Being diagnosed with cancer is devastating. But when the cancer cells
have to spread to form secondary colonies, the prognosis for the patient
is worse. If meaningful improvements in survival are to occur, then
control of metastasis will be a foundation. Relatively little is known
about the control of the metastatic process at the molecular level. This
volume begins to explore our current knowledge regarding the underlying
molecular and biochemical mechanisms controlling the metastatic
phenotype. While all of the authors attempted to put their findings into
a context for translation to the clinical situation, the
state-of-the-art does not fully allow this. Nonetheless, we write these
summaries of our work as an early effort toward that end. I am grateful
to all of the authors who have contributed generously of their time and
energies to make this volume a reality. To metastasize, neoplastic cells
dissociate from the primary tumor, enter a circulatory compartment
(typically lymphatics or blood vasculature), survive transport, arrest,
exit the circulation and finally proliferate at a discontinuous site in
response to local growth factors. Unless cells accomplish every step of
the metastatic cascade, metastases cannot develop. The process is highly
inefficient, i. e.,