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Article: Dopamine Receptors in Breast Cancer: Prevalence, Signaling, and Therapeutic Applications.

Ben-Jonathan, Nira / Borcherding, Dana C / Hugo, Eric R

2023 Volume 27, Issue 2, Page(s) 51–71

Abstract: Breast cancer (BC) is the most common malignancy among women, with over one million cases occurring annually worldwide. Although therapies against estrogen receptors and HER2 have improved response rate and survival, patients with advanced disease, who ... ...

Abstract	Breast cancer (BC) is the most common malignancy among women, with over one million cases occurring annually worldwide. Although therapies against estrogen receptors and HER2 have improved response rate and survival, patients with advanced disease, who are resistant to anti-hormonal therapy and/or to chemotherapy, have limited treatment options for reducing morbidity and mortality. These limitations provide major incentives for developing new, effective, and personalized therapeutic interventions. This review presents evidence on the involvement of dopamine (DA) and its type 1 receptors (D1R) in BC. DA is produced in multiple peripheral organs and is present in the systemic circulation in significant amounts. D1R is overexpressed in ~ 30% of BC cases and is associated with advanced disease and shortened patient survival. Activation of D1R, which signals via the cGMP/PKG pathway, results in apoptosis, inhibition of cell invasion, and increased chemosensitivity in multiple BC cell lines. Fenoldopam, a peripheral D1R agonist that does not penetrate the brain, dramatically suppressed tumor growth in mouse models with D1R-expressing BC xenografts. It is proposed that D1R should serve as a novel diagnostic/prognostic factor through the use of currently available D1R detection methods. Fenoldopam, which is FDA-approved to treat renal hypertension, could be repurposed as an effective therapeutic agent for patients with D1R-expressing tumors. Several drugs that interfere with the cGMP/PKG pathway and are approved for treating other diseases should also be considered as potential treatments for BC.
MeSH term(s)	Mice ; Animals ; Humans ; Female ; Fenoldopam/pharmacology ; Fenoldopam/therapeutic use ; Prevalence ; Receptors, Dopamine ; Signal Transduction ; Dopamine/therapeutic use ; Breast Neoplasms/diagnosis ; Breast Neoplasms/drug therapy ; Breast Neoplasms/epidemiology
Chemical Substances	Fenoldopam (INU8H2KAWG) ; Receptors, Dopamine ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2023-02-03
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	1036388-9
ISSN	0893-9675
ISSN	0893-9675
DOI	10.1615/CritRevOncog.2022043641
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Article: TYK2 in Cancer Metastases: Genomic and Proteomic Discovery.

Borcherding, Dana C / He, Kevin / Amin, Neha V / Hirbe, Angela C

Cancers

2021 Volume 13, Issue 16

Abstract: Advances in genomic analysis and proteomic tools have rapidly expanded identification of biomarkers and molecular targets important to cancer development and metastasis. On an individual basis, personalized medicine approaches allow better ... ...

Abstract	Advances in genomic analysis and proteomic tools have rapidly expanded identification of biomarkers and molecular targets important to cancer development and metastasis. On an individual basis, personalized medicine approaches allow better characterization of tumors and patient prognosis, leading to more targeted treatments by detection of specific gene mutations, overexpression, or activity. Genomic and proteomic screens by our lab and others have revealed tyrosine kinase 2 (
Language	English
Publishing date	2021-08-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13164171
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Article ; Online: Study Transportation of Drugs within Newly Established Murine Colon Organoid Systems.

Davoudi, Zahra / Atherly, Todd / Borcherding, Dana C / Jergens, Albert E / Wannemuehler, Michael / Barrett, Terrence A / Wang, Qun

Advanced biology

2023 Volume 7, Issue 12, Page(s) e2300103

Abstract: The development of 3D organoids of the small intestine is a tremendous breakthrough in drug development and biological research. However, the development of colonic organoids (i.e., colonoids) is particularly challenging due to a lack of simple, cost- ... ...

Abstract	The development of 3D organoids of the small intestine is a tremendous breakthrough in drug development and biological research. However, the development of colonic organoids (i.e., colonoids) is particularly challenging due to a lack of simple, cost-effective protocols for colonoid cultivation. Here, intestinal homogenates are described as a supplement to the culture medium for maintaining and replicating colonic stem cells. Colonoids generated by this cultivation protocol demonstrate substantial proliferation and differentiation (3 months). There is a similarity between cultured colonoids and primary colon tissue regarding structure and functionality. To evaluate the functionality of colonoids, permeability testing is performed with suspensions of 4 and 40 kDa fluorescein isothiocyanate-dextran (FITC-DEX). It is observed that neither can permeate the healthy epithelial barrier. The P-glycoprotein receptor, a vital drug efflux pump mitigating potential drug toxicity, is functionally manipulated, as evidenced by its inhibition function by verapamil and monitoring uptake of Rhodamin 123. In addition, Forskolin treatment which affects chloride transport results in organoid swelling; this confirms the functional expression of the CFTR transporter in the colonoids. This protocol to generate colonoids is promising for high-throughput drug screening, toxicity testing, and oral drug development.
MeSH term(s)	Mice ; Animals ; Colon ; Intestine, Small ; Organoids
Language	English
Publishing date	2023-08-21
Publishing country	Germany
Document type	Journal Article
ISSN	2701-0198
ISSN (online)	2701-0198
DOI	10.1002/adbi.202300103
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Article ; Online: Molecular Characterization of Multifocal Granular Cell Tumors.

Dehner, Carina A / Schroeder, Molly C / Lyu, Yang / Bell, Robert / Borcherding, Dana C / Moon, Tyler / Hirbe, Angela / Chrisinger, John S A

The American journal of surgical pathology

2022 Volume 47, Issue 3, Page(s) 326–332

Abstract: Granular cell tumors (GrCT) were recently found to be driven by inactivating mutations in vacuolar H + -ATPase (V-ATPase) genes, most frequently ATP6AP1 and ATP6AP2 . Multifocal presentation is present in ~10% of cases; however, the relationship between ... ...

Abstract	Granular cell tumors (GrCT) were recently found to be driven by inactivating mutations in vacuolar H + -ATPase (V-ATPase) genes, most frequently ATP6AP1 and ATP6AP2 . Multifocal presentation is present in ~10% of cases; however, the relationship between multifocal tumors in a given patient has not been elucidated. We hypothesized that benign-appearing multifocal GrCT are molecularly distinct whereas paired primary and metastatic malignant GrCT share identical mutations. To test this, we conducted targeted next-generation sequencing of the V-ATPase genes in multifocal GrCT and whole exome and Sanger sequencing in paired primary and metastatic malignant GrCT. Thirteen patients with≥2 GrCT were identified (total of 43 tumors). Forty-two tumors were successfully sequenced. Tumors showed somatic mutations in 3 of the 10 targeted genes in 32 of 42 samples (76%). Twenty tumors showed mutations in ATP6AP1 (48%), 10 tumors had mutations in ATP6AP2 (24%), and 2 tumors showed mutations in ATP6V0A4 (5%). Predicted loss-of-function mutations were found in ATP6AP1 in 17 tumors (40%), in ATP6AP2 in 10 tumors (24%), and in ATP6V0A4 in 1 tumor (2%). In 8 patients, mutually exclusive mutations were detected in at least 2 tumors per patient. Two patients were identified with malignant GrCT with material available from both primary and metastatic sites. Identical frameshift insertions were found in ATP6AP1 in 1 case and the second case showed identical nonsense mutations in ATP6AP1 . In conclusion, multifocal GrCT within an individual patient are molecularly distinct, while paired primary and metastatic GrCT share identical mutations.
MeSH term(s)	Humans ; Granular Cell Tumor/genetics ; Mutation ; Receptors, Cell Surface ; Vacuolar Proton-Translocating ATPases/genetics ; Vacuolar Proton-Translocating ATPases/metabolism ; Prorenin Receptor
Chemical Substances	Receptors, Cell Surface ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-) ; ATP6AP2 protein, human ; Prorenin Receptor ; ATP6AP1 protein, human
Language	English
Publishing date	2022-11-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	752964-8
ISSN	1532-0979 ; 0147-5185
ISSN (online)	1532-0979
ISSN	0147-5185
DOI	10.1097/PAS.0000000000001992
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Article ; Online: Activation of the cGMP/protein kinase G system in breast cancer by the dopamine receptor-1.

Ben-Jonathan, Nira / Borcherding, Dana C / Fox, Sejal / Hugo, Eric R

Cancer drug resistance (Alhambra, Calif.)

2019 Volume 2, Issue 4, Page(s) 933–947

Abstract: Despite recent advances in the detection and treatment of breast cancer, many shortcomings remain, providing incentives to search for new therapeutic targets. This review provides information on the expression and actions of dopamine receptor-1 (D1R) in ... ...

Abstract	Despite recent advances in the detection and treatment of breast cancer, many shortcomings remain, providing incentives to search for new therapeutic targets. This review provides information on the expression and actions of dopamine receptor-1 (D1R) in breast cancer. D1R is overexpressed in a significant number of primary breast tumors, characterized by having an aggressive phenotype and predicting a shorter survival time for patients. Activation of D1R in breast cancer cells by selective agonists caused suppression of cell viability, stimulation of apoptosis, inhibition of cell invasion, and an increase in chemosensitivity. Instead of being linked to the cAMP/PKA system as expected, D1R in breast cancer is linked to the activation of the cGMP/protein kinase G (PKG) pathway. Fenoldopam, a peripheral D1R agonist that does not penetrate the brain, dramatically suppressed the growth of breast cancer xenografts in immune-deficient mice. A new imaging system for detecting D1R-expressing tumors and metastases was also developed. The review offers a novel concept that D1R can serve as a biomarker for prognosis in advanced breast cancer and its agonists can be used as effective and personalized therapeutics in a subpopulation of patients with D1R-expressing breast tumors. Several drugs, some of which are FDA-approved, that bypass the D1R and directly activate the cGMP/PKG apoptotic system, are also identified.
Language	English
Publishing date	2019-12-19
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2578-532X
ISSN (online)	2578-532X
DOI	10.20517/cdr.2019.83
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Article: Suppression of Breast Cancer by Small Molecules That Block the Prolactin Receptor.

Borcherding, Dana C / Hugo, Eric R / Fox, Sejal R / Jacobson, Eric M / Hunt, Brian G / Merino, Edward J / Ben-Jonathan, Nira

Cancers

2021 Volume 13, Issue 11

Abstract: Prolactin (PRL) is a protein hormone which in humans is secreted by pituitary lactotrophs as well as by many normal and malignant non-pituitary sites. Many lines of evidence demonstrate that both circulating and locally produced PRL increase breast ... ...

Abstract	Prolactin (PRL) is a protein hormone which in humans is secreted by pituitary lactotrophs as well as by many normal and malignant non-pituitary sites. Many lines of evidence demonstrate that both circulating and locally produced PRL increase breast cancer (BC) growth and metastases and confer chemoresistance. Our objective was to identify and then characterize small molecules that block the tumorigenic actions of PRL in BC. We employed three cell-based assays in high throughput screening (HTS) of 51,000 small molecules and identified two small molecule inhibitors (SMIs), named SMI-1 and SMI-6. Both compounds bound to the extracellular domain (ECD) of the PRL receptor (PRLR) at 1-3 micromolar affinity and abrogated PRL-induced breast cancer cell (BCC) invasion and malignant lymphocyte proliferation. SMI-6 effectively reduced the viability of multiple BCC types, had much lower activity against various non-malignant cells, displayed high selectivity, and showed no apparent in vitro or in vivo toxicity. In athymic nude mice, SMI-6 rapidly and dramatically suppressed the growth of PRL-expressing BC xenografts. This report represents a pre-clinical phase of developing novel anti-cancer agents with the potential to become effective therapeutics in breast cancer patients.
Language	English
Publishing date	2021-05-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13112662
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Article ; Online: MEK Inhibition Synergizes with TYK2 Inhibitors in NF1-Associated Malignant Peripheral Nerve Sheath Tumors.

Borcherding, Dana C / Amin, Neha V / He, Kevin / Zhang, Xiaochun / Lyu, Yang / Dehner, Carina / Bhatia, Himanshi / Gothra, Angad / Daud, Layla / Ruminski, Peter / Pratilas, Christine A / Pollard, Kai / Sundby, Taylor / Widemann, Brigitte C / Hirbe, Angela C

Clinical cancer research : an official journal of the American Association for Cancer Research

2023 Volume 29, Issue 8, Page(s) 1592–1604

Abstract: Purpose: Malignant peripheral nerve sheath tumors (MPNST) are aggressive sarcomas with limited treatment options and poor survival rates. About half of MPNST cases are associated with the neurofibromatosis type 1 (NF1) cancer predisposition syndrome. ... ...

Abstract	Purpose: Malignant peripheral nerve sheath tumors (MPNST) are aggressive sarcomas with limited treatment options and poor survival rates. About half of MPNST cases are associated with the neurofibromatosis type 1 (NF1) cancer predisposition syndrome. Overexpression of TYK2 occurs in the majority of MPNST, implicating TYK2 as a therapeutic target. Experimental design: The effects of pharmacologic TYK2 inhibition on MPNST cell proliferation and survival were examined using IncuCyte live cell assays in vitro, and downstream actions were analyzed using RNA-sequencing (RNA-seq), qPCR arrays, and validation of protein changes with the WES automated Western system. Inhibition of TYK2 alone and in combination with MEK inhibition was evaluated in vivo using both murine and human MPNST cell lines, as well as MPNST PDX. Results: Pharmacologic inhibition of TYK2 dose-dependently decreased proliferation and induced apoptosis over time. RNA-seq pathway analysis on TYK2 inhibitor-treated MPNST demonstrated decreased expression of cell cycle, mitotic, and glycolysis pathways. TYK2 inhibition resulted in upregulation of the MEK/ERK pathway gene expression, by both RNA-seq and qPCR array, as well as increased pERK1/2 levels by the WES Western system. The compensatory response was tested with dual treatment with TYK2 and MEK inhibitors, which synergistically decreased proliferation and increased apoptosis in vitro. Finally, combination therapy was shown to inhibit growth of MPNST in multiple in vivo models. Conclusions: These data provide the preclinical rationale for the development of a phase I clinical trial of deucravacitinib and mirdametinib in NF1-assosciated MPNST.
MeSH term(s)	Humans ; Mice ; Animals ; Neurofibrosarcoma ; Neurofibromatosis 1/drug therapy ; Neurofibromatosis 1/genetics ; Cell Line ; Apoptosis ; Mitogen-Activated Protein Kinase Kinases/genetics ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Nerve Sheath Neoplasms/drug therapy ; Nerve Sheath Neoplasms/genetics ; Nerve Sheath Neoplasms/metabolism ; Cell Line, Tumor ; TYK2 Kinase/genetics ; TYK2 Kinase/metabolism ; TYK2 Kinase/pharmacology
Chemical Substances	Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; TYK2 protein, human (EC 2.7.10.2) ; TYK2 Kinase (EC 2.7.10.2)
Language	English
Publishing date	2023-02-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-22-3722
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Zs.A 4223: Show issues

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Article: Differential Transcriptomic Profiles Following Stimulation with Lipopolysaccharide in Intestinal Organoids from Dogs with Inflammatory Bowel Disease and Intestinal Mast Cell Tumor.

Sahoo, Dipak Kumar / Borcherding, Dana C / Chandra, Lawrance / Jergens, Albert E / Atherly, Todd / Bourgois-Mochel, Agnes / Ellinwood, N Matthew / Snella, Elizabeth / Severin, Andrew J / Martin, Martin / Allenspach, Karin / Mochel, Jonathan P

Cancers

2022 Volume 14, Issue 14

Abstract: Lipopolysaccharide (LPS) is associated with chronic intestinal inflammation and promotes intestinal cancer progression in the gut. While the interplay between LPS and intestinal immune cells has been well-characterized, little is known about LPS and the ... ...

Abstract	Lipopolysaccharide (LPS) is associated with chronic intestinal inflammation and promotes intestinal cancer progression in the gut. While the interplay between LPS and intestinal immune cells has been well-characterized, little is known about LPS and the intestinal epithelium interactions. In this study, we explored the differential effects of LPS on proliferation and the transcriptome in 3D enteroids/colonoids obtained from dogs with naturally occurring gastrointestinal (GI) diseases including inflammatory bowel disease (IBD) and intestinal mast cell tumor. The study objective was to analyze the LPS-induced modulation of signaling pathways involving the intestinal epithelia and contributing to colorectal cancer development in the context of an inflammatory (IBD) or a tumor microenvironment. While LPS incubation resulted in a pro-cancer gene expression pattern and stimulated proliferation of IBD enteroids and colonoids, downregulation of several cancer-associated genes such as
Language	English
Publishing date	2022-07-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14143525
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Article ; Online: The Impact of TSC-1 and -2 Mutations on Response to Therapy in Malignant PEComa: A Multicenter Retrospective Analysis.

Liu, Lawrence / Dehner, Carina / Grandhi, Nikhil / Lyu, Yang / Borcherding, Dana C / Chrisinger, John S A / Zhang, Xiao / Luo, Jingqin / Tao, Yu / Parkes, Amanda / Bui, Nam Q / Davis, Elizabeth J / Milhem, Mohammed M / Monga, Varun / Weiss, Mia / Tine, Brian Van / Hirbe, Angela C

Genes

2022 Volume 13, Issue 11

Abstract: Background: Perivascular epithelioid cell neoplasms (PEComas) are a diverse family of mesenchymal tumors with myomelanocytic differentiation that disproportionately affect women and can be associated with tuberous sclerosis (TS). Although mTOR ... ...

Abstract	Background: Perivascular epithelioid cell neoplasms (PEComas) are a diverse family of mesenchymal tumors with myomelanocytic differentiation that disproportionately affect women and can be associated with tuberous sclerosis (TS). Although mTOR inhibition is widely used as first-line treatment, it is unclear what genomic alterations exist in these tumors and how they influence the response to therapy. Methods: This was a multicenter study conducted at five sites within the US. The data were collected from 1 January 2004 to 31 January 2021. We conducted a retrospective analysis to identify PEComa patients with next-generation sequencing (NGS) data and compared outcomes based on mutations. Results: No significant differences in survival were identified between Conclusions: We were unable to detect differences in survival based on genomic alterations or PFS between mTOR inhibition versus other systemic therapies. Future studies should seek to identify other drivers of
MeSH term(s)	Female ; Humans ; Mutation ; Perivascular Epithelioid Cell Neoplasms/genetics ; Perivascular Epithelioid Cell Neoplasms/pathology ; Retrospective Studies ; TOR Serine-Threonine Kinases/genetics
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-10-24
Publishing country	Switzerland
Document type	Multicenter Study ; Journal Article
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13111932
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Article ; Online: Clinically-approved CFTR modulators rescue Nrf2 dysfunction in cystic fibrosis airway epithelia.

Borcherding, Dana C / Siefert, Matthew E / Lin, Songbai / Brewington, John / Sadek, Hesham / Clancy, John P / Plafker, Scott M / Ziady, Assem G

The Journal of clinical investigation

2019 Volume 129, Issue 8, Page(s) 3448–3463

Abstract: Cystic Fibrosis (CF) is a multi-organ progressive genetic disease caused by loss of functional cystic fibrosis transmembrane conductance regulator (CFTR) channel. Previously, we identified a significant dysfunction in CF cells and model mice of the ... ...

Abstract	Cystic Fibrosis (CF) is a multi-organ progressive genetic disease caused by loss of functional cystic fibrosis transmembrane conductance regulator (CFTR) channel. Previously, we identified a significant dysfunction in CF cells and model mice of the transcription factor nuclear-factor-E2-related factor-2 (Nrf2), a major regulator of redox balance and inflammatory signaling. Here we report that approved F508del CFTR correctors VX809/VX661 recover diminished Nrf2 function and colocalization with CFTR in CF human primary bronchial epithelia by proximity ligation assay, immunoprecipitation, and immunofluorescence, concordant with CFTR correction. F508del CFTR correctors induced Nrf2 nuclear translocation, Nrf2-dependent luciferase activity, and transcriptional activation of target genes. Rescue of Nrf2 function by VX809/VX661 was dependent on significant correction of F508del and was blocked by inhibition of corrected channel function, or high-level shRNA knockdown of CFTR or F508del-CFTR. Mechanistically, F508del-CFTR modulation restored Nrf2 phosphorylation and its interaction with the coactivator CBP. Our findings demonstrate that sufficient modulation of F508del CFTR function corrects Nrf2 dysfunction in CF.
MeSH term(s)	Active Transport, Cell Nucleus/genetics ; Animals ; Cell Line ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Cell Nucleus/pathology ; Cystic Fibrosis/genetics ; Cystic Fibrosis/metabolism ; Cystic Fibrosis/pathology ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Humans ; Mice ; Mice, Transgenic ; Mutation ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Phosphorylation/genetics ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/pathology
Chemical Substances	CFTR protein, human ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6)
Language	English
Publishing date	2019-05-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI96273
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