Platelets were unable to restore PAI-1 post silencing, demonstrating that although platelet-cancer cell interactions trigger PAI-1 transcription, increased PAI-1 is not merely an additive effect via platelet degranulation, but involves a molecular mechanism by which the platelets and cancer cells interact which results in the transcription and translation of intracellular PAI-1 in the cancer cells that may be excreted into the tumor microenvironment and the circulation. This evidence concerns the gene SERPINE1 and neoplasm.