Oncogenes, growth factors, and signal transduction

Article Abstract:

Biological signals in the form of small proteins are carried through the tissue fluid spaces and combine with receptors found on the surfaces of cells. The manner in which these external growth signals are then conveyed from the cell's surface membrane receptors to the cell nucleus, which holds the genetic code for the production of all proteins, remains largely unknown and an area of active scientific research. The mechanisms are considered to be of considerable importance in the control of normal cellular proliferation and in the uncontrolled growth of cancerous cells. Specific genes, oncogenes, are associated with the process of cancer formation or oncogenesis. The genes are considered a target of stimulation when various biological signals are encountered. For example, cells which have undergone cancerous transformation are stimulated to continuously multiply. Although the overall mechanism is at least partially understood, the mechanism that allows the proteins to communicate in this process is not clear. This study examines tyrosine kinase, a signal transducer, as a model system and as a means of investigating normal and cancerous cell proliferation.

Research, Cancer research, Cancer, Growth factors, Signal peptides

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Oncogenes

Article Abstract:

The elucidation of how oncogenes control cell proliferation is opening new avenues for cancer treatments. Growth is regulated via the transmission of messages from outside the cell to receptors at the cellular membrane. Messages are then relayed to the cell's nucleus. An important element in this sequence is the enzymatically-controlled addition of a phosphate group to certain molecules. This sets off a cascade of further activity as well as creating receptor sites for further interactions. Different growth regulating substances appear to initiate the growth-signalling message partially via a common pathway. Aberrations in one particular receptor protein, the Ras protein, plays a role in many tumors. Once activated, this protein initiates a series of events that commits the cell to a replication cycle. Techniques showing promise in the laboratory include molecules that compete for the Ras protein receptor site on the cellular membrane, disrupting bonding with the phosphorus group, and introducing genes coding for inhibitors of the Ras protein.

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Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia

Article Abstract:

A randomized trial was carried out to compare imatinib with interferon alfa plus cytarabine in the chronic phase of chronic myeloid leukemia (CML) to demonstrate the significant superiority of imatinib in all standard indicators of the disease within a median follow-up of 19 months. After 5 years of follow-up, continuous treatment of chronic-phase CML with imatinib as initial therapy was found to include durable responses in a high proportion of patients.

Drug therapy, Dosage and administration, Interferon alpha, Chronic myeloid leukemia, Imatinib mesylate, Clinical report

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