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You searched for +publisher:"Texas Medical Center" +contributor:("R. Eric Davis, M.D."). Showing records 1 – 2 of 2 total matches.

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Texas Medical Center

1. Teo, Albert. DIFFERENTIAL PAX5 LEVELS PROMOTE MCL DISPERSAL AND PROGRESSION AND PREDICT A POOR PROGNOSIS IN ADVANCED MCL PATIENTS.

Degree: PhD, 2014, Texas Medical Center

Although PAX5 conditional silencing in mice models led to aggressive lymphoma formation, there has been a lack of understanding in the precise functions of PAX5 in human B cell cancers. PAX5 expression is used to diagnose different B cell lymphoma in the clinic including mantle cell lymphoma (MCL), which is one of the most aggressive B cell cancers. PAX5 levels in MCL patients were significantly repressed compared to normal B cells. Surprisingly, we found there were quantitative differences in PAX5 expression levels within MCL patient tissues, which prompted us to silence PAX5 in MCL cell lines to characterize PAX5 functions in MCL disease progression. PAX5 silencing in MCL cells (PAX5) not only increased cell proliferation in vitro and in vivo but also contributed towards retention of quiescent PKH+ stem-like cells in xenograft bones. Decreased PAX5 signaling led to deregulation of the cell cycle and increased MCL survival pathways. PAX5 cells also exhibited increased dissemination and adhesion to bone marrow stromal cells. Analyses of clinical MCL cases further revealed that lower PAX5 levels are correlated with MCL dispersal and poorer overall survival in patients. In addition, aggressive blastoid variant MCL demonstrated lower levels of PAX5 compared to non-blastoid types, indicating a decreased PAX5 phenotype promotes MCL dispersal and progression. We also conducted a high throughput screening (HTS) of 3800 compounds to discover compounds that selectively target the aggressive MCL. The data revealed important properties of PAX5 MCL cells, which are highly drug resistant compared to parental cells. Several novel compounds were discovered through the HTS, which can be new potential therapeutic options for aggressive MCL. Collectively, our data support PAX5 functions as a tumor suppressor-like protein in MCL, and that PAX5 expression can predict advanced MCL patient prognosis. Advisors/Committee Members: Nami McCarty, Ph.D., Zhiqiang An, Ph.D., R. Eric Davis, M.D..

Subjects/Keywords: PAX5; Mantle Cell Lymphoma; High Throughput Screening; Medicine and Health Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Teo, A. (2014). DIFFERENTIAL PAX5 LEVELS PROMOTE MCL DISPERSAL AND PROGRESSION AND PREDICT A POOR PROGNOSIS IN ADVANCED MCL PATIENTS. (Doctoral Dissertation). Texas Medical Center. Retrieved from http://digitalcommons.library.tmc.edu/utgsbs_dissertations/533

Chicago Manual of Style (16th Edition):

Teo, Albert. “DIFFERENTIAL PAX5 LEVELS PROMOTE MCL DISPERSAL AND PROGRESSION AND PREDICT A POOR PROGNOSIS IN ADVANCED MCL PATIENTS.” 2014. Doctoral Dissertation, Texas Medical Center. Accessed October 16, 2019. http://digitalcommons.library.tmc.edu/utgsbs_dissertations/533.

MLA Handbook (7th Edition):

Teo, Albert. “DIFFERENTIAL PAX5 LEVELS PROMOTE MCL DISPERSAL AND PROGRESSION AND PREDICT A POOR PROGNOSIS IN ADVANCED MCL PATIENTS.” 2014. Web. 16 Oct 2019.

Vancouver:

Teo A. DIFFERENTIAL PAX5 LEVELS PROMOTE MCL DISPERSAL AND PROGRESSION AND PREDICT A POOR PROGNOSIS IN ADVANCED MCL PATIENTS. [Internet] [Doctoral dissertation]. Texas Medical Center; 2014. [cited 2019 Oct 16]. Available from: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/533.

Council of Science Editors:

Teo A. DIFFERENTIAL PAX5 LEVELS PROMOTE MCL DISPERSAL AND PROGRESSION AND PREDICT A POOR PROGNOSIS IN ADVANCED MCL PATIENTS. [Doctoral Dissertation]. Texas Medical Center; 2014. Available from: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/533


Texas Medical Center

2. Agollah, Germaine D. SRC HOMOLOGY 2 DOMAIN-CONTAINING 5’-INOSITOL PHOSPHATASE-2 (SHIP2) IS AN EFFECTOR OF LYMPHATIC DYSFUNCTION.

Degree: PhD, 2015, Texas Medical Center

The lymphatic system is essential for the transport of excess fluid, protein, and foreign materials from interstitial tissues to lymph nodes; for immune surveillance, and to maintain fluid homeostasis. Dysregulated lymphatics can be attributed to pathological conditions including tumor metastasis, inflammation, chronic wounds, obesity, blood vascular disorders, and lymphedema. Of these, lymphedema is the most extreme of lymphatic disorders and is represented by a spectrum of symptoms ranging from mild, subtle presentation to severe, disfiguring, overt presentation. Lymphedema is more manageable in the early stages of disease but severely reduces quality of life with progression. Due to lack of molecular knowledge and inadequate imaging techniques to safely, rapidly and non-invasively visualize the lymphatics, lymphedema remains under diagnosed and progresses to the irreversible stage if not diagnosed early. Candidate gene studies have identified a myriad of genes responsible for lymphedema, however, majority of patients do not harbor mutations in these putative genes, indicating many more unknown genes contribute to the pathology of this disease. In an effort to identify new polymorphisms that possibly effect lymphatic dysfunction, we combined investigational, non-invasive near-infrared fluorescence lymphatic imaging (NIRFLI) and next generation sequencing (NGS), to phenotype and genotype human subjects with familial lymphedema. We discovered that mutations in src homology 2-domain containing 5’-inositol phosphatase-2 (SHIP2), encoded by INPPL1, are associated with lymphatic abnormalities. SHIP2 is a phosphatidyIinositol (3,4,5) triphosphate (PIP3) 5’-phosphatase that negatively controls PIP3 levels thereby inhibiting the PI3K/AKT signaling, a pathway implicated in various lymphatic disorders. Our studies confirm this inhibitory role of SHIP2 against PI3K/AKT in lymphatic endothelial cells, and identify SHIP2 as a potential regulator of MAPK/ERK signaling, another pathway also recently identified as important in lymphatic malformations. Pharmacological inhibition of SHIP2 impedes lymphatic contractility and impairs the normal wound healing processes of lymphangiogenesis and angiogenesis in mice. These studies suggest that SHIP2 could have a previously unidentified effector role in lymphatic dysfunction. In elucidating the roles of SHIP2 in lymphatic dysfunction, the work presented herein expands our understanding of molecular basis of lymphatic failure which could have clinical implications affecting populations with lymphatic disorders, including the ever increasing population of cancer survivors who experience the chronic, disfiguring and incurable lymphedema. Advisors/Committee Members: Eva. M. Sevick-Muraca, Ph.D., R. Eric Davis, M.D., Jeffrey E. Gershenwald, M.D..

Subjects/Keywords: Lymphatic System; Lymphedema; SHIP2; INPPL1; Near Infrared Fluorescence Imaging; Next Generation Sequencing; PI3K/AKT; MAPK/ERK; AS1949490; Cancer Survivorship; Lymphangiogenesis; Angiogenesis; Endothelial Cell Biology; Cardiovascular System; Cell Biology; Diagnosis; Enzymes and Coenzymes; Genetic Phenomena; Hemic and Immune Systems; Hemic and Lymphatic Diseases; Immunopathology; Medical Biotechnology; Medicine and Health Sciences

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Agollah, G. D. (2015). SRC HOMOLOGY 2 DOMAIN-CONTAINING 5’-INOSITOL PHOSPHATASE-2 (SHIP2) IS AN EFFECTOR OF LYMPHATIC DYSFUNCTION. (Doctoral Dissertation). Texas Medical Center. Retrieved from http://digitalcommons.library.tmc.edu/utgsbs_dissertations/548

Chicago Manual of Style (16th Edition):

Agollah, Germaine D. “SRC HOMOLOGY 2 DOMAIN-CONTAINING 5’-INOSITOL PHOSPHATASE-2 (SHIP2) IS AN EFFECTOR OF LYMPHATIC DYSFUNCTION.” 2015. Doctoral Dissertation, Texas Medical Center. Accessed October 16, 2019. http://digitalcommons.library.tmc.edu/utgsbs_dissertations/548.

MLA Handbook (7th Edition):

Agollah, Germaine D. “SRC HOMOLOGY 2 DOMAIN-CONTAINING 5’-INOSITOL PHOSPHATASE-2 (SHIP2) IS AN EFFECTOR OF LYMPHATIC DYSFUNCTION.” 2015. Web. 16 Oct 2019.

Vancouver:

Agollah GD. SRC HOMOLOGY 2 DOMAIN-CONTAINING 5’-INOSITOL PHOSPHATASE-2 (SHIP2) IS AN EFFECTOR OF LYMPHATIC DYSFUNCTION. [Internet] [Doctoral dissertation]. Texas Medical Center; 2015. [cited 2019 Oct 16]. Available from: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/548.

Council of Science Editors:

Agollah GD. SRC HOMOLOGY 2 DOMAIN-CONTAINING 5’-INOSITOL PHOSPHATASE-2 (SHIP2) IS AN EFFECTOR OF LYMPHATIC DYSFUNCTION. [Doctoral Dissertation]. Texas Medical Center; 2015. Available from: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/548

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