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Being diagnosed with cancer is devastating. But when the cancer cells have to spread to form secondary colonies, the prognosis for the patient is worse. If meaningful improvements in survival are to occur, then control of metastasis will be a foundation. Relatively little is known about the control of the metastatic process at the molecular level. This volume begins to explore our current knowledge regarding the underlying molecular and biochemical mechanisms controlling the metastatic phenotype. While all of the authors attempted to put their findings into a context for translation to the clinical situation, the state-of-the-art does not fully allow this. Nonetheless, we write these summaries of our work as an early effort toward that end. I am grateful to all of the authors who have contributed generously of their time and energies to make this volume a reality. To metastasize, neoplastic cells dissociate from the primary tumor, enter a circulatory compartment (typically lymphatics or blood vasculature), survive transport, arrest, exit the circulation and finally proliferate at a discontinuous site in response to local growth factors. Unless cells accomplish every step of the metastatic cascade, metastases cannot develop. The process is highly inefficient, i. e. ,
List of contents
Metastasis-Suppressor Genes: A Review and Perspective on an Emerging Field.- The Roles of Map Kinases in Controling Cancer Metastasis.- Tumor Metastasis-Associated Human Mtal Gene: Role in Epithelial Cancer Cell Proplieration and Regulation.- Cooperative Integrin Interactions in the Regulation of Tumor Metastasis.- Brain-Metastasis Associated Genes.- Autocrine Motility Factor and Its Receptor as Regulators of Metastasis.- Nm23 Metastasis Suppressor Gene.- Gene Regulation in Melanoma Metastasis.- Heterochromatin-Associated Protein 1, HP1Hs?, in Breast Cancer Invasion and Metastasis.- Inhibition of Invasion and Metastasis During Specific Amino Acid Restriction Associated with Metastasis Suppressor and Other Gene Changes.- Role of BRMS1 in Breast Carcinoma Metastasis.- The Role of KISS1 in Melanoma Metastasis Suppression.- Osteopontin: A Ras-Regulated Gene That Contributes to Tumor Metastasis.- The Emerging Role for the mRNA Cap-Binding Protein, EIF-4E, in Metastatic Progression.
Summary
Being diagnosed with cancer is devastating. But when the cancer cells have to spread to form secondary colonies, the prognosis for the patient is worse. If meaningful improvements in survival are to occur, then control of metastasis will be a foundation. Relatively little is known about the control of the metastatic process at the molecular level. This volume begins to explore our current knowledge regarding the underlying molecular and biochemical mechanisms controlling the metastatic phenotype. While all of the authors attempted to put their findings into a context for translation to the clinical situation, the state-of-the-art does not fully allow this. Nonetheless, we write these summaries of our work as an early effort toward that end. I am grateful to all of the authors who have contributed generously of their time and energies to make this volume a reality. To metastasize, neoplastic cells dissociate from the primary tumor, enter a circulatory compartment (typically lymphatics or blood vasculature), survive transport, arrest, exit the circulation and finally proliferate at a discontinuous site in response to local growth factors. Unless cells accomplish every step of the metastatic cascade, metastases cannot develop. The process is highly inefficient, i. e. ,
