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Article ; Online: A multi-targeted approach to treating bone metastases.

Camacho, Daniel F / Pienta, Kenneth J

2014 Volume 33, Issue 2-3, Page(s) 545–553

Abstract: The treatment of bone-metastatic cancer now takes advantage of the unique biology of this clinical state. The complex interplay between the cancer cells and the bone microenvironment leads to a host of therapeutic targets, with agents in various stages ... ...

Abstract	The treatment of bone-metastatic cancer now takes advantage of the unique biology of this clinical state. The complex interplay between the cancer cells and the bone microenvironment leads to a host of therapeutic targets, with agents in various stages of clinical use or study. Targets include interactions between the cancer cells and osteoclasts, osteoblasts, endothelial cells, stromal cells, hematopoietic progenitor cells, cells of the immune system, and the bone matrix. Efforts at understanding specific mechanisms of drug resistance in the bone are also ongoing. Successful clinical outcomes will be the result of co-targeting and interrupting the various tumor-supportive elements and cooperating pathways at the level of the tumor cell, the primary and metastatic microenvironments, and systemic cancer effects, leading to a "scaled network disruption" to undermine the disease state.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Bone Matrix/drug effects ; Bone Matrix/metabolism ; Bone Neoplasms/drug therapy ; Bone Neoplasms/metabolism ; Bone Neoplasms/secondary ; Drug Resistance, Neoplasm ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Hematopoietic Stem Cells/drug effects ; Hematopoietic Stem Cells/metabolism ; Humans ; Immunity/drug effects ; Male ; Molecular Targeted Therapy ; Osteoblasts/drug effects ; Osteoblasts/metabolism ; Osteoclasts/drug effects ; Osteoclasts/metabolism ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Tumor Microenvironment/drug effects
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2014-09
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	604857-2
ISSN	1573-7233 ; 0167-7659
ISSN (online)	1573-7233
ISSN	0167-7659
DOI	10.1007/s10555-013-9476-y
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Article ; Online: Disrupting the networks of cancer.

Camacho, Daniel F / Pienta, Kenneth J

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

2012 Volume 18, Issue 10, Page(s) 2801–2808

Abstract: Ecosystems are interactive systems involving communities of species and their abiotic environment. Tumors are ecosystems in which cancer cells act as invasive species interacting with native host cell species in an established microenvironment within the ...

Abstract	Ecosystems are interactive systems involving communities of species and their abiotic environment. Tumors are ecosystems in which cancer cells act as invasive species interacting with native host cell species in an established microenvironment within the larger host biosphere. At its heart, to study ecology is to study interconnectedness. In ecologic science, an ecologic network is a representation of the biotic interactions in an ecosystem in which species (nodes) are connected by pairwise interactions (links). Ecologic networks and signaling network models have been used to describe and compare the structures of ecosystems. It has been shown that disruption of ecologic networks through the loss of species or disruption of interactions between them can lead to the destruction of the ecosystem. Often, the destruction of a single node or link is not enough to disrupt the entire ecosystem. The more complex the network and its interactions, the more difficult it is to cause the extinction of a species, especially without leveraging other aspects of the ecosystem. Similarly, successful treatment of cancer with a single agent is rarely enough to cure a patient without strategically modifying the support systems conducive to survival of cancer. Cancer cells and the ecologic systems they reside in can be viewed as a series of nested networks. The most effective new paradigms for treatment will be developed through application of scaled network disruption.
MeSH term(s)	Cell Nucleus/metabolism ; Chemokines/metabolism ; Cytokines/metabolism ; Humans ; Metabolic Networks and Pathways ; Models, Biological ; Neoplasm Metastasis ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Signal Transduction ; Tumor Microenvironment
Chemical Substances	Chemokines ; Cytokines
Language	English
Publishing date	2012-03-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-12-0366
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Article: IL-33 Drives Monocyte Recruitment to Lung Interstitium through Chemokine Upregulation.

Tjota, Melissa Y / Camacho, Daniel F / Turnquist, Heth R / Sperling, Anne I

ImmunoHorizons

2017 Volume 1, Issue 6, Page(s) 101–108

Abstract: Tissue infiltration by circulating monocytes is a critical step in the initiation and augmentation of type 2 inflammatory responses in the lungs. Our studies demonstrate that IL- ... ...

Abstract	Tissue infiltration by circulating monocytes is a critical step in the initiation and augmentation of type 2 inflammatory responses in the lungs. Our studies demonstrate that IL-33
Language	English
Publishing date	2017-08-01
Publishing country	United States
Document type	Journal Article
ISSN	2573-7732
ISSN	2573-7732
DOI	10.4049/immunohorizons.1700024
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Article ; Online: IRF4 expression by lung dendritic cells drives acute but not Trm cell-dependent memory Th2 responses.

Camacho, Daniel F / Velez, Tania E / Hollinger, Maile K / Wang, Esther / Howard, Chanie L / Darnell, Eli P / Kennedy, Domenick E / Krishack, Paulette A / Hrusch, Cara L / Clark, Marcus R / Moon, James J / Sperling, Anne I

JCI insight

2022 Volume 7, Issue 21

Abstract: Expression of the transcription factor interferon regulatory factor 4 (IRF4) is required for the development of lung conventional DCs type 2 (cDC2s) that elicit Th2 responses, yet how IRF4 functions in lung cDC2s throughout the acute and memory allergic ... ...

Abstract	Expression of the transcription factor interferon regulatory factor 4 (IRF4) is required for the development of lung conventional DCs type 2 (cDC2s) that elicit Th2 responses, yet how IRF4 functions in lung cDC2s throughout the acute and memory allergic response is not clear. Here, we used a mouse model that loses IRF4 expression after lung cDC2 development to demonstrate that mice with IRF4-deficient DCs display impaired memory responses to allergen. This defect in the memory response was a direct result of ineffective Th2 induction and impaired recruitment of activated effector T cells to the lung after sensitization. IRF4-deficient DCs demonstrated defects in their migration to the draining lymph node and in T cell priming. Finally, T cells primed by IRF4-competent DCs mediated potent memory responses independently of IRF4-expressing DCs, demonstrating that IRF4-expressing DCs are not necessary during the memory response. Thus, IRF4 controlled a program in mature DCs governing Th2 priming and effector responses, but IRF4-expressing DCs were dispensable during tissue-resident memory T cell-dependent memory responses.
MeSH term(s)	Animals ; Mice ; Allergens ; Dendritic Cells ; Gene Expression Regulation ; Interferon Regulatory Factors/genetics ; Interferon Regulatory Factors/metabolism ; Lung/pathology ; Memory T Cells/immunology ; Th2 Cells ; Immunologic Memory
Chemical Substances	Allergens ; Interferon Regulatory Factors
Language	English
Publishing date	2022-11-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.140384
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Article: Leveraging Framework Instability: A Journey from Energy Storage to Drug Delivery

Suresh, Kuthuru / López-Mejías, Vilmalí / Roy, Saikat / Camacho, Daniel F. / Matzger, Adam J.

Synlett

2020 Volume 31, Issue 16, Page(s) 1573–1580

Abstract: Amorphous pharmaceuticals often suffer from poor physical stability, which can negate their high solubility, fast dissolution rate, and better oral bioavailability vs. crystalline forms. This represents a major hurdle to processing, storage, and delivery ...

Abstract	Amorphous pharmaceuticals often suffer from poor physical stability, which can negate their high solubility, fast dissolution rate, and better oral bioavailability vs. crystalline forms. This represents a major hurdle to processing, storage, and delivery of amorphous pharmaceuticals. Several approaches to addressing these problems have been pursued, but there is still a need for a general method for stabilizing the amorphous form. We describe a novel approach using a water-unstable metal-organic framework as a drug delivery vehicle that demonstrates improved amorphous form stability accompanied by remarkably enhanced solubility and a fast dissolution rate. This research project spanned eleven years from conception to realization and dissemination. With origins in understanding the stability or porous solids for energy storage materials, the work also highlights potential of basic science understanding to illuminate new areas of application.
Keywords	pharmaceuticals ; amorphous form ; metal-organic frameworks ; stability ; solubility and dissolution rate
Language	English
Publishing date	2020-06-18
Publisher	© Georg Thieme Verlag
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	2042012-2
ISSN	1437-2096 ; 0936-5214
ISSN (online)	1437-2096
ISSN	0936-5214
DOI	10.1055/s-0040-1707139
Database	Thieme publisher's database

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Article ; Online: Adjuvant-free nanofiber vaccine induces in situ lung dendritic cell activation and T

Si, Youhui / Tian, Qiaomu / Zhao, Fan / Kelly, Sean H / Shores, Lucas S / Camacho, Daniel F / Sperling, Anne I / Andrade, Michael S / Collier, Joel H / Chong, Anita S

Science advances

2020 Volume 6, Issue 32, Page(s) eaba0995

Abstract: The current paradigm that subunit vaccines require adjuvants to optimally activate innate immunity implies that increased vaccine reactogenicity will invariably be linked to improved immunogenicity. Countering this paradigm, nanoparticulate vaccines have ...

Abstract	The current paradigm that subunit vaccines require adjuvants to optimally activate innate immunity implies that increased vaccine reactogenicity will invariably be linked to improved immunogenicity. Countering this paradigm, nanoparticulate vaccines have been reported to act as delivery systems for vaccine antigens and induce immunity without the need for exogenous adjuvants or local inflammation; however, the mechanisms underlying the immunogenicity of nanoparticle vaccines are incompletely identified. Here, we show that antigens displayed on self-assembling nanofiber scaffolds and delivered intranasally are presented by CD103
MeSH term(s)	Adjuvants, Immunologic ; Dendritic Cells ; Lung ; Nanofibers ; Vaccines, Subunit
Chemical Substances	Adjuvants, Immunologic ; Vaccines, Subunit
Language	English
Publishing date	2020-08-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.aba0995
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Article ; Online: Pro-lymphangiogenic VEGFR-3 signaling modulates memory T cell responses in allergic airway inflammation.

Maisel, Katharina / Hrusch, Cara L / Medellin, Jorge E G / Potin, Lambert / Chapel, David B / Nurmi, Harri / Camacho, Daniel F / Gleyzer, Rachel / Alitalo, Kari / Sperling, Anne I / Swartz, Melody A

Mucosal immunology

2020 Volume 14, Issue 1, Page(s) 144–151

Abstract: In allergic airway inflammation, VEGFR-3-mediated lymphangiogenesis occurs in humans and mouse models, yet its immunological roles, particularly in adaptive immunity, are poorly understood. Here, we explored how pro-lymphangiogenic signaling affects the ... ...

Abstract	In allergic airway inflammation, VEGFR-3-mediated lymphangiogenesis occurs in humans and mouse models, yet its immunological roles, particularly in adaptive immunity, are poorly understood. Here, we explored how pro-lymphangiogenic signaling affects the allergic response to house dust mite (HDM). In the acute inflammatory phase, the lungs of mice treated with blocking antibodies against VEGFR-3 (mF4-31C1) displayed less inflammation overall, with dramatically reduced innate and T-cell numbers and reduced inflammatory chemokine levels. However, when inflammation was allowed to resolve and memory recall was induced 2 months later, mice treated with mF4-31C1 as well as VEGF-C/-D knockout models showed exacerbated type 2 memory response to HDM, with increased Th2 cells, eosinophils, type 2 chemokines, and pathological inflammation scores. This was associated with lower CCL21 and decreased T
MeSH term(s)	Allergens ; Animals ; Biomarkers ; Disease Susceptibility ; Immunologic Memory ; Immunophenotyping ; Lymphangiogenesis/genetics ; Mice ; Pyroglyphidae/immunology ; Respiratory Hypersensitivity/etiology ; Respiratory Hypersensitivity/metabolism ; Respiratory Hypersensitivity/pathology ; Signal Transduction ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Vascular Endothelial Growth Factor C/genetics ; Vascular Endothelial Growth Factor C/metabolism ; Vascular Endothelial Growth Factor Receptor-3/genetics ; Vascular Endothelial Growth Factor Receptor-3/metabolism
Chemical Substances	Allergens ; Biomarkers ; Vascular Endothelial Growth Factor C ; vascular endothelial growth factor C, mouse ; Vascular Endothelial Growth Factor Receptor-3 (EC 2.7.10.1)
Language	English
Publishing date	2020-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2411370-0
ISSN	1935-3456 ; 1933-0219
ISSN (online)	1935-3456
ISSN	1933-0219
DOI	10.1038/s41385-020-0308-4
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Article ; Online: Protection against Staphylococcus aureus bacteremia-induced mortality depends on ILC2s and eosinophils.

Krishack, Paulette A / Louviere, Tyler J / Decker, Trevor S / Kuzel, Timothy G / Greenberg, Jared A / Camacho, Daniel F / Hrusch, Cara L / Sperling, Anne I / Verhoef, Philip A

JCI insight

2019 Volume 4, Issue 6

Abstract: The dysregulated, unbalanced immune response of sepsis results in a mortality exceeding 20%, yet recent findings by our group indicate that patients with allergic, type 2-mediated immune diseases are protected from developing sepsis. We evaluated CD4+ Th ...

Abstract	The dysregulated, unbalanced immune response of sepsis results in a mortality exceeding 20%, yet recent findings by our group indicate that patients with allergic, type 2-mediated immune diseases are protected from developing sepsis. We evaluated CD4+ Th cell polarization among patients with Staphylococcus aureus bacteremia and confirmed that survivors had a higher percentage of circulating Th2 cells but lower frequencies of Th17 cells and neutrophils early in the course of infection. To establish the mechanism of this protection, we used a mouse model of lethal S. aureus bacteremia and found that intratracheal pretreatment with the type 2-initiating cytokine IL-33 activated pulmonary type 2 innate lymphoid cells (ILC2s) and promoted eosinophilia. In addition, stimulation of type 2 immunity before lethal infection suppressed the pulmonary neutrophilic response to S. aureus. Mice lacking functional ILC2s did not respond to IL-33 and were not protected from lethal bacteremia, but treatment of these mice with the type 2 cytokines IL-5 and IL-13 rescued them from death. Depletion of eosinophils abrogated IL-33-mediated protection, indicating that eosinophilia is also necessary for the survival benefit. Thus, we have identified a potentially novel mechanism by which type 2 immunity can balance dysregulated septic inflammatory responses, thereby clarifying the protective benefit of type 2 immune diseases on sepsis mortality.
MeSH term(s)	Animals ; Antigens, CD1d/genetics ; Asthma/immunology ; Bacteremia/mortality ; Bacteremia/prevention & control ; Cytokines/metabolism ; Disease Models, Animal ; Eosinophils/immunology ; Eosinophils/metabolism ; Humans ; Hypersensitivity ; Immunity, Innate ; Interleukin-13 ; Interleukin-33/immunology ; Interleukin-5 ; Lung/metabolism ; Lung/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neutrophils/immunology ; Promyelocytic Leukemia Zinc Finger Protein/genetics ; Pulmonary Edema/immunology ; Pulmonary Edema/pathology ; Staphylococcal Infections/immunology ; Staphylococcus aureus/immunology ; Th17 Cells/immunology ; Th2 Cells/immunology
Chemical Substances	Antigens, CD1d ; CD1d antigen, mouse ; Cytokines ; IL33 protein, human ; Il33 protein, mouse ; Interleukin-13 ; Interleukin-33 ; Interleukin-5 ; Promyelocytic Leukemia Zinc Finger Protein ; Zbtb16 protein, mouse
Language	English
Publishing date	2019-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.124168
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Article ; Online: Mechanisms of cancer cell metastasis to the bone: a multistep process.

Patel, Lalit R / Camacho, Daniel F / Shiozawa, Yusuke / Pienta, Kenneth J / Taichman, Russell S

Future oncology (London, England)

2011 Volume 7, Issue 11, Page(s) 1285–1297

Abstract: For metastasis to occur, tumor cells must first detach from their tissue of origin. This requires altering both the tissue of origin and the cancer cell. Once detached, cancer cells in circulation must also acquire survival mechanisms. Although many may ... ...

Abstract	For metastasis to occur, tumor cells must first detach from their tissue of origin. This requires altering both the tissue of origin and the cancer cell. Once detached, cancer cells in circulation must also acquire survival mechanisms. Although many may successfully disseminate, variation exists in the efficiency with which circulating tumor cells home to and invade the bone marrow as metastastic seeds. Disseminated tumor cells that do successfully invade the marrow are secured by cell-cell and cell-extracellular matrix adhesion. However, establishing a foothold in the marrow is not sufficient for disseminated tumor cells to create metastases. A significant latent phase must be overcome by either rescuing cellular proliferation or attenuating micrometastatic mass dormancy programs. Finally, growing metastases fuel osteolysis, osteoblastogenesis and T-cell differentiation, creating a variety of tumor phenotypes. Each step in the metastatic cascade is rich in biological targets and mechanistic pathways.
MeSH term(s)	Bone Marrow/metabolism ; Bone Marrow/pathology ; Bone Neoplasms/mortality ; Bone Neoplasms/pathology ; Bone Neoplasms/secondary ; Breast Neoplasms/pathology ; Cell Adhesion ; Chemokines/metabolism ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Female ; Humans ; Lung Neoplasms/pathology ; Male ; Neoplasm Invasiveness ; Neoplasm Metastasis/pathology ; Neoplasm Metastasis/physiopathology ; Neoplastic Cells, Circulating ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Prostatic Neoplasms/pathology
Chemical Substances	Chemokines
Language	English
Publishing date	2011-11-21
Publishing country	England
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. ; Review
ZDB-ID	2274956-1
ISSN	1744-8301 ; 1479-6694
ISSN (online)	1744-8301
ISSN	1479-6694
DOI	10.2217/fon.11.112
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Zs.A 6478: Show issues

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Article ; Online: Role of transcriptional corepressor CtBP1 in prostate cancer progression.

Wang, Rui / Asangani, Irfan A / Chakravarthi, Balabhadrapatruni V S K / Ateeq, Bushra / Lonigro, Robert J / Cao, Qi / Mani, Ram-Shankar / Camacho, Daniel F / McGregor, Natalie / Schumann, Taibriana E W / Jing, Xiaojun / Menawat, Radhika / Tomlins, Scott A / Zheng, Heng / Otte, Arie P / Mehra, Rohit / Siddiqui, Javed / Dhanasekaran, Saravana M / Nyati, Mukesh K /

Pienta, Kenneth J / Palanisamy, Nallasivam / Kunju, Lakshmi P / Rubin, Mark A / Chinnaiyan, Arul M / Varambally, Sooryanarayana

Neoplasia (New York, N.Y.)

2012 Volume 14, Issue 10, Page(s) 905–914

Abstract: Transcriptional repressors and corepressors play a critical role in cellular homeostasis and are frequently altered in cancer. C-terminal binding protein 1 (CtBP1), a transcriptional corepressor that regulates the expression of tumor suppressors and ... ...

Abstract	Transcriptional repressors and corepressors play a critical role in cellular homeostasis and are frequently altered in cancer. C-terminal binding protein 1 (CtBP1), a transcriptional corepressor that regulates the expression of tumor suppressors and genes involved in cell death, is known to play a role in multiple cancers. In this study, we observed the overexpression and mislocalization of CtBP1 in metastatic prostate cancer and demonstrated the functional significance of CtBP1 in prostate cancer progression. Transient and stable knockdown of CtBP1 in prostate cancer cells inhibited their proliferation and invasion. Expression profiling studies of prostate cancer cell lines revealed that multiple tumor suppressor genes are repressed by CtBP1. Furthermore, our studies indicate a role for CtBP1 in conferring radiation resistance to prostate cancer cell lines. In vivo studies using chicken chorioallantoic membrane assay, xenograft studies, and murine metastasis models suggested a role for CtBP1 in prostate tumor growth and metastasis. Taken together, our studies demonstrated that dysregulated expression of CtBP1 plays an important role in prostate cancer progression and may serve as a viable therapeutic target.
MeSH term(s)	Alcohol Oxidoreductases/antagonists & inhibitors ; Alcohol Oxidoreductases/genetics ; Alcohol Oxidoreductases/metabolism ; Animals ; Apoptosis ; Blotting, Western ; Cell Movement ; Cell Proliferation ; Chick Embryo ; Chorioallantoic Membrane/metabolism ; Chorioallantoic Membrane/pathology ; Chromatin Immunoprecipitation ; DNA-Binding Proteins/antagonists & inhibitors ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Gene Expression Profiling ; Genes, Tumor Suppressor ; Humans ; Immunoenzyme Techniques ; Lung Neoplasms/genetics ; Lung Neoplasms/prevention & control ; Lung Neoplasms/secondary ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Invasiveness ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Prostatic Neoplasms/prevention & control ; RNA, Small Interfering/genetics ; Radiation Tolerance ; Tumor Cells, Cultured
Chemical Substances	DNA-Binding Proteins ; RNA, Small Interfering ; Alcohol Oxidoreductases (EC 1.1.-) ; C-terminal binding protein (EC 1.1.1.-)
Language	English
Publishing date	2012-10-05
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	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1593/neo.121192
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