Calcium Signalling in Cancer

A treatise on the transduction signals induced by calcium. It examines a range of topics, from mechanisms and significance of calcium homeostasis for normal cell function to calcium signaling pathways and the transduction of the calcium signal in proliferation and cell motility with an emphasis on the role played by calcium binding proteins.

Calcium signalling occupies a preeminent position in the signal transduction system of the cell by virtue of its participation in a wide range of physiological functions together with the biological events associated with genetic expression, cell proliferation and apoptosis, as well as cell differentiation and morphogenesis. It is an important feature of cell adhesion and motility; the integrity of the calcium binding proteins themselves is a basic requirement of normal biological function. In fact, the deregulation of calcium signaling is now regarded as the primary event in the pathogenesis, growth, invasion, and secondary spread of cancer.

Calcium Signalling in Cancer is a concise up-to-date treatise on the transduction signals induced by calcium that considers how alterations in this calcium-dependent signal transduction pathway are related to a number of human diseases, especially neoplastic transformation. This authoritative text examines a broad range of topics-from mechanisms and significance of calcium homeostasis for normal cell function to calcium signalling pathways and the transduction of the calcium signal, especially in proliferation, cell motility, cancer invasion,, and metastasis.

Clearly organized, it covers all aspects of the subject including specific sections on the regulation of the genes whose products are required for signal transduction by calcium, such as Alzheimer''s disease, Darier''s disease, Duchenne and limb girdle dystrophies, psoriasis and some forms of ichthyosis, and cancer associated retinopathy. With an extensive bibliography and over 2,500 references, Calcium Signalling in Cancer is an invaluable reference source.