OHSU

Schedin Lab


The long term objective of the Schedin Lab research program is to develop breast cancer chemopreventive strategies that are targeted to specific windows of breast development. By understanding normal mammary gland development and homeostasis, it should possible to identify both mammary specific and life cycle specific chemopreventive strategies. The focus of my lab is on characterizing extracellular matrix (ECM) proteins that mediate mammary epithelial cell death during key windows of normal mammary gland differentiation, such as adolescent mammary gland development, the estrous cycle, and the pregnancy/lactation/involution cycle. Major areas of investigation include adolescent mammary development, mammary epithelial cell-stromal interactions, tissue remodeling, mammary carcinogenesis, and chemoprevention in rodent models. 

Current Research Projects Include:

Determine the mechanism of pregnancy-associated breast cancer. I have proposed that the natural tissue remodeling that occurs in the mammary gland following pregnancy and lactation promotes breast cancer progression, accounting for 'the dual effect' of pregnancy. I propose that the tumor promoting activity of physiologic mammary gland regression is due to an inflammation-like microenvironment that is present during gland regression. The hypothesis that mammary stroma from an actively involuting mammary gland promotes tumor progression is being evaluated using both in vivo and in vitro model systems. ECM proteins that activate tumor cells invasion are being identified using proteomic approaches. 

Identify the ECM proteomes of the 'breast-cancer protected' and 'at-risk' mammary gland. For these studies, we are isolating mammary ECM proteins from mammary glands of female rats at reduced risk of developing breast cancer due to tamoxifen treatment or parity, and from control, 'at-risk' rats. The ECM proteins will be identified by proteomics and proteins in common to the 'protected-glands', but absent or reduced in the 'at-risk' glands, will be candidates for ECM proteins that mediate protection. 

The identification of dietary interventions that result in the development of mammary tissue that is resistant to carcinogenic insult. To this end, we are currently evaluating how vitamin A modifies adolescent mammary development, mammotrophic hormone signaling, and subsequent risk for carcinogenesis.

Laboratory Manager / Research Coordinator

Jane Wiesen PhD

Jane Wiesen, Ph.D.

Education: Ph.D., Cellular and Molecular Biology, University of Michigan, 1992

Postdoctoral training: The University of California, San Francisco, Departments of OB/GYN and Anatomy


Research Assistant Professor

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Sonali Jindal M.D.

Education: MBBS, M.D. (Pathology) J.N. Medical College, India 2008

Scientific Interest: The focus of my research is to understand the tumor-host environment including immune cell interactions in normal and pathological breast development on histological platform which can aid in development of chemo preventive and treatment strategies for pregnancy associated breast cancer among younger women. We have shown that histologically postpartum breast involution window in women occurs in about 12 months. The identification of this period in a women's life time can be used chemo prophylactically resulting in decreased tumor progression and metastasis of pregnancy associated breast cancers. Another significant advantage of this defined involution period is that that it helps us in identification of unique biomarkers for risk assessment, prognosis, and targeted therapeutics. Another focus of my research is to understand the pathological differences in tumor characteristics, tumor cell -host environment interactions and survival differences between younger premenopausal women with and without pregnancy associated breast cancers and older postmenopausal women with breast cancer. I have been doing comparative histology on tumor and adjacent normal histology using semi-quantitative analysis on tissue sections stained for single /dual immunohistochemistry markers via novel Aperio software.


Graduate Students

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Courtney Betts, M.S.

Education: Ph.D. (in progress), Cell and Developmental Biology, Oregon Health & Science University; M.S., Cell Biology and Cancer Research, Albany Medical College (2010); B.S., Biology, Hobart and William Smith Colleges (2007)

Scientific Interests: I am specifically interested in understanding if the dendritic cell-T cell axis is altered by mammary gland involution, and furthermore if this contributes to tumor progression. This works aims to bridge a gap between normal biology and cancer, as well as investigate the potential use of immunotherapies within the unique developmental window of mammary gland involution.


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Erica Goddard, B.S. 

Education: Ph.D. (in progress), Cancer Biology, Oregon Health and Science University; B.S., Microbiology, University of Kansas (2011)

Scientific Interests:My scientific interests include understanding the tissue microenvironment as it pertains to tumor initiation, progression, and metastasis. I am working to understand why women diagnosed with postpartum breast cancer are at an increased risk for developing metastasis. I have the unique opportunity to study how normal liver biology during the postpartum period may induce tissue changes that promote metastasis. I not only investigate the process of involution by which the postpartum liver returns to a state of homeostasis, but also how distinct extracellular matrix proteins and immune cell populations in the liver during the postpartum window may be promoting liver metastasis of postpartum breast cancers.


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Qiuchen Guo, B.A. 

Education: Ph.D. (in progress) Cancer Biology, Oregon Health & Science University; B.A. Biotechnology, University of Science and Technology of China (2010).

Scientific interests: understanding how microenvironment of post-partum mammary gland involution influences fibroblast and macrophage function in tumor promotional collagen deposition and organization. Also, finding target therapy to switch back this collagen phenotype in order to reduce the risk of post-partum breast cancer.