Current Search: Inflammation (x)
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- Title
- Adhesion molecules thatregulate inflammatory cell interactions.
- Creator
- Wegner, C. D., Wallace, R. W., Harbor Branch Oceanographic Institute
- Date Issued
- 1993
- PURL
- http://purl.flvc.org/fau/fd/FA00007308
- Subject Headings
- Cell Adhesion Molecules, Cellular immunity, Inflammation--Immunological aspects
- Format
- Document (PDF)
- Title
- Investigation of cell stiffness and cytoskeletal remodeling in response to inflammatory mediators using atomic force microscopy (AFM).
- Creator
- Magny, Sherlyne, Wojcikiewicz, Ewa P.
- Date Issued
- 2013-04-05
- PURL
- http://purl.flvc.org/fcla/dt/3361120
- Subject Headings
- Atomic force microscopy, Inflammation--Mediators, Cancer cells, Cytoskeleton
- Format
- Document (PDF)
- Title
- ROLE OF INTERLEUKIN-1 RECEPTOR-ASSOCIATED KINASES IN CHRONIC INFLAMMATION AND PROSTATE TUMORIGENESIS.
- Creator
- Oseni, Saheed Oluwasina, Kumi-Diaka, James, Florida Atlantic University, Department of Biological Sciences, Charles E. Schmidt College of Science
- Abstract/Description
-
The oncogenic role of many of inflammatory genes in prostate cancer (PCa) remains unexplored despite the increasing association of chronic inflammation with PCa initiation, progression, and therapy resistance. The overarching goal of this project was to identify dysregulated inflammatory genes that correlate with PCa progression and seek to understand their molecular mechanisms and the therapeutic potential of targeting them. To achieve this, we utilized cutting-edge integrative (epi) genomic...
Show moreThe oncogenic role of many of inflammatory genes in prostate cancer (PCa) remains unexplored despite the increasing association of chronic inflammation with PCa initiation, progression, and therapy resistance. The overarching goal of this project was to identify dysregulated inflammatory genes that correlate with PCa progression and seek to understand their molecular mechanisms and the therapeutic potential of targeting them. To achieve this, we utilized cutting-edge integrative (epi) genomic and transcriptomic techniques to identify and characterize inflammatory genes whose deregulation or (epi) genetic alterations correlate with PCa progression. Weighted Gene Co-expression Network Analysis and other multivariate analysis techniques identified IRAK1 as one of the inflammatory signatures found to be overexpressed in over 80% of prostate adenocarcinoma (PRAD) samples. We also explored the diagnostic and prognostic potential of IRAK1 as a biomarker using Kaplan Meier Survival Analysis and AUROC Analysis. DNA methylation analysis showed that IRAK1 is hypomethylated and found to negatively correlate with its overexpression in PRAD patients. We also found some missense and truncated mutations in some patients and reported a high level of IRAK1 gene amplification in castration-resistant and neuroendocrine PCa patients.
Show less - Date Issued
- 2021
- PURL
- http://purl.flvc.org/fau/fd/FA00013713
- Subject Headings
- Prostate--Cancer, Interleukin-1 Receptor-Associated Kinases, Inflammation
- Format
- Document (PDF)
- Title
- The synergistic effects of concurrent stress on the inflammatory response in healthy individuals.
- Creator
- McAlpine, David, Huang, Chun-Jung
- Date Issued
- 2012-04-06
- PURL
- http://purl.flvc.org/fcla/dt/3349030
- Subject Headings
- Pentraxin 3, Inflammation, PTX3 protein, Vascular Diseases, Blood Vessels, C-Reactive Protein, Inflammation --blod, Parasympathetic Nervous System, Stress --psychological
- Format
- Document (PDF)
- Title
- Investigating the Role of CHI3L1 in Promoting Tumor Growth and Metastasis Using Mammary Tumor Models.
- Creator
- Libreros, Stephania, Iragavarapu-Charyulu, Vijaya, Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
- Abstract/Description
-
Metastasis is the primary cause of mortality in women with breast cancer. Recently, elevated serum levels of a glycoprotein known as chitinase-3 likeprotein- 1 (CHI3L1) has been correlated with poor prognosis and shorter survival of patients with cancer and inflammatory diseases. The biological and physiological functions of CHI3L1 in tumor progression have not yet been elucidated. In this document, we describe the role of CHI3L1 in tumor growth and metastasis and its relationship with...
Show moreMetastasis is the primary cause of mortality in women with breast cancer. Recently, elevated serum levels of a glycoprotein known as chitinase-3 likeprotein- 1 (CHI3L1) has been correlated with poor prognosis and shorter survival of patients with cancer and inflammatory diseases. The biological and physiological functions of CHI3L1 in tumor progression have not yet been elucidated. In this document, we describe the role of CHI3L1 in tumor growth and metastasis and its relationship with inflammation. Using well-established models of breast cancer, we show that CHI3L1 is increased in the serum of tumor bearing mice. We found that CHI3L1 levels are increased at both the “pre-metastatic” and “metastatic stage” and that tumor cells, splenic, alveolar and interstitial macrophages; and myeloid derived population produce CHI3L1. Furthermore, we demonstrated that CHI3L1 has an inhibitory role on the expression of interferon-gamma (IFN γ) by T cells, while enhancing the production of pro-inflammatory mediators by macrophages such as Cchemokine ligand 2 (CCL2/MCP-1), Chemokine CX motif ligand 2 (CXCL2/IL-8) and matrix metalloproteinase-9 (MMP-9), all of which promote tumor growth and metastasis. We demonstrated that in vivo treatment of tumor-bearing mice with chitin microparticles, a TH1 adjuvant and a substrate for CHI3L1, promoted immune effector functions with increased production of IFN-γ but decreased CCL2/MCP-1, CXCL2/IL-8 and MMP-9 expression by splenic and pulmonary macrophages. Significantly, in vivo administration of chitin microparticles decreased tumor growth and pulmonary metastasis in mammary tumor bearing mice. These results suggest that CHI3L1 may play a role in tumor progression. Inflammation plays a pivotal role during tumor progression and metastasis by promoting the production of pro-inflammatory molecules such as CHI3L1. However, little is known about how CHI3L1 expression can affect secondary sites to enhance metastasis. In these studies, we demonstrated that CHI3L1 alters the cellular composition and inflammatory mediators that aid in the establishment of a metastatic niche for the support of infiltrating tumor cells leading to accelerated tumor progression. Since previous studies showed that CHI3L1 modulates inflammation, we determined the role of CHI3L1 in the context of pre-existing inflammation and metastasis. We found that CHI3L1 deficient mice with preexisting inflammation had decreased pro-inflammatory mediators, and significant reduction in tumor volume and metastasis compared to wild type controls. Preexisting inflammation and CHI3L1 may be driving the establishment of a premetastatic milieu in the lungs and aiding in the establishment of metastasis. Understanding the role of CHI3L1 in inflammation during tumor progression could result in the design of targeted therapies for breast cancer patients.
Show less - Date Issued
- 2015
- PURL
- http://purl.flvc.org/fau/fd/FA00004517, http://purl.flvc.org/fau/fd/FA00004517
- Subject Headings
- Biopharmaceutics, Breast -- Cancer -- Etiology, Breast -- Cancer -- Molecular aspects, Cell differentiation, Chitinase, Glycoproteins -- Metabolism, Inflammation, Mice as laboratory animals
- Format
- Document (PDF)