1. Mutations can be be fixed by enzymes before they cause trouble. There are many enzymes that repair damage DNA in a cell. Some enzymes remove damaged pieces of DNA and fill in the gap with the proper bases, using the opposite strand of DNA as a guide. Other repair enzymes scan the chromosomes for mismatched bases. When a mismatch is discovered, the enzymes remove the wrong base, and replace it with the correct one.

2. Cancer cells replication patterns is controlled by the cyclins. Mitosis has S, G2, M, G1 stages and movement between the stages are controlled by cyclin-dependant Kinases. A cell's progress through the cell cycle is controlled by a group of proteins known as cyclins. For example, cyclin D1 increases as a cell prepares to enter the S stage of mitosis. Only when the right cyclins are at the right level in a cell will it enter the next stage of mitosis. In some cancers cells, it appears that some of the cell cycle genes, both cyclins and th cyclin-dependent kinases, have been mutated. D1 mutations can be found in some cancer cells. Cycline E protein in higher in breast cancer cells. Cycline E may also increase as breast cancers become more aggressive. These changes stimulate the cell to perpetually divide.

3. The mitosis checkpoints fail in cancer cells. The cell continues to divide with gene defects. The checkpoints may allow a cell to resume progress through the cycle even though the damaged remains unrepaired; the cell seems to become accustomed to the damage and sees it as normal. Some scientist think that the checkpoints themselves may have mutated.

4. In normal cells, the cyclins do not act on their own; they are controlled by growth factors, hormones and other growth-stimulating proteins. These proteins are usually manufactured by one type of cell and sent to a different type of cell. They attach to receptors on the cell and send signals inside which, ultimately, control the cyclins and stimulate cell division.

5. When growth factors or other cell stimulants send signals inside the cells, internal molecules must transmit those signals. One of the more commonly mutated oncognese in tumors is call Ras. The Ras protein is part of the signaling pathway which usually leads to cell growth. In some tumors, drugs which can suppress Ras can block the growth of cancer.

6. When a tumor suppressor gene mutates, its ability to prevent uncontrolled growth is turned off. For most tumor suppressors, both tumor suppressor geens in a cell must be damaged in order to promote cancer. Tumor suppressor gene and associated cancers: p53 (Sarcomas, breast cancer), RB (Retinoblastoma), APC (Colon Cancer), DCP4 (Cancer of the pancreas), PTCH (Basal cell carcinoma, skin cancer), BRCA1 & BRCA2 (breast cancer). Cell with mutated genes with an intact p53 can not be repaired, p53 turns on a set of proteins which kill the cell. The process of cell sucide is called apoptosis.

7. As many as 80% of women who inherit mutations in BRCA1 and BRCA2 will develop breast cancer.

8. The mainstays of cancer therapy is surgery, radiation, and chemotherapy. Not all cancers can bee effectively with all three.

9. Radiotheraphy basically works by bombarding the cancer with very energetic particles such as x-rays or gamma rays. The energy is absorbed by cells, and can split water moleculs in the cells, producing free radicals. Free radicals are very unstable molecules which have temporarily captured an extra electron. This extra electron give a free radical the ability to combine with any other molecule nearby. The free radicals bounce around in the cell, wreaking havoc as they damage cricical molecules. Scientist believe that the radiation therapy amy trigger apoptsis (cell sucide). The drug CBLB502 is being tested to help delay apoptsis during radiation treatment allowing healthy cells to survive and cancer cells to die.

10. With complex calculations and multiple beams from different directions, radiation can now match even the shape of the tumor. The exciting field of optical Coherence Tomography may someday allow doctors to probe tissue layers interactively and remove cancer by very focused radiation burst.

11. Japan is perfection the heavy-ion treatment system for killing certain cancer. Heavy ions concentrate more destructive energy directly at the tumor. The Tokyo Heavy-Ion Medical Accelerator in Chiba, or Himac is the first large accellerator in the world dedicated to cancer treatment. The accelerator cost $300 million to build and $50 million a year to treat 1,000 patients. The device uses 25 megawatts of electrical power, the capacity to supply 8,000 homes. Heavy ions are particularly useful for treating tumors in areas that can be damaged by radiation, such as the eye and spinal cord.

12. Chemicals called radiosensitizers make tumors more sensitive to radiation.

13. Porphyrins are useful molecules in the body. Among their duties, they carry oxygen and iron in the blood. Porphyrins also tend to accumulate in cancer cells and not in normal cells. This characteristic has made them important in phototherapy treatment .Johnathan Sessler built a bigger porphyrin carried by cancer drugs into the cancer cell. The drug was called Texaphyrin. When Texaphyrin is attached to gadolinium, it seems to make free radicals last longer.

14. 5-fluorouracil (5 FU) stops the cell from making the base thymine by blocking the enzyme thymidylate synthase, which makes thymine from uracil. 5-FU inhibits thymidylate synthetase. Cancer cells need to make and repair DNA in order to grow and multiply. 5FU stop cells making and repairing DNA. The taking of 5-FU causes a temporary drop in the number of white blood cells produced by the bone marrow. 5-FU are part of a group of chemotherapy drugs know at anti-metabolites. Anti-metabolites often stop cells making and repairing DNA.

15. Cancer carrying Fas-L receptors connect with T cell Fas receptor and the T-cell commits suicide. Cancer cells have antigen blockers on their receptors and do not bind with the T-cell and the cancer cell and T-cell survive. Cancer cell with the Fas gen have fas receptors that bind with Cancers with Fas-L receptors and the cancer cell dies.