User:Simoncaulton/sandbox
Definitions
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
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
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
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. They do this by either altering the mechanisms that detect abnormalities, the following signalling that activates apoptosis; or the proteins involved in apoptosis itself.[6][9]
Enabling of a limitless replicative potential
Induction and sustainment of angiogenesis
Activation of metastasis and invasion of tissue
The progression from normal cells to cells that can form a discernible mass to outright cancer involves multiple steps known as malignant progression.[5][10]
- ^ Cite error: The named reference
WHO2014
was invoked but never defined (see the help page). - ^ "Defining Cancer". National Cancer Institute. Retrieved 10 June 2014.
- ^ "Cancer Glossary". cancer.org. American Cancer Society. Retrieved September 11, 2013.
- ^ "What is cancer?". cancer.gov. National Cancer Institute. Retrieved September 11, 2013.
- ^ 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.
- ^ a b c Hanahan, D; Weinberg, RA (4 March 2011). "Hallmarks of cancer: the next generation". Cell. 144 (5): 646–74. PMID 21376230.
- ^ Evan, GI; Vousden, KH (17 May 2001). "Proliferation, cell cycle and apoptosis in cancer". Nature. 411 (6835): 342–8. PMID 11357141.
- ^ McClatchey, AI; Yap, AS (October 2012). "Contact inhibition (of proliferation) redux". Current opinion in cell biology. 24 (5): 685–94. PMID 22835462.
- ^ Elmore, S (June 2007). "Apoptosis: a review of programmed cell death". Toxicologic pathology. 35 (4): 495–516. PMID 17562483.
- ^ 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.