malignant melanoma are analyzed and found to have an elevated ability to bind to laminin; they also secrete much higher than normal levels of a certain proteolytic enzyme activity. How would these differences from normal, control cells promote metastasis of these cancer cells? (2) In contrast to the situation described in question 1, it has recently been found that nearly 25% of melanomas have mutations in matrix metalloproteinases (MMPs). Why is this contradictory and what does this suggest about the likelihood of MMP inhibitors being effect chemotherapy agents? (3) Why would cells that express less E-cadherin be more likely to become malignant and give rise to epithelial cell tumors?
Cancer is a complicated series of diseases characterized by over-proliferation of cells within a tissue. While in some instances the primary tumor is the ultimate cause of death, in many cases the primary tumor metastasizes, or moves, through the lymph system to invade other tissues. The migration of tumor cells requires changes in the adhesion properties of the cell that allow it to move and invade more readily.
There are several molecules involved in cell-to-cell connections and cellular architecture: laminins, matrix metalloproteinases, cadherins, and integrins. While mutations in genes that control the cell cycle or recognize DNA damage are the causes of tumor cell formation, tumor cell spread to other tissues may be caused by mutations in the genes the code for these extracellular proteins. The loss of cellular connections, cellular identification and signaling, and tissue structure may lead to the release of expanding tumor cells into the circulatory and lymphatic systems. Once tumor cells have access to blood and lymph vessels, they can travel to most parts of the body. This spread of tumor cells is called metastasis.
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