Primary melanoma tumor inhibits metastasis through alterations in systemic hemostasis.

Progression from a primary tumor to distant metastases requires extensive interactions between tumor cells and their microenvironment. The primary tumor is not only the source of metastatic cells but also can also modulate host responses to these cells, leading to an enhancement or inhibition of metastasis. Tumor-mediated stimulation of bone marrow can result in pre-metastatic niche formation and increased metastasis.

Micrometastatic disease and metastatic outgrowth: clinical issues and experimental approaches.

Metastasis from the primary tumor to distant organs is the principal cause of mortality in patients with cancer. While prognostic factors can predict which patients are likely to have their cancer recur, these are not perfect predictors, and some patient's cancers recur even decades after apparently successful treatment. This phenomenon is referred to as dormancy.

Effect of anti-fibrinolytic therapy on experimental melanoma metastasis.

Anti-fibrinolytic agents such as aprotinin and epsilon-aminocaproic acid (EACA) are used clinically to decrease peri-operative bleeding. Use of these treatments during cancer-related surgeries has led to investigation of the effect of fibrinolysis inhibition on cancer cell spread. The ability of aprotinin to reduce proteolytic activity of proteases required for metastasis suggests that it could have an anti-metastatic effect in patients undergoing tumor resection.