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Erika L. Spaeth

Researcher at University of Texas MD Anderson Cancer Center

Publications -  35
Citations -  4453

Erika L. Spaeth is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Mesenchymal stem cell & Tumor microenvironment. The author has an hindex of 18, co-authored 27 publications receiving 4017 citations.

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Mesenchymal Stem Cell Transition to Tumor-Associated Fibroblasts Contributes to Fibrovascular Network Expansion and Tumor Progression

TL;DR: Evidence is provided that TAF are derived from mesenchymal stem cells that acquire a TAF phenotype following exposure to or systemic recruitment into adenocarcinoma xenograft models including breast, pancreatic, and ovarian and under long-term tumor conditioning in vitro, MSC express TAF–like proteins.
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Direct evidence of mesenchymal stem cell tropism for tumor and wounding microenvironments using in vivo bioluminescent imaging.

TL;DR: Conditions under which MSC tropism and selective engraftment in sites of inflammation can be monitored by bioluminescent imaging are identified and consistent findings were independent of tumor type, immunocompetence, and route of MSC delivery.
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Inflammation and tumor microenvironments: defining the migratory itinerary of mesenchymal stem cells

TL;DR: The role of inflammatory signaling in attracting MSC to tumors is discussed and radiation enhancesinflammatory signaling in the tumor microenvironment and may be used to potentiate site-specific MSC migration.
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Concise Review: Dissecting a Discrepancy in the Literature: Do Mesenchymal Stem Cells Support or Suppress Tumor Growth?

TL;DR: It is found that the timing of MSC introduction into tumors may be a critical element to safely develop MSCs as a therapeutic tool and to advance the understanding of the role of tumor stroma in carcinogenesis.
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Origins of the Tumor Microenvironment: Quantitative Assessment of Adipose-Derived and Bone Marrow–Derived Stroma

TL;DR: Through multicolored tissue transplant procedures, quantitatively determined the contribution of bone marrow-derived and adipose-derived cells to stromal populations within syngeneic ovarian and breast murine tumors.