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Transcript
The Cell Cycle,Cancer !! THE CELL CYCLE AND CANCER A disease caused by severe disruption of the mechanisms that normally controlled the cell cycle. DIFFERENCE BETWEEN CANCER CELL AND NORMAL CELL There are some differences in between cancer cell and the normal cell. These cells behave differently than normal cell in the body. Many of these differences are related to cell division. 1. Cancer cell can multiply in culture without any growth factor where as normal cells needs growth factor in culture for multiplication. 2. Normal cell show contact inhibition. Because of this, they form a single layer on the bottom of a culture dish. Cancer cells, in contrast, keep dividing and pile on top of each other in lumpy layers. 3. Normal cells divide poorly if they are floating in liquid or soft gel, a property called anchorage dependence. Cancer cells lose anchorage dependence and grow fine in liquid or gel. 4. Cancer cells are called as “immortal”. They can grow and divide in culture for long periods of time, years or even decades. Normal cells only divide a certain number of times in culture before they stop dividing and eventually die. 5. Cancer cells are also different from normal cell in ways that are not directly cell cycle related. This difference helps them to grow, divide and form tumors.For instance cancer cells may not undergo programmed cell death or apoptosis, under conditions that would trigger this process in normal cell. 6. Cancer cell also gain the ability to migrate from the initial site of a tumor to other part of the body. This process is known as metastasis. CELL CYCLE REGULATORS AND CANCER Different types of cancer involve different types of mutation and each individual tumor has a unique genome and set of genetic alteration. Positive regulators may be over activated (become oncogenic) while negative regulators, also called tumor suppressor may be inactivated. ONCOGENES Positive regulators that move the cell cycle forward may be overactive cancer. A growth factor receptor may send signals even when growth factors are not there, or a cyclin may be expressed at abnormally high levels. These overactive forms of genes are called oncogenes and the normal forms of genes are called as proto oncogenes. Mutation that turns proto oncogenes into oncogenes can take variety of different forms. Some change the amino acid sequence of the protein, altering its shape and trapping it in an ‘always on’ state. Other involve amplification, in which a cell acquires extra copies of a gene (errors in DNA replication or repair).the extra copies of the gene result in higher levels of protein, which drive increased or inappropriate cell cycle progression. Many of the proteins that transmit growth factor signals are encoded by proto oncogenes. Normally these proteins drive cell cycle progression only when growth factors are available. In this simplified growth factor signalling pathway, the growth factor receptor, the G protein Ras and the signalling enzyme Raf are encoded by proto oncogenes. This overactive form of proteins is commonly found in cancer cell.oncogenic Ras mutations are found in an estimated 90% of pancreatic cancer. TUMOR SUPPRESSORS Negative regulators that block cell cycle progression may be less active in cancer cells. Tumor suppressor genes are family of normal genes that instruct cells to produce proteins that restrains cell growth and division. Sence,tumor suppressor genes code for proteins that slow down cell growth and division, the loss of such proteins allows a cell to grow and divide in an uncontrolled fashion. One of the most important tumor suppressors is tumor protein p 53 , which plays a key role in the cellular response to DNA damage. It acts primarily at the G1 checkpoint, where it blocks cell cycle progression in response to damaged DNA and other unfavourable conditions. When a cell DNA is damaged, a sensor protein activates p53, which halts the cell cycle at G1 checkpoint by triggering production of a protein called Cdk inhibitor. This inhibitor binds to cyclin Cdk complexes and inactivates them, preventing the cell from moving into S phase. 53 If the damaged is successfully fixed, p will release the cell allowing to continue through the cell cycle. If the damage is not fixable, p53 will play a final role, triggering apoptosis (programmed cell death) so that damaged DNA is not passed on. When p53 is defected a cell with damaged DNA may proceed with cell division rather than pausing the cell cycle, attempting DNA repairs or undergoing apoptosis. The daughter cells produced in such a division are likely to inherit mutations due to the unpaired DNA of the mother cell. Over generation, cells with faulty p53 tend to rapidly accumulate mutations, some of which may convert proto oncogenes to oncogenes or inactive other tumor suppressor and thus lead to the development of cancer. This is the general notes on The Cell cycle and Cancer. The Cell Cycle and Cancer Tutorial Video : Thank you for reading.