The overexpression of another cell adhesion molecule L1 gene was associated with LDN-193189 metastasis in malignant melanoma. Cancer is a fatal disease whereby invasive local tumor growth and metastatic spread to distant vital organs resulting in dormant and/or active growth and inevitable death of patients. Contrary to previous models new evidence suggested that metastatic cells might be created already during initial growth of a primary local tumor. These cells then succeed in cell migration/WZ8040 invasion, embolization, survival in the circulation, arrest in a distant capillary bed, and extravasation into and multiplication within the distant organ parenchyma. Failure at any of these steps could block the entire metastatic process and may lead to ����dormant cancer cells and dormant micrometastases����. Surgical removal of the primary tumor might then lead to active growth. Because tumor spread is responsible for the majority of deaths of cancer patients, the development of therapeutic agents that inhibit tumor metastasis is of paramount importance. One of us predicted previously that the cytoplasmic end of CHL1 protein might interact with the cytoskeleton and might induce/regulate filopodia formation driving tumor cell migration and invasion. CHL1 behavior in cancer is thus strikingly similar to L1 and LOX which both work through the actin network. This study suggested that CHL1 might contribute to cancer invasive growth and metastasis. It might act either as a tumorsuppressor or oncogene. CHL1 therefore could belong to the new rapidly growing category of cancer genes that may function either as TSGs or oncogenes. During initial growth CHL1 is not expressed in tumor cells to facilitate in situ tumor growth. Re-expression of CHL1 on the edge of the tumor mass and around tumor vessels could promote migration and local invasive growth and furthermore allow initiating the metastatic process. Thus, our results along with the findings that CHL1 was a mutated candidate cancer-associated gene in colon cancer suggested that this type of recognition receptors may indeed have dual roles in carcinogenesis. The mutations discovered in the extra-cellular part of CHL1 could afford a therapeutic antibody to selectively treat patients. This validates CHL1 as a novel target for personalized immune intervention in cancers expressing mutated CHL1. New therapeutic small inhibitors directed at CHL1 could be effective in restraining new tumor formation from dormant micrometastases.