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Pepper Schedin

Researcher at Oregon Health & Science University

Publications -  139
Citations -  6867

Pepper Schedin is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Breast cancer & Cancer. The author has an hindex of 39, co-authored 122 publications receiving 5848 citations. Previous affiliations of Pepper Schedin include University of Colorado Boulder & University of Colorado Hospital.

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Mammary Gland ECM Remodeling, Stiffness, and Mechanosignaling in Normal Development and Tumor Progression

TL;DR: Understanding the role of forces in the mammary gland is crucial to understanding both normal developmental and pathological processes.
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Pregnancy-associated breast cancer and metastasis

TL;DR: The mammary microenvironment might become tumour-promoting after pregnancy because of the remodelling of the mammary gland to its pre-pregnant state, and this remodelling, which is associated with pro-inflammatory and wound-healing mechanisms, is proposed to support tumours dissemination.
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Postpartum mammary gland involution drives progression of ductal carcinoma in situ through collagen and COX-2

TL;DR: A mouse model of postpartum breast cancer that identifies mammary gland involution as a driving force of tumor progression is described and data support further research to determine whether women at high risk for postpartums breast cancer would benefit from treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) during post partum involution.
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Alternatively Activated Macrophages and Collagen Remodeling Characterize the Postpartum Involuting Mammary Gland across Species

TL;DR: Fibrillar collagen levels and proteolysis increased dramatically during involution, and denatured collagen I acted as a strong chemoattractant for macrophages in cell culture, suggesting proteolyzed fibrillsar collagen as a candidate ECM mediator of macrophage recruitment.
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Remodeling of the mammary microenvironment after lactation promotes breast tumor cell metastasis.

TL;DR: It is suggested that the mammary gland microenvironment becomes promotional for tumor cell dissemination during involution, thus providing a plausible mechanism to explain the high rate of metastases that occur with pregnancy-associated breast cancer.