) remains the most diagnosed non-skin cancer amongst the American male population. Treatment for localized prostate cancer consists of androgen deprivation therapies (ADTs), which typically inhibit androgen production and the androgen receptor (AR). Though initially effective, a subset of patients will develop resistance to ADTs and the tumors will transition to castration-resistant prostate cancer (CRPC). Second generation hormonal therapies such as abiraterone acetate and enzalutamide are typically given to men with CRPC. However, these treatments are not curative and typically prolong survival only by a few months. Several resistance mechanisms contribute to this lack of efficacy such as the emergence of AR mutations, AR amplification, lineage plasticity, AR splice variants (AR-Vs) and increased kinase signaling. Having identified SRC kinase as a key tyrosine kinase enriched in CRPC patient tumors from our previous work, we evaluated whether inhibition of SRC kinase synergizes with enzalutamide or chemotherapy in several prostate cancer cell lines expressing variable AR isoforms. We observed robust synergy between the SRC kinase inhibitor, saracatinib, and enzalutamide, in the AR-FL+/AR-V+ CRPC cell lines, LNCaP95 and 22Rv1. We also observed that saracatinib significantly decreases AR Y
Language	English
Publishing date	2023-06-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2023.1210487
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Article ; Online: Unraveling the Global Proteome and Phosphoproteome of Prostate Cancer Patient-Derived Xenografts.

Sychev, Zoi E / Day, Abderrahman / Bergom, Hannah E / Larson, Gabrianne / Ali, Atef / Ludwig, Megan / Boytim, Ella / Coleman, Ilsa / Corey, Eva / Plymate, Stephen R / Nelson, Peter S / Hwang, Justin H / Drake, Justin M

Molecular cancer research : MCR

2024 Volume 22, Issue 5, Page(s) 452–464

Abstract: Resistance to androgen-deprivation therapies leads to metastatic castration-resistant prostate cancer (mCRPC) of adenocarcinoma (AdCa) origin that can transform into emergent aggressive variant prostate cancer (AVPC), which has neuroendocrine (NE)-like ... ...

Abstract	Resistance to androgen-deprivation therapies leads to metastatic castration-resistant prostate cancer (mCRPC) of adenocarcinoma (AdCa) origin that can transform into emergent aggressive variant prostate cancer (AVPC), which has neuroendocrine (NE)-like features. In this work, we used LuCaP patient-derived xenograft (PDX) tumors, clinically relevant models that reflect and retain key features of the tumor from advanced prostate cancer patients. Here we performed proteome and phosphoproteome characterization of 48 LuCaP PDX tumors and identified over 94,000 peptides and 9,700 phosphopeptides corresponding to 7,738 proteins. We compared 15 NE versus 33 AdCa samples, which included six different PDX tumors for each group in biological replicates, and identified 309 unique proteins and 476 unique phosphopeptides that were significantly altered and corresponded to proteins that are known to distinguish these two phenotypes. Assessment of concordance from PDX tumor-matched protein and mRNA revealed increased dissonance in transcriptionally regulated proteins in NE and metabolite interconversion enzymes in AdCa. Implications: Overall, our study highlights the importance of protein-based identification when compared with RNA and provides a rich resource of new and feasible targets for clinical assay development and in understanding the underlying biology of these tumors.
MeSH term(s)	Humans ; Male ; Proteome/metabolism ; Animals ; Mice ; Phosphoproteins/metabolism ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/pathology ; Heterografts ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Adenocarcinoma/metabolism ; Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Xenograft Model Antitumor Assays ; Proteomics/methods
Chemical Substances	Proteome ; Phosphoproteins
Language	English
Publishing date	2024-01-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-23-0976
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Article ; Online: DNA Damage and Oxidative Stress of Tobacco Smoke Condensate in Human Bladder Epithelial Cells.

Bellamri, Medjda / Walmsley, Scott J / Brown, Christina / Brandt, Kyle / Konorev, Dmitri / Day, Abderrahman / Wu, Chia-Fang / Wu, Ming Tsang / Turesky, Robert J

Chemical research in toxicology

2022 Volume 35, Issue 10, Page(s) 1863–1880

Abstract: Smoking is a major risk factor for bladder cancer (BC), with up to 50% of BC cases being attributed to smoking. There are 70 known carcinogens in tobacco smoke; however, the principal chemicals responsible for BC remain uncertain. The aromatic amines 4- ... ...

Abstract	Smoking is a major risk factor for bladder cancer (BC), with up to 50% of BC cases being attributed to smoking. There are 70 known carcinogens in tobacco smoke; however, the principal chemicals responsible for BC remain uncertain. The aromatic amines 4-aminobiphenyl (4-ABP) and 2-naphthylamine (2-NA) are implicated in BC pathogenesis of smokers on the basis of the elevated BC risk in factory workers exposed to these chemicals. However, 4-ABP and 2-NA only occur at several nanograms per cigarette and may be insufficient to induce BC. In contrast, other genotoxicants, including acrolein, occur at 1000-fold or higher levels in tobacco smoke. There is limited data on the toxicological effects of tobacco smoke in human bladder cells. We have assessed the cytotoxicity, oxidative stress, and DNA damage of tobacco smoke condensate (TSC) in human RT4 bladder cells. TSC was fractionated by liquid-liquid extraction into an acid-neutral fraction (NF), containing polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, phenols, and aldehydes, and a basic fraction (BF) containing aromatic amines, heterocyclic aromatic amines, and
MeSH term(s)	Humans ; 2-Naphthylamine/metabolism ; 2-Naphthylamine/pharmacology ; Acrolein/metabolism ; Aldehydes/metabolism ; Carcinogens/chemistry ; Cresols/metabolism ; Cresols/pharmacology ; DNA/metabolism ; DNA Damage ; Epithelial Cells ; Glutathione/metabolism ; Hydroquinones/metabolism ; Lipid Peroxides/metabolism ; Nitroso Compounds/metabolism ; Oxidative Stress ; Smoke/adverse effects ; Smoke/analysis ; Nicotiana/chemistry ; Tobacco Smoke Pollution ; Urinary Bladder/metabolism ; Urinary Bladder Neoplasms/metabolism
Chemical Substances	2-Naphthylamine (CKR7XL41N4) ; Acrolein (7864XYD3JJ) ; Aldehydes ; Carcinogens ; Cresols ; DNA (9007-49-2) ; Glutathione (GAN16C9B8O) ; Hydroquinones ; Lipid Peroxides ; Nitroso Compounds ; Smoke ; Tobacco Smoke Pollution
Language	English
Publishing date	2022-07-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639353-6
ISSN	1520-5010 ; 0893-228X
ISSN (online)	1520-5010
ISSN	0893-228X
DOI	10.1021/acs.chemrestox.2c00153
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Article ; Online: Divergent immune microenvironments in two tumor nodules from a patient with mismatch repair-deficient prostate cancer.

Bergom, Hannah E / Sena, Laura A / Day, Abderrahman / Miller, Benjamin / Miller, Carly D / Lozada, John R / Zorko, Nicholas / Wang, Jinhua / Shenderov, Eugene / Lobo, Francisco Pereira / Caramella-Pereira, Fernanda / Marchionni, Luigi / Drake, Charles G / Lotan, Tamara / De Marzo, Angelo M / Hwang, Justin / Antonarakis, Emmanuel S

NPJ genomic medicine

2024 Volume 9, Issue 1, Page(s) 7

Abstract: Patients with prostate cancer (PC) generally do not respond favorably to immune checkpoint inhibitors, which may be due to a low abundance of tumor-infiltrating lymphocytes even when mutational load is high. Here, we identified a patient who presented ... ...

Abstract	Patients with prostate cancer (PC) generally do not respond favorably to immune checkpoint inhibitors, which may be due to a low abundance of tumor-infiltrating lymphocytes even when mutational load is high. Here, we identified a patient who presented with high-grade primary prostate cancer with two adjacent tumor nodules. While both nodules were mismatch repair-deficient (MMRd), exhibited pathogenic MSH2 and MSH6 alterations, had a high tumor mutational burden (TMB), and demonstrated high microsatellite instability (MSI), they had markedly distinct immune phenotypes. The first displayed a dense infiltrate of lymphocytes ("hot nodule"), while the second displayed significantly fewer infiltrating lymphocytes ("cold nodule"). Whole-exome DNA analysis found that both nodules shared many identical mutations, indicating that they were derived from a single clone. However, the cold nodule appeared to be sub-clonal relative to the hot nodule, suggesting divergent evolution of the cold nodule from the hot nodule. Whole-transcriptome RNA analysis found that the cold nodule demonstrated lower expression of genes related to antigen presentation (HLA) and, paradoxically, classical tumor immune tolerance markers such as PD-L1 (CD274) and CTLA-4. Immune cell deconvolution suggested that the hot nodule was enriched not only in CD8+ and CD4 + T lymphocytes, but also in M1 macrophages, activated NK cells, and γδ T cells compared to the cold nodule. This case highlights that MMRd/TMB-high PC can evolve to minimize an anti-tumor immune response, and nominates downregulation of antigen presentation machinery (HLA loss) as a potential mechanism of adaptive immune evasion in PC.
Language	English
Publishing date	2024-01-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2813848-X
ISSN	2056-7944 ; 2056-7944
ISSN (online)	2056-7944
ISSN	2056-7944
DOI	10.1038/s41525-024-00392-1
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Article: ZBTB7A as a novel vulnerability in neuroendocrine prostate cancer.

Bae, Song Yi / Bergom, Hannah E / Day, Abderrahman / Greene, Joseph T / Sychev, Zoi E / Larson, Gabrianne / Corey, Eva / Plymate, Stephen R / Freedman, Tanya S / Hwang, Justin H / Drake, Justin M

Frontiers in endocrinology

2023 Volume 14, Page(s) 1093332

Abstract: Neuroendocrine prostate cancer (NEPC) is a highly aggressive subtype of prostate cancer. NEPC is characterized by the loss of androgen receptor (AR) signaling and transdifferentiation toward small-cell neuroendocrine (SCN) phenotypes, which results in ... ...

Abstract	Neuroendocrine prostate cancer (NEPC) is a highly aggressive subtype of prostate cancer. NEPC is characterized by the loss of androgen receptor (AR) signaling and transdifferentiation toward small-cell neuroendocrine (SCN) phenotypes, which results in resistance to AR-targeted therapy. NEPC resembles other SCN carcinomas clinically, histologically and in gene expression. Here, we leveraged SCN phenotype scores of various cancer cell lines and gene depletion screens from the Cancer Dependency Map (DepMap) to identify vulnerabilities in NEPC. We discovered ZBTB7A, a transcription factor, as a candidate promoting the progression of NEPC. Cancer cells with high SCN phenotype scores showed a strong dependency on RET kinase activity with a high correlation between RET and ZBTB7A dependencies in these cells. Utilizing informatic modeling of whole transcriptome sequencing data from patient samples, we identified distinct gene networking patterns of ZBTB7A in NEPC versus prostate adenocarcinoma. Specifically, we observed a robust association of ZBTB7A with genes promoting cell cycle progression, including apoptosis regulating genes. Silencing ZBTB7A in a NEPC cell line confirmed the dependency on ZBTB7A for cell growth
MeSH term(s)	Humans ; Male ; Transcription Factors/metabolism ; DNA-Binding Proteins/genetics ; Cell Line, Tumor ; Prostatic Neoplasms/pathology ; Neuroendocrine Tumors/genetics ; Neuroendocrine Tumors/pathology
Chemical Substances	Transcription Factors ; DNA-Binding Proteins ; ZBTB7A protein, human
Language	English
Publishing date	2023-03-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1093332
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Article: Unraveling the Global Proteome and Phosphoproteome of Prostate Cancer Patient-Derived Xenografts.

bioRxiv : the preprint server for biology

2023

Abstract: Resistance to androgen deprivation therapies leads to metastatic castration-resistant prostate cancer (mCRPC) of adenocarcinoma (AdCa) origin that can transform to emergent aggressive variant prostate cancer (AVPC) which has neuroendocrine (NE)-like ... ...

Abstract	Resistance to androgen deprivation therapies leads to metastatic castration-resistant prostate cancer (mCRPC) of adenocarcinoma (AdCa) origin that can transform to emergent aggressive variant prostate cancer (AVPC) which has neuroendocrine (NE)-like features. To this end, we used LuCaP patient-derived xenograft (PDX) tumors, clinically relevant models that reflects and retains key features of the tumor from advanced prostate cancer patients. Here we performed proteome and phosphoproteome characterization of 48 LuCaP PDX tumors and identified over 94,000 peptides and 9,700 phosphopeptides corresponding to 7,738 proteins. When we compared 15 NE versus 33 AdCa PDX samples, we identified 309 unique proteins and 476 unique phosphopeptides that were significantly altered and corresponded to proteins that are known to distinguish these two phenotypes. Assessment of protein and RNA concordance from these tumors revealed increased dissonance in transcriptionally regulated proteins in NE and metabolite interconversion enzymes in AdCa.
Language	English
Publishing date	2023-08-05
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.08.02.551697
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Article ; Online: ALAN is a computational approach that interprets genomic findings in the context of tumor ecosystems.

Bergom, Hannah E / Shabaneh, Ashraf / Day, Abderrahman / Ali, Atef / Boytim, Ella / Tape, Sydney / Lozada, John R / Shi, Xiaolei / Kerkvliet, Carlos Perez / McSweeney, Sean / Pitzen, Samuel P / Ludwig, Megan / Antonarakis, Emmanuel S / Drake, Justin M / Dehm, Scott M / Ryan, Charles J / Wang, Jinhua / Hwang, Justin

Communications biology

2023 Volume 6, Issue 1, Page(s) 417

Abstract: Gene behavior is governed by activity of other genes in an ecosystem as well as context-specific cues including cell type, microenvironment, and prior exposure to therapy. Here, we developed the Algorithm for Linking Activity Networks (ALAN) to compare ... ...

Abstract	Gene behavior is governed by activity of other genes in an ecosystem as well as context-specific cues including cell type, microenvironment, and prior exposure to therapy. Here, we developed the Algorithm for Linking Activity Networks (ALAN) to compare gene behavior purely based on patient -omic data. The types of gene behaviors identifiable by ALAN include co-regulators of a signaling pathway, protein-protein interactions, or any set of genes that function similarly. ALAN identified direct protein-protein interactions in prostate cancer (AR, HOXB13, and FOXA1). We found differential and complex ALAN networks associated with the proto-oncogene MYC as prostate tumors develop and become metastatic, between different cancer types, and within cancer subtypes. We discovered that resistant genes in prostate cancer shared an ALAN ecosystem and activated similar oncogenic signaling pathways. Altogether, ALAN represents an informatics approach for developing gene signatures, identifying gene targets, and interpreting mechanisms of progression or therapy resistance.
MeSH term(s)	Male ; Humans ; Ecosystem ; Prostatic Neoplasms/pathology ; Genes, myc ; Genomics ; Signal Transduction/genetics ; Tumor Microenvironment/genetics
Language	English
Publishing date	2023-04-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-023-04795-1
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Article: Integrative molecular analyses define correlates of high B7-H3 expression in metastatic castrate-resistant prostate cancer.

Shi, Xiaolei / Day, Abderrahman / Bergom, Hannah E / Tape, Sydney / Baca, Sylvan C / Sychev, Zoi E / Larson, Gabrianne / Bozicevich, Asha / Drake, Justin M / Zorko, Nicholas / Wang, Jinhua / Ryan, Charles J / Antonarakis, Emmanuel S / Hwang, Justin

NPJ precision oncology

2022 Volume 6, Issue 1, Page(s) 80

Abstract: B7-H3 (CD276) is an immune checkpoint overexpressed in prostate cancer with minimal expression in normal tissues and associated with poor prognosis, making it an excellent therapy target. We interrogated B7-H3 expression and its regulation in metastatic ... ...

Abstract	B7-H3 (CD276) is an immune checkpoint overexpressed in prostate cancer with minimal expression in normal tissues and associated with poor prognosis, making it an excellent therapy target. We interrogated B7-H3 expression and its regulation in metastatic castration-resistant prostate cancer (mCRPC). We found greater expression of B7-H3 transcript relative to other immunotherapy targets (CTLA-4, PD-L1/2), including in tumors that lacked expression of prostate-specific membrane antigen (PSMA). Enzalutamide-resistant mCRPC cells demonstrated increased amounts of B7-H3, and this was associated with resistance signaling pathways. Using a machine-learning algorithm, the gene network of B7-H3 was strongly correlated with androgen receptor (AR) and AR co-factor (HOXB13, FOXA1) networks. In mCRPC samples, the B7-H3 promoter and distal enhancer regions exhibited enhanced transcriptional activity and were directly bound by AR and its co-factors. Altogether, our study characterizes molecular profiles and epigenetic regulation of B7-H3-expressing mCRPC tumors, which informs optimal precision-oncology approaches for mCRPC patients.
Language	English
Publishing date	2022-11-02
Publishing country	England
Document type	Journal Article
ISSN	2397-768X
ISSN	2397-768X
DOI	10.1038/s41698-022-00323-2
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Article ; Online: Nicotinamide enhances natural killer cell function and yields remissions in patients with non-Hodgkin lymphoma.

Science translational medicine

2023 Volume 15, Issue 705, Page(s) eade3341

Abstract: Allogeneic natural killer (NK) cell adoptive transfer has shown the potential to induce remissions in relapsed or refractory leukemias and lymphomas, but strategies to enhance NK cell survival and function are needed to improve clinical efficacy. Here, ... ...

Abstract	Allogeneic natural killer (NK) cell adoptive transfer has shown the potential to induce remissions in relapsed or refractory leukemias and lymphomas, but strategies to enhance NK cell survival and function are needed to improve clinical efficacy. Here, we demonstrated that NK cells cultured ex vivo with interleukin-15 (IL-15) and nicotinamide (NAM) exhibited stable induction of l-selectin (CD62L), a lymphocyte adhesion molecule important for lymph node homing. High frequencies of CD62L were associated with elevated transcription factor forkhead box O1 (FOXO1), and NAM promoted the stability of FOXO1 by preventing proteasomal degradation. NK cells cultured with NAM exhibited metabolic changes associated with elevated glucose flux and protection against oxidative stress. NK cells incubated with NAM also displayed enhanced cytotoxicity and inflammatory cytokine production and preferentially persisted in xenogeneic adoptive transfer experiments. We also conducted a first-in-human phase 1 clinical trial testing adoptive transfer of NK cells expanded ex vivo with IL-15 and NAM (GDA-201) combined with monoclonal antibodies in patients with relapsed or refractory non-Hodgkin lymphoma (NHL) and multiple myeloma (MM) (NCT03019666). Cellular therapy with GDA-201 and rituximab was well tolerated and yielded an overall response rate of 74% in 19 patients with advanced NHL. Thirteen patients had a complete response, and 1 patient had a partial response. GDA-201 cells were detected for up to 14 days in blood, bone marrow, and tumor tissues and maintained a favorable metabolic profile. The safety and efficacy of GDA-201 in this study support further development as a cancer therapy.
MeSH term(s)	Humans ; Interleukin-15/metabolism ; Niacinamide/metabolism ; Lymphoma, Non-Hodgkin/therapy ; Lymphoma, Non-Hodgkin/metabolism ; Rituximab/metabolism ; Killer Cells, Natural
Chemical Substances	Interleukin-15 ; Niacinamide (25X51I8RD4) ; Rituximab (4F4X42SYQ6)
Language	English
Publishing date	2023-07-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.ade3341
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