Research Images

The Ostrowski lab focuses on understanding interactions between signaling pathways locating in the different cell compartments involved in complex biological processes of cancer cell progression and normal cellular differentiation.

Genetic Analysis of the Tumor Microenvironment

A breast tumor is composed of not only the epithelial-cell derived tumor cells, but also stromal cells, endothelial cells, and various immune cells including macrophages, B-cells and T-cells. The molecular dialogue between the tumor cell and these “normal” cell types is critical for tumor progression and metastasis, and strategies for disrupting this crosstalk may provide new ways to block tumor growth and spread.   The lab team uses a combination of genetic mouse models, human samples, genomic technology and molecular genetics to attack these problems. For example, we have demonstrated that deletion of the tumor suppressor PTEN in tumor stromal fibroblasts increases the malignancy of Her2-mediated mammary cancer in mouse models.

Research 1a

IHC of Pten in Human IBC


Importantly, PTEN expression is  is also decreased in the stroma of Her2+ human breast cancers,  and this correlates with worsened patient outcomes.




PU.1 and MITF: Regulation of Osteoclast Differentiation

Research 2

Osteoclasts are cells required for normal bone growth and homeostasis, but they  inappropriately destroy bone in human diseases, including in osteoporosis, rheumatoid arthritis and tumor metastasis to bone.  Our work has taken advantage of genetic modeling and functional genomic approaches to study how osteoclasts are formed and regulated in mice.  This work provides a paradigm-shifting insights into how osteoclasts are regulating, demonstrating that the transcription factors PU.1 and MITF regulate a transcription factor network that is required for osteoclast differentiation and function.   Our current work is geared to define the mechanisms that regulate osteoclasts as implied by our genomic studies and to attempt to translate these finding to  osteoclast dysfunction in human diseases.