Metastasis is the process at which cells depart the primary tumor site, survive and shuttle through the circulation or lymph and then invade to distant organs and expand. This multi steps process is extremely complex from physical, molecular, cellular and physiological and levels. Worldwide, more than 7 million cancer related mortalities each year, are due to progression of metastatic processes. We intrigued by the fact that the distribution of the metastasizing cells to distant organs is a non-random process that known as "organotropism" Approximately 40% of newly diagnosed cancers will involve bone, disrupting the bone balanced turnover and causing damage in the form of osteolytic lesions or osteoblastic deformations.  In particularly, bone metastases occurs in approximately 60% of patients with metastatic breast or prostate cancer. This unique and crucial microenvironment, on one hand, may provide a complex niches, safeguard and trigger harsh relapse of the disease on the other. Despite the great occurrence of bone metastasis following breast and prostate cancer, many of the molecular mechanisms driving metastatic character remain unclear.

The focus of our laboratory lies from the basic cell and molecular mechanisms by which metastatic cell behavior originates,  depart the primary site,  survive, home  and  colonize the bone and interacts within the microenvironment. We suggest that stemming from the mineral and organic nature of the bone tissue various ques, acting together, spatially and temporally to enable anchorage, survival, dormancy and reactivation of the invading cell decades after the onset of the disease.          

With the conjunction and continuation of our biomedical research amid regeneration of hard tissues, we introduced new bone-related methodologies.  We developed three-dimensional models that closely resemble a living natural bone, and heavily used to study cellular and molecular cues in bone metastasis. For example, using this model we showed that the mineral phase might have an important role on cellular characteristics such as, proliferation rates and tumorigenicity. We also revealed that interactions with mesenchymal stem cells increased migration and invasion capacities along with osteosarcomas (OS) proliferation. We also showed that via regulation of pathways such Wnt, cadherins, Notch and their downstream target genes such as c-Myc, these capacities are further enhanced following accommodation with the bone like biolattice and interaction with MSCs.

In addition, we also strive to identify specific molecular targets and therapeutic methodologies and interventions for better treatment of metastatic disease. We are currently developing new strategies for treatment of metastatic bone diseases.