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Article ; Online: An NIH National Center for Advancing Translational Sciences: is a focus on drug discovery the best option?

Littman, Bruce H

2011 Volume 10, Issue 6, Page(s) 471

MeSH term(s)	Drug Discovery/methods ; Drug Discovery/trends ; Drug Industry/trends ; Humans ; National Institutes of Health (U.S.)/trends ; Precision Medicine/methods ; Precision Medicine/trends ; Translational Medical Research/methods ; Translational Medical Research/trends ; United States
Language	English
Publishing date	2011-05-20
Publishing country	England
Document type	Comment ; Letter
ZDB-ID	2062954-0
ISSN	1474-1784 ; 1474-1776
ISSN (online)	1474-1784
ISSN	1474-1776
DOI	10.1038/nrd3357-c1
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Article: Tocilizumab and missed personalized medicine opportunities for patients with rheumatoid arthritis?

Littman, Bruce H

Arthritis and rheumatism

2009 Volume 60, Issue 5, Page(s) 1565–1566

MeSH term(s)	Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized ; Antirheumatic Agents/therapeutic use ; Arthritis, Rheumatoid/drug therapy ; Humans ; Patient Care/methods
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Antirheumatic Agents ; tocilizumab (I031V2H011)
Language	English
Publishing date	2009-05
Publishing country	United States
Document type	Letter
ZDB-ID	127294-9
ISSN	1529-0131 ; 0004-3591 ; 2326-5191
ISSN (online)	1529-0131
ISSN	0004-3591 ; 2326-5191
DOI	10.1002/art.24474
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Article: Translational strategies to implement personalized medicine: rheumatoid arthritis examples.

Littman, Bruce H

Personalized medicine

2009 Volume 6, Issue 4, Page(s) 429–437

Abstract: Advances in the molecular definition of disease, biomarker technologies and informatics have brought us to the threshold of a new way to individualize treatment for patients - personalized medicine. However, while the clinical translation of drug ... ...

Abstract	Advances in the molecular definition of disease, biomarker technologies and informatics have brought us to the threshold of a new way to individualize treatment for patients - personalized medicine. However, while the clinical translation of drug metabolism and cancer-related genomics data has resulted in accepted individualized treatment paradigms, this has not occurred as frequently or efficiently for patients with common chronic diseases such as rheumatoid arthritis. This gap between the rapidly increasing amount of disease-related genomic information and its clinical translation can be addressed through the creation and testing of personalized medicine treatment hypotheses using the same strategies that translational medicine scientists utilize to achieve proof-of-concept for drugs with novel targets. This is illustrated with three testable personalized medicine hypotheses for rheumatoid arthritis where known genetic markers in patients can potentially be used to select the most appropriate treatments and dose. Incentives resulting from changes in government and regulatory agency policies, investments in sample and data repositories, acceptance of new economic models by pharmaceutical companies and third party payers as well as more training, research support and academic opportunities for translational medicine scientists are all needed to speed up the implementation of personalized medicine for patients with rheumatoid arthritis and other common chronic diseases.
Language	English
Publishing date	2009-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2299146-3
ISSN	1744-828X ; 1741-0541
ISSN (online)	1744-828X
ISSN	1741-0541
DOI	10.2217/pme.09.17
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Article ; Online: Targeting B-Raf inhibitor resistant melanoma with novel cell penetrating peptide disrupters of PDE8A - C-Raf.

Blair, Connor M / Walsh, Nicola M / Littman, Bruce H / Marcoux, Frank W / Baillie, George S

BMC cancer

2019 Volume 19, Issue 1, Page(s) 266

Abstract: Background: Recent advances in the treatment of melanoma that involve immunotherapy and B-Raf inhibition have revolutionised cancer care for this disease. However, an un-met clinical need remains in B-Raf inhibitor resistant patients where first- ... ...

Abstract	Background: Recent advances in the treatment of melanoma that involve immunotherapy and B-Raf inhibition have revolutionised cancer care for this disease. However, an un-met clinical need remains in B-Raf inhibitor resistant patients where first-generation B-Raf inhibitors provide only short-term disease control. In these cases, B-Raf inhibition leads to paradoxical activation of the C-Raf - MEK - ERK signalling pathway, followed by metastasis. PDE8A has been shown to directly interact with and modulate the cAMP microdomain in the vicinity of C-Raf. This interaction promotes C-Raf activation by attenuating the PKA-mediated inhibitory phosphorylation of the kinase. Methods: We have used a novel cell-penetrating peptide agent (PPL-008) that inhibits the PDE8A - C-Raf complex in a human malignant MM415 melanoma cell line and MM415 melanoma xenograft mouse model to investigate ERK MAP kinase signalling. Results: We have demonstrated that the PDE8A - C-Raf complex disruptor PPL-008 increased inhibitory C-Raf-S259 phosphorylation and significantly reduced phospho-ERK signalling. We have also discovered that the ability of PPL-008 to dampen ERK signalling can be used to counter B-Raf inhibitor-driven paradoxical activation of phospho-ERK in MM415 cells treated with PLX4032 (Vemurafenib). PPL-008 treatment also significantly retarded the growth of these cells. When applied to a MM415 melanoma xenograft mouse model, PPL-008C penetrated tumour tissue and significantly reduced phospho-ERK signalling in that domain. Conclusion: Our data suggests that the PDE8A-C-Raf complex is a promising therapeutic treatment for B-Raf inhibitor resistant melanoma.
MeSH term(s)	3',5'-Cyclic-AMP Phosphodiesterases/metabolism ; Animals ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Cell-Penetrating Peptides/administration & dosage ; Cell-Penetrating Peptides/pharmacology ; Drug Resistance, Neoplasm/drug effects ; Female ; Humans ; MAP Kinase Signaling System/drug effects ; Melanoma/drug therapy ; Melanoma/metabolism ; Mice ; Protein Binding/drug effects ; Proto-Oncogene Proteins c-raf/metabolism ; Vemurafenib/administration & dosage ; Vemurafenib/pharmacology ; Xenograft Model Antitumor Assays
Chemical Substances	Cell-Penetrating Peptides ; Vemurafenib (207SMY3FQT) ; Proto-Oncogene Proteins c-raf (EC 2.7.11.1) ; Raf1 protein, human (EC 2.7.11.1) ; 3',5'-Cyclic-AMP Phosphodiesterases (EC 3.1.4.17) ; PDE8A protein, human (EC 3.1.4.17)
Language	English
Publishing date	2019-03-25
Publishing country	England
Document type	Journal Article
ISSN	1471-2407
ISSN (online)	1471-2407
DOI	10.1186/s12885-019-5489-4
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Enforced gut homing of murine regulatory T cells reduces early graft-versus-host disease severity.

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons

2023 Volume 23, Issue 8, Page(s) 1102–1115

Abstract: Damage to the gastrointestinal tract following allogeneic hematopoietic stem cell transplantation is a significant contributor to the severity and perpetuation of graft-versus-host disease. In preclinical models and clinical trials, we showed that ... ...

Abstract	Damage to the gastrointestinal tract following allogeneic hematopoietic stem cell transplantation is a significant contributor to the severity and perpetuation of graft-versus-host disease. In preclinical models and clinical trials, we showed that infusing high numbers of regulatory T cells reduces graft-versus-host disease incidence. Despite no change in in vitro suppressive function, transfer of ex vivo expanded regulatory T cells transduced to overexpress G protein-coupled receptor 15 or C-C motif chemokine receptor 9, specific homing receptors for colon or small intestine, respectively, lessened graft-versus-host disease severity in mice. Increased regulatory T cell frequency and retention within the gastrointestinal tissues of mice that received gut homing T cells correlated with lower inflammation and gut damage early post-transplant, decreased graft-versus-host disease severity, and prolonged survival compared with those receiving control transduced regulatory T cells. These data provide evidence that enforced targeting of ex vivo expanded regulatory T cells to the gastrointestinal tract diminishes gut injury and is associated with decreased graft-versus-host disease severity.
MeSH term(s)	Animals ; Mice ; T-Lymphocytes, Regulatory ; Graft vs Host Disease/etiology ; Graft vs Host Disease/prevention & control ; Graft vs Host Disease/drug therapy ; Hematopoietic Stem Cell Transplantation/adverse effects ; Intestine, Small ; Inflammation
Language	English
Publishing date	2023-03-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2060594-8
ISSN	1600-6143 ; 1600-6135
ISSN (online)	1600-6143
ISSN	1600-6135
DOI	10.1016/j.ajt.2023.01.030
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Article ; Online: Create a translational medicine knowledge repository--research downsizing, mergers and increased outsourcing have reduced the depth of in-house translational medicine expertise and institutional memory at many pharmaceutical and biotech companies: how will they avoid relearning old lessons?

Littman, Bruce H / Marincola, Francesco M

Journal of translational medicine

2011 Volume 9, Page(s) 56

Abstract: Pharmaceutical industry consolidation and overall research downsizing threatens the ability of companies to benefit from their previous investments in translational research as key leaders with the most knowledge of the successful use of biomarkers and ... ...

Abstract	Pharmaceutical industry consolidation and overall research downsizing threatens the ability of companies to benefit from their previous investments in translational research as key leaders with the most knowledge of the successful use of biomarkers and translational pharmacology models are laid off or accept their severance packages. Two recently published books may help to preserve this type of knowledge but much of this type of information is not in the public domain. Here we propose the creation of a translational medicine knowledge repository where companies can submit their translational research data and access similar data from other companies in a precompetitive environment. This searchable repository would become an invaluable resource for translational scientists and drug developers that could speed and reduce the cost of new drug development.
MeSH term(s)	Academies and Institutes/economics ; Academies and Institutes/organization & administration ; Biotechnology/economics ; Biotechnology/organization & administration ; Databases as Topic ; Drug Discovery/economics ; Drug Discovery/organization & administration ; Drug Industry/economics ; Drug Industry/organization & administration ; Health Facility Merger ; Humans ; Knowledge ; Outsourced Services/economics ; Outsourced Services/organization & administration ; Personnel Downsizing/economics ; Personnel Downsizing/organization & administration ; Professional Competence ; Translational Medical Research/economics ; Translational Medical Research/organization & administration
Language	English
Publishing date	2011-05-10
Publishing country	England
Document type	Editorial
ISSN	1479-5876
ISSN (online)	1479-5876
DOI	10.1186/1479-5876-9-56
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book: Translational medicine and drug discovery

Littman, Bruce H / Krishna, Rajesh

2011

Abstract: Focuses on the new discipline of translational medicine as it pertains to drug development within the pharmaceutical and biotechnology industry"--Provided by publisher. ...

Author's details	edited by Bruce H. Littman, Rajesh Krishna
Abstract	"Focuses on the new discipline of translational medicine as it pertains to drug development within the pharmaceutical and biotechnology industry"--Provided by publisher.
MeSH term(s)	Drug Discovery ; Translational Medical Research/methods
Language	English
Size	xx, 361 p. :, ill.
Publisher	Cambridge University Press
Publishing place	Cambridge
Document type	Book
ISBN	9780521886451 ; 0521886457
Database	Catalogue of the US National Library of Medicine (NLM)

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Article: The ultimate model organism: progress in experimental medicine.

Littman, Bruce H / Williams, Stephen A

Nature reviews. Drug discovery

2005 Volume 4, Issue 8, Page(s) 631–638

Abstract: Experimental medicine is the use of innovative measurements, models and designs in studying human subjects for establishing proof of mechanism and concept of new drugs, for exploring the potential for market differentiation for successful drug candidates, ...

Abstract	Experimental medicine is the use of innovative measurements, models and designs in studying human subjects for establishing proof of mechanism and concept of new drugs, for exploring the potential for market differentiation for successful drug candidates, and for efficiently terminating the development of unsuccessful ones. Humans are the ultimate 'model' because of the uncertain validity and efficacy of novel targets and drug candidates that emerge from genomics, combinatorial chemistry and high-throughput screening and the use of poorly predictive preclinical models. The in-depth investigation of the effects of drugs and the nature of disease progression is becoming ever more feasible because of advances in clinical biomarkers.
MeSH term(s)	Animals ; Clinical Trials as Topic/classification ; Clinical Trials as Topic/methods ; Clinical Trials as Topic/trends ; Connecticut ; Disease Models, Animal ; Drug Industry/methods ; Drug Industry/organization & administration ; Drug Industry/trends ; History, 20th Century ; Human Experimentation/ethics ; Human Experimentation/history ; Human Experimentation/standards ; Humans ; Technology, Pharmaceutical/methods ; Technology, Pharmaceutical/trends
Language	English
Publishing date	2005-08
Publishing country	England
Document type	Historical Article ; Journal Article ; Review
ZDB-ID	2062954-0
ISSN	1474-1784 ; 1474-1776
ISSN (online)	1474-1784
ISSN	1474-1776
DOI	10.1038/nrd1800
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Article ; Online: Create a translational medicine knowledge repository - Research downsizing, mergers and increased outsourcing have reduced the depth of in-house translational medicine expertise and institutional memory at many pharmaceutical and biotech companies

Marincola Francesco M / Littman Bruce H

Journal of Translational Medicine, Vol 9, Iss 1, p

how will they avoid relearning old lessons?

2011 Volume 56

Abstract: Abstract Pharmaceutical industry consolidation and overall research downsizing threatens the ability of companies to benefit from their previous investments in translational research as key leaders with the most knowledge of the successful use of ... ...

Abstract	Abstract Pharmaceutical industry consolidation and overall research downsizing threatens the ability of companies to benefit from their previous investments in translational research as key leaders with the most knowledge of the successful use of biomarkers and translational pharmacology models are laid off or accept their severance packages. Two recently published books may help to preserve this type of knowledge but much of this type of information is not in the public domain. Here we propose the creation of a translational medicine knowledge repository where companies can submit their translational research data and access similar data from other companies in a precompetitive environment. This searchable repository would become an invaluable resource for translational scientists and drug developers that could speed and reduce the cost of new drug development.
Keywords	Medicine ; R
Subject code	020
Language	English
Publishing date	2011-05-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Anti-inflammatory Activity of MTL-CEBPA, a Small Activating RNA Drug, in LPS-Stimulated Monocytes and Humanized Mice.

Zhou, Jiehua / Li, Haitang / Xia, Xin / Herrera, Alberto / Pollock, Nicolette / Reebye, Vikash / Sodergren, Mikael H / Dorman, Stephanie / Littman, Bruce H / Doogan, Declan / Huang, Kai-Wen / Habib, Robert / Blakey, David / Habib, Nagy A / Rossi, John J

Molecular therapy : the journal of the American Society of Gene Therapy

2019 Volume 27, Issue 5, Page(s) 999–1016

Abstract: Excessive or inappropriate inflammatory responses can cause serious and even fatal diseases. The CCAAT/enhancer-binding protein alpha (CEBPA) gene encodes C/EBPα, a transcription factor that plays a fundamental role in controlling maturation of the ... ...

Abstract	Excessive or inappropriate inflammatory responses can cause serious and even fatal diseases. The CCAAT/enhancer-binding protein alpha (CEBPA) gene encodes C/EBPα, a transcription factor that plays a fundamental role in controlling maturation of the myeloid lineage and is also expressed during the late phase of inflammatory responses when signs of inflammation are decreasing. MTL-CEBPA, a small activating RNA targeting for upregulation of C/EBPα, is currently being evaluated in a phase 1b trial for treatment of hepatocellular carcinoma. After dosing, subjects had reduced levels of pro-inflammatory cytokines, and we therefore hypothesized that MTL-CEBPA has anti-inflammatory potential. The current study was conducted to determine the effects of C/EBPα saRNA - CEBPA-51 - on inflammation in vitro and in vivo after endotoxin challenge. CEBPA-51 led to increased expression of the C/EBPα gene and inhibition of pro-inflammatory cytokines in THP-1 monocytes previously stimulated by E. coli-derived lipopolysaccharide (LPS). Treatment with MTL-CEBPA in an LPS-challenged humanized mouse model upregulated C/EBPα mRNA, increased neutrophils, and attenuated production of several key pro-inflammatory cytokines, including TNF-α, IL-6, IL-1β, and IFN-γ. In addition, a Luminex analysis of mouse serum revealed that MTL-CEBPA reduced pro-inflammatory cytokines and increased the anti-inflammatory cytokine IL-10. Collectively, the data support further investigation of MTL-CEBPA in acute and chronic inflammatory diseases where this mechanism has pathogenic importance.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; CCAAT-Enhancer-Binding Proteins/antagonists & inhibitors ; CCAAT-Enhancer-Binding Proteins/genetics ; Gene Expression Regulation/drug effects ; Humans ; Inflammation/chemically induced ; Inflammation/genetics ; Inflammation/pathology ; Inflammation/therapy ; Interleukin-10/genetics ; Interleukin-1beta/genetics ; Lipopolysaccharides/toxicity ; Mice ; Monocytes/drug effects ; Monocytes/metabolism ; RNA/genetics ; RNA/pharmacology ; RNA, Messenger/genetics ; Tumor Necrosis Factor-alpha/genetics
Chemical Substances	Anti-Inflammatory Agents ; CCAAT-Enhancer-Binding Proteins ; CEBPA protein, human ; IL10 protein, human ; IL1B protein, human ; Interleukin-1beta ; Lipopolysaccharides ; RNA, Messenger ; Tumor Necrosis Factor-alpha ; Interleukin-10 (130068-27-8) ; RNA (63231-63-0)
Language	English
Publishing date	2019-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1016/j.ymthe.2019.02.018
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