Causes, Smoking: p53
This series of animations shows how mutations in the p53 gene are found in 70% of lung tumors, the highest rate for any cancer.
P53 Mutations in the p53 gene are found in 70% of lung tumors, the highest rate for any cancer. The p53 protein is a tumor suppressor, analogous to car brakes, because its activity helps counter tumor development. P53 occupies a "checkpoint" in the cycle of cell division, where it "senses" DNA damage or mutations. The cell cycle is composed of four stages: During the first Gap Phase (G1) the cell grows and replenishes its resources. During S Phase (S) the cell synthesizes DNA in preparation for cell division. During the second Gap Phase (G2) the cell synthesizes proteins and other cellular components needed for cell division. During Mitosis Phase (M) the cell divides into two daughter cells. P53 acts as a checkpoint into the critical Synthesis (S) and Mitosis (M) Phases. After receiving information from DNA repair systems, p53 can signal the cell to stop dividing, allowing time for a mutation to be repaired before it is passed on to daughter cells. For example, p53 arrests the cell cycle, allowing time to repair G-T mutations induced by benzo[a]pyrene. If the DNA damage is too great to repair, p53 can signal the cell to commit suicide by the process called apoptosis, or programmed cell death. Mutations in p53 cause a loss of checkpoint control, allowing mutations and DNA damage to accumulate in a cell lineage.
p53 acts, p53 mutations, p53 protein, p53 gene, cell lineage, lung tumors, daughter cells, tumor suppressor, dna repair, dna damage, cellular components, smoking smoke, tumor development, cell death, pyrene, checkpoint, damage, DNA
- ID: 960
- Source: DNALC.IC
This section explains that lung cancer is the leading cause of cancer deaths in the United States and it is almost entirely preventable, since the vast majority of cases are due to cigarette smoking.
This section reviews K-ras and p53, two genes most frequently mutated in smoking-related lung cancers, one tar component, benzo[a]pyrene, is specifically linked to known mutations in these genes.
Leland Hartwell describes how cells regulate the timing of growth and cell division. Bob Horvitz and Mike Hengartner explain control mechanisms for cell death.
How does p53, a tumor-suppressor gene, affect cell death?
How do the cell death proteins interact?
The role of p53 in chemo- and radiotherapy given its role in programmed cell death.
The importance of cell death in cancer.
Scott Lowe's research has shown how the regulation of the cell cycle affect cancer.
Human homologue to C. elegans ced-4 gene.
Aflatoxin causes DNA damage and with prolonged exposure to aflatoxin, cells accumulate DNA mutations and thus are at increased risk of developing into cancer cells.