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Article ; Online: Distinct uptake and elimination profiles for trastuzumab, human IgG and biocytin-TMR in experimental HER2+ brain metastases of breast cancer.

Silvestri, Vanesa L / Tran, Andy D / Chung, Monika / Chung, Natalie / Gril, Brunilde / Robinson, Christina / Difilippantonio, Simone / Wei, Debbie / Kruhlak, Michael J / Peer, Cody J / Figg, W Douglas / Khan, Imran / Steeg, Patricia S

Neuro-oncology

2024

Abstract: Background: The aim of this study is an improved understanding of drug distribution in brain metastases. Rather than single point snapshots, we analyzed the time course and route of drug/probe elimination (clearance), focusing on the Intramural ... ...

Abstract	Background: The aim of this study is an improved understanding of drug distribution in brain metastases. Rather than single point snapshots, we analyzed the time course and route of drug/probe elimination (clearance), focusing on the Intramural Periarterial Drainage (IPAD) pathway. Methods: Mice with JIMT1-BR HER2+ experimental brain metastases were injected with biocytin-TMR and either trastuzumab or human IgG. Drugs/probes circulated for 5 min-48h, followed by perfusion. Brain sections were stained for human IgG, vascular basement membrane proteins laminin or collagen IV, and periarterial α-SMA. A machine learning algorithm was developed to identify metastases, metastatic microenvironment, and uninvolved brain in confocally scanned brain sections. Drug/probe intensity over time and total imaged drug exposure (iAUC) were calculated for 27,249 lesions and co-immunofluorescence with IPAD- vascular matrix analyzed in 11,668 metastases. Results: In metastases, peak trastuzumab levels were 5-fold higher than human IgG but 4-fold less than biocytin-TMR. The elimination phase constituted 85-93% of total iAUC for all drugs/probes tested. For trastuzumab, total iAUC during uptake was similar to the small molecule drug probe biocytin-TMR, but slower trastuzumab elimination resulted in a 1.7-fold higher total iAUC. During elimination trastuzumab and IgG were preferentially enriched in the α-SMA+ periarterial vascular matrix, consistent with the IPAD clearance route; biocytin-TMR showed heterogeneous elimination pathways. Conclusions: Drug/probe elimination is an important component of drug development for brain metastases. We identified a prolonged elimination pathway for systemically administered antibodies through the periarterial vascular matrix that may contribute to the sustained presence and efficacy of large antibody therapeutics.
Language	English
Publishing date	2024-02-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2028601-6
ISSN	1523-5866 ; 1522-8517
ISSN (online)	1523-5866
ISSN	1522-8517
DOI	10.1093/neuonc/noae025
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Zs.A 5307: Show issues

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Article: The Pharm.D. investigator in clinical pharmacology: supply and demand.

Figg, W D

Clinical pharmacology and therapeutics

2009 Volume 84, Issue 4, Page(s) 526–529

Abstract: The field of clinical pharmacology is the discipline engaged in optimal drug discovery, development, and use, based on an in-depth knowledge of human pharmacology and therapeutics. Although many think clinical pharmacology is simply the study of ... ...

Abstract	The field of clinical pharmacology is the discipline engaged in optimal drug discovery, development, and use, based on an in-depth knowledge of human pharmacology and therapeutics. Although many think clinical pharmacology is simply the study of pharmacokinetics, pharmacodynamics, and pharmacogenetics, the role of the clinical pharmacologists covers all avenues of drug discovery, development, therapeutics, optimal drug therapy, and education. This expanded understanding is important as we start to address the overwhelming mandate and the unfortunate shortage of qualified investigators in the field (both physicians and non-physicians).
MeSH term(s)	Biomedical Research/organization & administration ; Education, Pharmacy, Graduate/organization & administration ; Humans ; Pharmacology, Clinical ; Schools, Pharmacy/organization & administration ; United States ; Workforce
Language	English
Publishing date	2009-02-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	123793-7
ISSN	1532-6535 ; 0009-9236
ISSN (online)	1532-6535
ISSN	0009-9236
DOI	10.1038/sj.clpt.6100423
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Article ; Online: Enhanced toxicity to chemoradiation in a patient with Anti-Jo-1-antisynthetase syndrome.

Valle, Luca / Katz, James / Duffy, Austin / Hueman, Matthew / Wang, Hao-Wei / Hughes, Marybeth / Sissung, Tristan / Figg, William / Citrin, Deborah

BJR case reports

2022 Volume 8, Issue 3, Page(s) 20210188

Abstract: Appropriate counseling of patients with autoimmune connective tissue disorders (ACTDs) is often challenging for radiation oncologists, especially regarding anticipated side-effects of radiation treatment. These patients can have highly variable and ... ...

Abstract	Appropriate counseling of patients with autoimmune connective tissue disorders (ACTDs) is often challenging for radiation oncologists, especially regarding anticipated side-effects of radiation treatment. These patients can have highly variable and unpredictable sequelae from radiation therapy, and the uncertainty builds when radiation is convoluted by the addition of concurrent chemotherapy. While many patients may experience a mild intensification of toxicity above what is expected, some patients experience much more severe toxicity. These patients become critical learning cases, enabling a better understanding of the delicate and complex ways in which radiation response is altered in the context of ACTDs while allowing other patients with similar ACTD profiles to benefit from past experience. Our report makes an important contribution to this space by describing a particularly severe case of toxicity that manifested in such a patient and the ensuing clinical decision-making. Comprehensive genotyping of classic pharmacokinetic and pharmacodynamic pathway genes (including mutations in DPD and CDA) did not reveal any signatures that might explain her enhanced toxicity and we demonstrate that severe toxicity can still manifest in the era of modern conformal radiation treatments for rectal cancer. We urge caution in the treatment of patients with rare ACTDs, but also emphasize that curative treatment should not be withheld in such patients. We conclude by advocating for the development and maintenance of a prospective multiinstitutional database of patients with ACTDs to help inform and improve future practice.
Language	English
Publishing date	2022-02-24
Publishing country	England
Document type	Case Reports
ISSN	2055-7159
ISSN (online)	2055-7159
DOI	10.1259/bjrcr.20210188
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Article: Biological Effects of Modifications of the Englerin A Glycolate.

Seenadera, Sarath P D / Long, Sarah A / Akee, Rhone / Bermudez, Gabriela / Parsonage, Gregory / Strope, Jonathan / Peer, Cody / Figg, W Douglas / Parker, Kathlyn A / Beech, David J / Beutler, John A

ACS medicinal chemistry letters

2022 Volume 13, Issue 9, Page(s) 1472–1476

Abstract: Modifications at the glycolate moiety of englerin A were made to explore variations at the most sensitive site on the molecule for activity in the NCI 60 screen, wherein englerin A is highly potent and selective for renal cancer cells. Replacement of the ...

Abstract	Modifications at the glycolate moiety of englerin A were made to explore variations at the most sensitive site on the molecule for activity in the NCI 60 screen, wherein englerin A is highly potent and selective for renal cancer cells. Replacement of the glycolate by other functionalities as well as esterification of the glycolate hydroxyl yielded compounds which displayed excellent selectivity and potency compared with the natural product. TRPC4/5 ion channel experiments with five compounds showed delayed or reduced agonism with TRPC5, at much higher concentrations than englerin A. With TRPC4, these compounds all had no effect at 10 μM. The same compounds were not detectable in mouse serum after a single oral dose of 12.5 mg/kg. At 100 mg/kg p.o., no toxicity was observed, and blood levels were barely detectable. Intravenous administration led to toxicity but at substantially lower doses than for englerin A.
Language	English
Publishing date	2022-08-22
Publishing country	United States
Document type	Journal Article
ISSN	1948-5875
ISSN	1948-5875
DOI	10.1021/acsmedchemlett.2c00258
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Article ; Online: GNRH2

Sissung, Tristan M / Lochrin, Sarah / Liu, Tyler / Schmidt, Keith / Strope, Jonathan / Risdon, Emily / Choo-Wosoba, Hyoyoung / Venzon, David J / Lassoued, Wiem / Sater, Houssein A / Walter-Rodriguez, Beatriz / Price, Douglas K / Figg, William D

Anticancer research

2023 Volume 43, Issue 9, Page(s) 4023–4030

Abstract: Background/aim: Gonadotropin-releasing hormone 2 (GNRH2) is a poorly-studied peptide hormone that is widely distributed in the central nervous system and expressed in peripheral tissues of mammals. The non-synonymous rs6051545 variant in GNRH2 (A16V) ... ...

Abstract	Background/aim: Gonadotropin-releasing hormone 2 (GNRH2) is a poorly-studied peptide hormone that is widely distributed in the central nervous system and expressed in peripheral tissues of mammals. The non-synonymous rs6051545 variant in GNRH2 (A16V) has been linked to higher serum testosterone concentrations. This study investigated whether the A16V variant is associated with altered androgen-deprivation therapy (ADT) progression-free survival (PFS) and overall survival (OS). Patients and methods: We examined the expression of GNRH2 in prostate tissue microarrays comprising normal tissue, prostatic hyperplasia, and prostate cancer using immunofluorescence. We also evaluated the GNRH2 genotype in 131 patients with prostate cancer who received ADT and compared PFS and OS between the variant and wild-type genotypes. Results: GNRH2 was detected in all prostate tissues, although expression did not vary with Gleason grade or disease stage (p=0.71). The GNRH2 A16V genotype was not associated with PFS or OS; however, univariate and multivariate analyses revealed Gleason score and definitive local therapy were each associated with PFS (p≤0.0074), whereas age and Gleason score were associated with OS (p≤0.0046). Conclusion: GNRH2 is expressed in normal, hyperplastic, and neoplastic prostate tissues; the A16V variant is not related to treatment outcome or survival.
MeSH term(s)	Animals ; Male ; Humans ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Androgen Antagonists/therapeutic use ; Gonadotropin-Releasing Hormone/genetics ; Androgens ; Prostatic Hyperplasia ; Mammals
Chemical Substances	Androgen Antagonists ; Gonadotropin-Releasing Hormone (33515-09-2) ; Androgens
Language	English
Publishing date	2023-08-29
Publishing country	Greece
Document type	Journal Article
ZDB-ID	604549-2
ISSN	1791-7530 ; 0250-7005
ISSN (online)	1791-7530
ISSN	0250-7005
DOI	10.21873/anticanres.16590
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Zs.A 1642: Show issues

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Article ; Online: Immunotherapy reverses glioma-driven dysfunction of immune system homeostasis.

DiVita Dean, Bayli / Wildes, Tyler / Dean, Joseph / Yegorov, Oleg / Yang, Changlin / Shin, David / Francis, Connor / Figg, John W / Sebastian, Mathew / Font, Laura Falceto / Jin, Dan / Reid, Alexandra / Moore, Ginger / Fernandez, Brandon / Wummer, Brandon / Kuizon, Carmelle / Mitchell, Duane / Flores, Catherine T

Journal for immunotherapy of cancer

2023 Volume 11, Issue 2

Abstract: Background: Glioma-induced immune dysregulation of the hematopoietic system has been described in a limited number of studies. In this study, our group further demonstrates that gliomas interrupt the cellular differentiation programming and outcomes of ... ...

Abstract	Background: Glioma-induced immune dysregulation of the hematopoietic system has been described in a limited number of studies. In this study, our group further demonstrates that gliomas interrupt the cellular differentiation programming and outcomes of hematopoietic stem and progenitor cells (HSPCs) in the bone marrow. HSPCs from glioma-bearing mice are reprogrammed and driven towards expansion of myeloid lineage precursors and myeloid-derived suppressor cells (MDSCs) in secondary lymphoid organs. However, we found this expansion is reversed by immunotherapy. Adoptive cellular therapy (ACT) has been demonstrably efficacious in multiple preclinical models of central nervous system (CNS) malignancies, and here we describe how glioma-induced dysfunction is reversed by this immunotherapeutic platform. Methods: The impact of orthotopic KR158B-luc glioma on HSPCs was evaluated in an unbiased fashion using single cell RNAseq (scRNAseq) of lineage Results: Using scRNAseq, we observed an altered HSPC landscape in glioma-bearing versus non-tumor-bearing mice . In addition, an expansion of myeloid lineage subsets, including granulocyte macrophage precursors (GMPs) and MDSCs, were observed in glioma-bearing mice relative to non-tumor-bearing controls. Furthermore, MDSCs from glioma-bearing mice demonstrated increased suppressive capacity toward tumor-specific T cells as compared with MDSCs from non-tumor-bearing hosts. Interestingly, treatment with ACT overcame these suppressive properties. When HSPCs from glioma-bearing mice were transferred in the context of ACT, we observed significant survival benefit and long-term cures in orthotopic glioma models compared with mice treated with ACT using non-glioma-bearing HSPCs.
MeSH term(s)	Mice ; Animals ; Cell Line, Tumor ; Glioma/pathology ; Immunotherapy ; Hematopoietic Stem Cells ; T-Lymphocytes ; Central Nervous System Neoplasms
Language	English
Publishing date	2023-02-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1136/jitc-2022-004805
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Article ; Online: Inhibition of p38α MAPK restores neuronal p38γ MAPK and ameliorates synaptic degeneration in a mouse model of DLB/PD.

Iba, Michiyo / Kim, Changyoun / Kwon, Somin / Szabo, Marcell / Horan-Portelance, Liam / Peer, Cody J / Figg, William D / Reed, Xylena / Ding, Jinhui / Lee, Seung-Jae / Rissman, Robert A / Cookson, Mark R / Overk, Cassia / Wrasidlo, Wolf / Masliah, Eliezer

Science translational medicine

2023 Volume 15, Issue 695, Page(s) eabq6089

Abstract: Alterations in the p38 mitogen-activated protein kinases (MAPKs) play an important role in the pathogenesis of dementia with Lewy bodies (DLB) and Parkinson's disease (PD). Activation of the p38α MAPK isoform and mislocalization of the p38γ MAPK isoform ... ...

Abstract	Alterations in the p38 mitogen-activated protein kinases (MAPKs) play an important role in the pathogenesis of dementia with Lewy bodies (DLB) and Parkinson's disease (PD). Activation of the p38α MAPK isoform and mislocalization of the p38γ MAPK isoform are associated with neuroinflammation and synaptic degeneration in DLB and PD. Therefore, we hypothesized that p38α might be associated with neuronal p38γ distribution and synaptic dysfunction in these diseases. To test this hypothesis, we treated in vitro cellular and in vivo mouse models of DLB/PD with SKF-86002, a compound that attenuates inflammation by inhibiting p38α/β, and then investigated the effects of this compound on p38γ and neurodegenerative pathology. We found that inhibition of p38α reduced neuroinflammation and ameliorated synaptic, neurodegenerative, and motor behavioral deficits in transgenic mice overexpressing human α-synuclein. Moreover, treatment with SKF-86002 promoted the redistribution of p38γ to synapses and reduced the accumulation of α-synuclein in mice overexpressing human α-synuclein. Supporting the potential value of targeting p38 in DLB/PD, we found that SKF-86002 promoted the redistribution of p38γ in neurons differentiated from iPS cells derived from patients with familial PD (carrying the A53T α-synuclein mutation) and healthy controls. Treatment with SKF-86002 ameliorated α-synuclein-induced neurodegeneration in these neurons only when microglia were pretreated with this compound. However, direct treatment of neurons with SKF-86002 did not affect α-synuclein-induced neurotoxicity, suggesting that SKF-86002 treatment inhibits α-synuclein-induced neurotoxicity mediated by microglia. These findings provide a mechanistic connection between p38α and p38γ as well as a rationale for targeting this pathway in DLB/PD.
MeSH term(s)	Humans ; Mice ; Animals ; Parkinson Disease/drug therapy ; Parkinson Disease/pathology ; alpha-Synuclein/metabolism ; Mitogen-Activated Protein Kinase 14/metabolism ; Neuroinflammatory Diseases ; Neurons/metabolism ; Mice, Transgenic
Chemical Substances	alpha-Synuclein ; Mitogen-Activated Protein Kinase 14 (EC 2.7.11.24) ; 6-(4-fluorophenyl)-2,3-dihydro-5-(4-pyridinyl)imidazo(2,1-b)thiazole (9R6QDF1UO7)
Language	English
Publishing date	2023-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.abq6089
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Article ; Online: Targeting the microenvironment of pancreatic cancer: overcoming treatment barriers and improving local immune responses.

Strauss, J / Alewine, C / Figg, W D / Duffy, A

Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico

2015 Volume 18, Issue 7, Page(s) 653–659

Abstract: Historically, patients diagnosed with metastatic pancreatic cancer have faced a grim prognosis. The survival benefit seen with systemic chemotherapies and even combinations thereof have been disappointing. However, growing data suggest that the ... ...

Abstract	Historically, patients diagnosed with metastatic pancreatic cancer have faced a grim prognosis. The survival benefit seen with systemic chemotherapies and even combinations thereof have been disappointing. However, growing data suggest that the microenvironment of pancreatic cancer may be contributing to this poor prognosis. This microenvironment has a dense fibrotic stroma, and is hypoxic and highly immunosuppressive, all of which pose barriers to treatment. Newer strategies looking to disrupt the fibrotic stroma, target hypoxic areas, and improve local immune responses in the tumor microenvironment are currently undergoing clinical evaluation and seem to offer great promise. In addition to these therapies, preclinical work evaluating novel cytotoxic agents including nanoparticles has also been encouraging. While much research still needs to be done, these strategies offer new hope for patients with pancreatic cancer.
MeSH term(s)	Carcinoma, Pancreatic Ductal/immunology ; Carcinoma, Pancreatic Ductal/pathology ; Humans ; Pancreatic Neoplasms/immunology ; Pancreatic Neoplasms/pathology ; Tumor Microenvironment/immunology
Language	English
Publishing date	2015-12-11
Publishing country	Italy
Document type	Journal Article ; Review
ZDB-ID	2397359-6
ISSN	1699-3055 ; 1699-048X
ISSN (online)	1699-3055
ISSN	1699-048X
DOI	10.1007/s12094-015-1459-8
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Article ; Online: A Very Long-Acting PARP Inhibitor Suppresses Cancer Cell Growth in DNA Repair-Deficient Tumor Models.

Fontaine, Shaun D / Ashley, Gary W / Houghton, Peter J / Kurmasheva, Raushan T / Diolaiti, Morgan / Ashworth, Alan / Peer, Cody J / Nguyen, Ryan / Figg, William D / Beckford-Vera, Denis R / Santi, Daniel V

Cancer research

2020 Volume 81, Issue 4, Page(s) 1076–1086

Abstract: PARP inhibitors are approved for treatment of cancers ... ...

Abstract	PARP inhibitors are approved for treatment of cancers with
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Cell Line, Tumor ; DNA Repair/drug effects ; DNA Repair/genetics ; DNA Repair-Deficiency Disorders/drug therapy ; DNA Repair-Deficiency Disorders/genetics ; DNA Repair-Deficiency Disorders/pathology ; Delayed-Action Preparations/therapeutic use ; Female ; Genes, BRCA2 ; Genes, Wilms Tumor ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Nude ; Mice, SCID ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Phthalazines/chemistry ; Phthalazines/therapeutic use ; Poly(ADP-ribose) Polymerase Inhibitors/therapeutic use ; Polyethylene Glycols/chemistry ; Polyethylene Glycols/therapeutic use ; Prodrugs/therapeutic use ; Xenograft Model Antitumor Assays ; Zirconium/chemistry ; Zirconium/therapeutic use
Chemical Substances	Antineoplastic Agents ; Delayed-Action Preparations ; Phthalazines ; Poly(ADP-ribose) Polymerase Inhibitors ; Prodrugs ; Polyethylene Glycols (3WJQ0SDW1A) ; talazoparib (9QHX048FRV) ; Zirconium (C6V6S92N3C)
Language	English
Publishing date	2020-12-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-20-1741
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Article ; Online: Metastasis-Specific Gene Expression in Autochthonous and Allograft Mouse Mammary Tumor Models: Stratification and Identification of Targetable Signatures.

Ross, Christina / Szczepanek, Karol / Lee, Maxwell / Yang, Howard / Peer, Cody J / Kindrick, Jessica / Shankarappa, Priya / Lin, Zhi-Wei / Sanford, Jack D / Figg, William D / Hunter, Kent W

Molecular cancer research : MCR

2020 Volume 18, Issue 9, Page(s) 1278–1289

Abstract: Breast cancer metastasis is a leading cause of cancer-related death of women in the United States. A hurdle in advancing metastasis-targeted intervention is the phenotypic heterogeneity between primary and secondary lesions. To identify metastasis- ... ...

Abstract	Breast cancer metastasis is a leading cause of cancer-related death of women in the United States. A hurdle in advancing metastasis-targeted intervention is the phenotypic heterogeneity between primary and secondary lesions. To identify metastasis-specific gene expression profiles we performed RNA-sequencing of breast cancer mouse models; analyzing metastases from models of various drivers and routes. We contrasted the models and identified common, targetable signatures. Allograft models exhibited more mesenchymal-like gene expression than genetically engineered mouse models (GEMM), and primary culturing of GEMM-derived metastatic tissue induced mesenchymal-like gene expression. In addition, metastasis-specific transcriptomes differed between tail vein and orthotopic injection of the same cell line. Gene expression common to models of spontaneous metastasis included sildenafil response and nicotine degradation pathways. Strikingly,
MeSH term(s)	Allografts ; Animals ; Cell Line, Tumor ; Chromatography, Liquid/methods ; Female ; Gene Expression Regulation, Neoplastic ; Male ; Mammary Neoplasms, Experimental/genetics ; Mammary Neoplasms, Experimental/metabolism ; Mammary Neoplasms, Experimental/pathology ; Mice ; Mice, Inbred C57BL ; Neoplasm Metastasis ; Neoplasm Transplantation ; Tandem Mass Spectrometry/methods
Language	English
Publishing date	2020-06-08
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-20-0046
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