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Definitions[edit]

Cancers are a large family of diseases that involve abnormal cell growth with the potential to invade or spread to other parts of the body.[1][2] They form a subset of neoplasms. A neoplasm or tumor is a group of cells that have undergone unregulated growth, and will often form a mass or lump, but may be distributed diffusely.[3][4]

All tumor cells show the six hallmarks of cancer. These are characteristics that the cancer cells need to produce a malignant tumor. They include:[5]

Sustained growth and division[edit]

Typically, cells of the body require hormones and other molecules that act as signals for them to grow and divide. Cancer cells, however, have the ability to grow without these external signals. There are multiple ways in which cancer cells can do this: by producing these signals themselves, known as autocrine signalling; by permanently activating the signalling pathways that respond to these signals; or by destroying 'off switches' that prevents excessive growth from these signals (negative feedback). In addition, cell division in normal, non-cancerous cells is tightly controlled. In cancer cells, these processes are deregulated because the proteins that control them are altered, leading to increased growth and cell division within the tumor.[6][7]

Preventing growth suppression[edit]

To counteract and control signals that tell cells when to grow and divide, they also have processes within the cells that prevent cell growth and division. These processes are orchestrated by proteins known as tumor supressor genes. These genes take information from the cell to ensure that it is ready to divide, and will halt division if not (when the DNA is damaged, for example). In cancer, these tumour suppressor proteins are altered so that they don't effectively prevent cell division, even when the cell has severe abnormalities. Normal cells will also stop dividing when the cells fill up the space they are in and touch other cells; known as contact inhibition. Cancer cells do not have contact inhibition, and so will continue to grow and divide, regardless of their surroundings.[6][8]

Resisting cell death[edit]

Cells have the ability to 'self-destruct'; a process known as apoptosis. This is required for organisms to grow and develop properly, for maintaining tissues of the body, and is also initiated when a cell is damaged or infected. Cancer cells, however, lose this ability; even though cells may become grossly abnormal, they do not apoptose. The cancer cells may do this by altering the mechanisms that detect the damage or abnormalities. This means that proper signalling cannot occur, thus apoptosis cannot activate. They may also have defects in the downstream signalling itself, or the proteins involved in apoptosis.[6][9]

Immortalisation[edit]

Cells of the body don't normally have the ability to divide indefinitely. They have a limited number of divisions before the cells become unable to divide (senescence), or die (crisis). The cause of these barriers is primarily due to the DNA at the end of chromosomes, known as telomeres. Telomeric DNA shortens with every cell division, until it becomes so short it activates senescence, so the cell stops dividing. Cancer cells bypass this barrier by manipulating enzymes that increase the length of telomeres. Thus, they can divide indefinitely, without initiating senescence.[6][10]

Developing blood vessels[edit]

Normal tissues of the body have blood vessels running through them that deliver oxygen from the lungs. Cells must be close to the blood vessels to get enough oxygen for them to survive. New blood vessels are formed during the development of embryos, during wound repair and during the female reproductive cycle. An expanding tumour requires new blood vessels to deliver adequate oxygen to the cancer cells, and thus exploits these normal physiological processes for its benefit. To do this, the cancer cells acquire the ability to orchestrate production of new vasculature by activating what is known as the 'angiogenic switch'. In doing so they control non-cancerous cells that are present in the tumor that can form blood vessels by reducing the production of factors that inhibit blood vessel production, and increase the production of factors that promote blood vessel formation.[6][11]

Metastasis and invasion[edit]

One of the most well known properties of cancer cells is their ability to invade neighboring tissues. It is what dictates whether the tumor is benign or malignant, and is the reason for their dissemination around the body. The cancer cells have to undergo a multitude of changes in order for them to aquire the ability to metastasize. It is a multistep process that starts with local invasion of the cells into the surrounding tissues. They then have to invade blood vessels, survive in the harsh environment of the circulatory system, exit this system and then start dividing in the new tissue.[6][12]





The progression from normal cells to cells that can form a discernible mass to outright cancer involves multiple steps known as malignant progression.[5][13]

  1. ^ Cite error: The named reference WHO2014 was invoked but never defined (see the help page).
  2. ^ "Defining Cancer". National Cancer Institute. Retrieved 10 June 2014. 
  3. ^ "Cancer Glossary". cancer.org. American Cancer Society. Retrieved September 11, 2013. 
  4. ^ "What is cancer?". cancer.gov. National Cancer Institute. Retrieved September 11, 2013. 
  5. ^ a b Hanahan, Douglas; Weinberg, Robert A. (January 7, 2000). "The hallmarks of cancer". Cell. 100 (1): 57–70. doi:10.1016/S0092-8674(00)81683-9. PMID 10647931. 
  6. ^ a b c d e f Hanahan, D; Weinberg, RA (4 March 2011). "Hallmarks of cancer: the next generation". Cell. 144 (5): 646–74. PMID 21376230. 
  7. ^ Evan, GI; Vousden, KH (17 May 2001). "Proliferation, cell cycle and apoptosis in cancer". Nature. 411 (6835): 342–8. PMID 11357141. 
  8. ^ McClatchey, AI; Yap, AS (October 2012). "Contact inhibition (of proliferation) redux". Current opinion in cell biology. 24 (5): 685–94. PMID 22835462. 
  9. ^ Elmore, S (June 2007). "Apoptosis: a review of programmed cell death". Toxicologic pathology. 35 (4): 495–516. PMID 17562483. 
  10. ^ Greenberg, RA (March 2005). "Telomeres, crisis and cancer". Current molecular medicine. 5 (2): 213–8. PMID 15974875. 
  11. ^ Bergers, G; Benjamin, LE (June 2003). "Tumorigenesis and the angiogenic switch". Nature reviews. Cancer. 3 (6): 401–10. PMID 12778130. 
  12. ^ van Zijl, F; Krupitza, G; Mikulits, W (2011). "Initial steps of metastasis: cell invasion and endothelial transmigration". Mutation research. 728 (1-2): 23–34. PMID 21605699. 
  13. ^ Hanahan, Douglas; Weinberg, Robert A. (2011). "Hallmarks of Cancer: The Next Generation". Cell. 144 (5): 646–74. doi:10.1016/j.cell.2011.02.013. PMID 21376230.