Watch this video titled Normal vs. Cancer Cells.
Please note this is NOT a narrated video clip; it has no audio.
Cancer cells are cells that divide abnormally and exhibit uncontrolled growth. Under normal circumstances, cells will divide only when necessary and will stop dividing when their cell membrane encounters another cell membrane (referred to as contact inhibition). Cell division can be altered by the presence of particular proteins that act as chemical signals. For example, when you cut your skin, cells will be destroyed and you bleed. Chemical signals, in the form of proteins, are released by platelets (found in the blood) to increase the rate of cell division in that area. This, in conjunction with several other processes that take place, aids the healing process. Once the new cells fill in the wound and encounter each other’s cell membrane, the increased division of cells will stop, and the rate of cell division in the area returns to what is normal.
What are these chemical signals? These signals are proteins classified as cyclins. The term cyclin should help you recall the cell cycle, as this class of proteins regulates that process. One set of cyclins ensure that there are smooth transitions between cell cycle phases, and a second set oversees checkpoints in the cell cycle. Checkpoints are able to sense problems with critical events in the cell cycle, such as incorrect DNA replication, and will delay the progression of the cell cycle. However, it is crucial to note that checkpoint function is not required for every cell cycle.
Since cancer is a disorder where cells divide abnormally and uncontrollably, it would seem logical to focus on the mechanism of the cell cycle for answers regarding what causes cancer. It has been determined that mutations (changes in the DNA nucleotides) in a specific set of genes (proto-oncogenes) leads to an increased rate of cell division. In addition, mutations in a group of tumor suppressor genes have been shown to directly affect the cell cycle. Tumor suppressor genes code for proteins that are involved with the checkpoint functions. One in particular, a protein known as p53, is essential to halting the cell cycle when damage to the DNA or to the chromosomes is present. By stopping the cell from reproducing, p53 sentences the cell to death. If the gene coding for this protein is mutated, p53 will no longer function correctly, allowing defective cells to reproduce. The cumulative effects of errors in proto-oncogenes and tumor suppressor genes are thought to play a significant role in the development and progression of cancer.
It would be incorrect to assume that there is a single cause for the development of cancer. While genetics certainly plays a role, the question remains in terms of what can influence or directly cause changes in the genes themselves. It has been shown that smoking, consuming a diet high in fats, and working with toxic chemicals increase the risk of adults developing cancer. In addition, certain viruses, specifically Epstein-Barr and HIV, have been linked with the development of certain types of childhood cancers including Hodgkin’s lymphoma. In this case, it is thought that the virus alters the cells directly and these altered cells then continue to divide, producing disease. Prolonged and consistent exposure to UV (ultraviolet) light , including that found in sunlight, increases a person’s risk for skin cancers, such as melanoma and basal cell carcinoma. Research has also been done investigating how exposure to pesticides, fertilizers, and power lines may influence the development of cancer, especially in children. The search continues to establish definitive causes and to develop more effective treatments for this cell cycle disorder.
1. Watch the video titled The Cell Cycle and Cancer
2. Summarize what changes in the cell cycle can lead to the development of cancer cells.
3. List any questions you have.
4. Find the answers to your questions using the resources available: your peers, your instructor, the internet
5. Share your questions and answers as directed by your instructor.