{"id":1090,"date":"2024-02-21T20:55:47","date_gmt":"2024-02-22T01:55:47","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=1090"},"modified":"2026-05-27T13:44:51","modified_gmt":"2026-05-27T17:44:51","slug":"dna-mutations-and-cancer","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/dna-mutations-and-cancer\/","title":{"raw":"DNA Mutations and Cancer","rendered":"DNA Mutations and Cancer"},"content":{"raw":"<h3><strong>What is Cancer?\u00a0 How do Cells become Cancerous?<\/strong><\/h3>\r\n<strong>Cancer<\/strong> is characterized by the accumulation of cells due to excessive rates of cell cycling and\/or lack of apoptosis.\u00a0 Often cancerous cells no longer respond to normal cues to exit the cell cycle and unfortunately continue to repeatedly undergo cell division.\u00a0 Cancer can also occur when cells no longer respond to cues to become dormant and undergo apoptosis.\u00a0 As a result of impaired control of rates of cell cycling and\/or apoptosis, cells begin to accumulate forming a mass, which can spread, not only negatively affect neighbouring tissue but also disrupting distant locations throughout the body that cancerous cells migrate to.\r\n\r\n<strong>Impaired Control of Cell Cycling and Apoptosis\u00a0 \u00a0 \u00a0\u00a0<\/strong>\r\n\r\nYou may recall that the cell cycle consists of interphase (consisting of 3 phases:\u00a0 G<sub>1<\/sub> phase, S-phase, and G<sub>2<\/sub> phase), and mitosis (consisting of 4 stages: prophase, metaphase, anaphase, telophase), following by cytokinesis.\u00a0 In the process of 1 cell cycle, one cell grows, duplicates its organelles and DNA and then divides into two identical daughter cells.\u00a0 This entire process is tightly regulated by specific genes known as regulator genes.\u00a0 For example, there are regulatory genes that code for growth factors that stimulate cell cycling as well as growth-inhibiting factors that limit the rate of mitosis.\r\n\r\n[caption id=\"attachment_5862\" align=\"alignnone\" width=\"300\"]<a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Cancer-Increased-Cell-Division-and-Decreased-Apoptosis.png\" target=\"_blank\" rel=\"noopener\"><img class=\"wp-image-5862 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Cancer-Increased-Cell-Division-and-Decreased-Apoptosis-300x225.png\" alt=\"Cell Division and Apoptosis. In an adult organism, normal cell division is balanced by apoptosis (programmed cell death) to maintain a constant cell number in homeostasis. Either an increase in cell division or a decrease in apoptosis leads an increase in the number of cells and tumor formation. Credit: Rao, A. and Ryan, K. Department of Biology, Texas A&amp;M University.\" width=\"300\" height=\"225\" \/><\/a> Cell Division and Apoptosis. In an adult organism, normal cell division is balanced by apoptosis (programmed cell death) to maintain a constant cell number in homeostasis. Either an increase in cell division or a decrease in apoptosis leads an increase in the number of cells and tumor formation. Credit: Rao, A. and Ryan, K. Department of Biology, Texas A&amp;M University.[\/caption]\r\n\r\n<strong>Regulator genes<\/strong> code for <strong>growth factors<\/strong> and <strong>growth-inhibiting factors<\/strong>, controlling the <span style=\"text-decoration: underline\"><strong>rate<\/strong><\/span> of mitosis and apoptosis (cell death).\u00a0 Mutations in regulatory genes can therefore lead to excessive mitosis or a lack of apoptosis, both of which contribute to cancer development.\r\n\r\nThere are several c<span style=\"font-size: 1em\">auses of DNA mutation, which include:<\/span>\r\n<ul>\r\n \t<li><span style=\"font-size: 1em\"> <strong>Viruses<\/strong> (e.g., Human Papilloma Virus, HPV is considered an oncovirus in that it can mutate DNA and has been linked to the development of cervical cancer), <\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\"><strong>Radiation<\/strong> which includes:<\/span>\r\n<ul>\r\n \t<li><span style=\"font-size: 1em\"><strong>UV light<\/strong> is a risk factor for skin cancer as it can cause thymine dimers in DNA which leads to errors during DNA duplication, <\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\"><strong>Gamma rays<\/strong> are associated with radioactive isotopes which have been found to cause DNA mutations), <\/span><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><span style=\"font-size: 1em\"><strong>Chemicals<\/strong> (e.g., asbestos, cigarette smoke), and <\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\"><strong>Spontaneous errors<\/strong> during DNA synthesis.<\/span><\/li>\r\n \t<li style=\"font-weight: 400\"><strong>Rapid rates of mitosis<\/strong> during injury repair may increase the risk of errors occurring, potentially leading to cancer.<\/li>\r\n<\/ul>\r\n[caption id=\"attachment_5854\" align=\"alignnone\" width=\"300\"]<a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-scaled.png\"><img class=\"size-medium wp-image-5854\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-300x231.png\" alt=\"\" width=\"300\" height=\"231\" \/><\/a> <strong>Both UVA and UVB radiation are risk factors for skin cancer<\/strong>.\u00a0 <strong>UVA photons<\/strong> can cause indirect DNA damage by increasing <strong>ROS (Reactive Oxygen Species)<\/strong> within in a cell. <strong>UVB photons<\/strong> can cause direct DNA damage specifically by causing aberrant covalent bonds to form between adjacent pyrimidine bases, producing a dimer. Most UV-induced pyrimidine dimers in DNA are repaired however, <strong>pyrimidine dimers<\/strong> that escape this repair process can induce a form of programmed cell death (apoptosis) or can cause DNA replication errors leading to mutation and therefore risk of developing <strong>skin cancer<\/strong>.[\/caption]\r\n\r\nTerry Fox is a Canadian Hero who attempted to run across Canada in order to raise money in support of cancer research. Of course, we know he started in St. John's Newfoundland and was stopped short in Thunder Bay when the cancer had spread to his lungs and he could no longer run.\u00a0 Until that point, he had been running the distance of one marathon per day for 143 days.\u00a0 This is an astounding feat given that one of his legs had been amputated due to cancer of the bone and he was running with the use of a fairly rudimentary (and certainly not comfortable) prosthetic limb.\u00a0 Terry Fox had a cancer called osteosarcoma. Now, before he was diagnosed with cancer in that that bone, he'd actually been in a in a vehicle accident and had sustained damage to that same leg.\u00a0 \u00a0When he was later diagnosed with cancer in that same leg, he thought it was quite the coincidence. He started speculating this, maybe during the healing of his leg, cancer had formed.\u00a0 During healing when there were rapid rates of mitosis, it may have been that DNA errors were created in regulatory genes that caused cells to become cancerous.\u00a0 Terry's Marathon of Hope was stopped short and he died at age 22 as the cancer metastasized to his lungs.\r\n\r\n[caption id=\"attachment_5824\" align=\"alignnone\" width=\"300\"]<a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/terry-fox-photo.png\" target=\"_blank\" rel=\"noopener\"><img class=\"wp-image-5824 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/terry-fox-photo-300x180.png\" alt=\"Terry Fox\" width=\"300\" height=\"180\" \/><\/a> Figure 1.\u00a0 Terry Fox running in his Marathon of Hope, May 25, 1980. In 1980, the young Canadian athlete Terry Fox, who had grown up in British Columbia and had lost his right leg to cancer, embarked on an ambitious cross-country run using a prosthetic leg. His journey, known as the Marathon of Hope, was intended to raise funds and awareness for cancer research. The run began on April 12, 1980, in St. John\u2019s, Newfoundland, and was intended to conclude in Victoria, British Columbia. As Fox made his way from town to town across Canada, his fame grew exponentially. He set himself a grueling 26 mile (~42 km) daily regime, eventually covering over 3,339 miles (5,374 km) in 143 days. Having completed half of his projected journey, Fox ended his run near Thunder Bay, Ontario, on September 1. He died the following year at the age of 22. Photograph: The Terry Fox Foundation.[\/caption]\r\n<h3><strong>Cancer is a Disease of the Genes?\u00a0<\/strong><\/h3>\r\nIt may seem odd that cancer is considered a genetic disease as it is <strong>rarely inherited<\/strong>, and more often is acquired through exposure to various mutagenic risk factors (some of which are mentioned above).\u00a0 Cancer is certainly a disease caused by <strong>gene mutations<\/strong>, specifically in regulatory genes required for cell cycling and\/or apoptosis as well as for ensuring proper and error-free DNA duplication.\u00a0 To date over 290 different gene mutations have been linked to cancer.\r\n<h3><strong>What is the difference between a genetic disease, an inherited disease and a congenital disease?<\/strong><\/h3>\r\nAlthough some cancers are <strong>inherited<\/strong> (e.g., retinoblastoma), most inherited diseases are not cancerous.\u00a0 For example, Cystic Fibrosis and Huntington's Disease both occur when DNA mutations are inherited.\u00a0 In both of these cases the DNA mutations occur in genes that are involved other cellular processes that do cause problems, but do not result in cancer.\r\n\r\nSide note:\u00a0 Not all <strong>congenital diseases<\/strong> are inherited or genetic.\u00a0 Congenital is a term that translates to \"born with\".\u00a0 For example, cerebral palsy is a congenital disease, though it is not genetic and is not inherited.\u00a0 Cerebral palsy is thought to occur when a brain lesion takes place either before or shortly after birth.","rendered":"<h3><strong>What is Cancer?\u00a0 How do Cells become Cancerous?<\/strong><\/h3>\n<p><strong>Cancer<\/strong> is characterized by the accumulation of cells due to excessive rates of cell cycling and\/or lack of apoptosis.\u00a0 Often cancerous cells no longer respond to normal cues to exit the cell cycle and unfortunately continue to repeatedly undergo cell division.\u00a0 Cancer can also occur when cells no longer respond to cues to become dormant and undergo apoptosis.\u00a0 As a result of impaired control of rates of cell cycling and\/or apoptosis, cells begin to accumulate forming a mass, which can spread, not only negatively affect neighbouring tissue but also disrupting distant locations throughout the body that cancerous cells migrate to.<\/p>\n<p><strong>Impaired Control of Cell Cycling and Apoptosis\u00a0 \u00a0 \u00a0\u00a0<\/strong><\/p>\n<p>You may recall that the cell cycle consists of interphase (consisting of 3 phases:\u00a0 G<sub>1<\/sub> phase, S-phase, and G<sub>2<\/sub> phase), and mitosis (consisting of 4 stages: prophase, metaphase, anaphase, telophase), following by cytokinesis.\u00a0 In the process of 1 cell cycle, one cell grows, duplicates its organelles and DNA and then divides into two identical daughter cells.\u00a0 This entire process is tightly regulated by specific genes known as regulator genes.\u00a0 For example, there are regulatory genes that code for growth factors that stimulate cell cycling as well as growth-inhibiting factors that limit the rate of mitosis.<\/p>\n<figure id=\"attachment_5862\" aria-describedby=\"caption-attachment-5862\" style=\"width: 300px\" class=\"wp-caption alignnone\"><a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Cancer-Increased-Cell-Division-and-Decreased-Apoptosis.png\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-5862 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Cancer-Increased-Cell-Division-and-Decreased-Apoptosis-300x225.png\" alt=\"Cell Division and Apoptosis. In an adult organism, normal cell division is balanced by apoptosis (programmed cell death) to maintain a constant cell number in homeostasis. Either an increase in cell division or a decrease in apoptosis leads an increase in the number of cells and tumor formation. Credit: Rao, A. and Ryan, K. Department of Biology, Texas A&amp;M University.\" width=\"300\" height=\"225\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Cancer-Increased-Cell-Division-and-Decreased-Apoptosis-300x225.png 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Cancer-Increased-Cell-Division-and-Decreased-Apoptosis-1024x768.png 1024w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Cancer-Increased-Cell-Division-and-Decreased-Apoptosis-768x576.png 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Cancer-Increased-Cell-Division-and-Decreased-Apoptosis-65x49.png 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Cancer-Increased-Cell-Division-and-Decreased-Apoptosis-225x169.png 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Cancer-Increased-Cell-Division-and-Decreased-Apoptosis-350x263.png 350w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Cancer-Increased-Cell-Division-and-Decreased-Apoptosis.png 1200w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><figcaption id=\"caption-attachment-5862\" class=\"wp-caption-text\">Cell Division and Apoptosis. In an adult organism, normal cell division is balanced by apoptosis (programmed cell death) to maintain a constant cell number in homeostasis. Either an increase in cell division or a decrease in apoptosis leads an increase in the number of cells and tumor formation. Credit: Rao, A. and Ryan, K. Department of Biology, Texas A&amp;M University.<\/figcaption><\/figure>\n<p><strong>Regulator genes<\/strong> code for <strong>growth factors<\/strong> and <strong>growth-inhibiting factors<\/strong>, controlling the <span style=\"text-decoration: underline\"><strong>rate<\/strong><\/span> of mitosis and apoptosis (cell death).\u00a0 Mutations in regulatory genes can therefore lead to excessive mitosis or a lack of apoptosis, both of which contribute to cancer development.<\/p>\n<p>There are several c<span style=\"font-size: 1em\">auses of DNA mutation, which include:<\/span><\/p>\n<ul>\n<li><span style=\"font-size: 1em\"> <strong>Viruses<\/strong> (e.g., Human Papilloma Virus, HPV is considered an oncovirus in that it can mutate DNA and has been linked to the development of cervical cancer), <\/span><\/li>\n<li><span style=\"font-size: 1em\"><strong>Radiation<\/strong> which includes:<\/span>\n<ul>\n<li><span style=\"font-size: 1em\"><strong>UV light<\/strong> is a risk factor for skin cancer as it can cause thymine dimers in DNA which leads to errors during DNA duplication, <\/span><\/li>\n<li><span style=\"font-size: 1em\"><strong>Gamma rays<\/strong> are associated with radioactive isotopes which have been found to cause DNA mutations), <\/span><\/li>\n<\/ul>\n<\/li>\n<li><span style=\"font-size: 1em\"><strong>Chemicals<\/strong> (e.g., asbestos, cigarette smoke), and <\/span><\/li>\n<li><span style=\"font-size: 1em\"><strong>Spontaneous errors<\/strong> during DNA synthesis.<\/span><\/li>\n<li style=\"font-weight: 400\"><strong>Rapid rates of mitosis<\/strong> during injury repair may increase the risk of errors occurring, potentially leading to cancer.<\/li>\n<\/ul>\n<figure id=\"attachment_5854\" aria-describedby=\"caption-attachment-5854\" style=\"width: 300px\" class=\"wp-caption alignnone\"><a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-scaled.png\"><img loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-5854\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-300x231.png\" alt=\"\" width=\"300\" height=\"231\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-300x231.png 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-1024x788.png 1024w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-768x591.png 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-1536x1182.png 1536w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-2048x1576.png 2048w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-65x50.png 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-225x173.png 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Pyrimidine-Dimers-DNA-mutation-caused-by-UV-350x269.png 350w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><figcaption id=\"caption-attachment-5854\" class=\"wp-caption-text\"><strong>Both UVA and UVB radiation are risk factors for skin cancer<\/strong>.\u00a0 <strong>UVA photons<\/strong> can cause indirect DNA damage by increasing <strong>ROS (Reactive Oxygen Species)<\/strong> within in a cell. <strong>UVB photons<\/strong> can cause direct DNA damage specifically by causing aberrant covalent bonds to form between adjacent pyrimidine bases, producing a dimer. Most UV-induced pyrimidine dimers in DNA are repaired however, <strong>pyrimidine dimers<\/strong> that escape this repair process can induce a form of programmed cell death (apoptosis) or can cause DNA replication errors leading to mutation and therefore risk of developing <strong>skin cancer<\/strong>.<\/figcaption><\/figure>\n<p>Terry Fox is a Canadian Hero who attempted to run across Canada in order to raise money in support of cancer research. Of course, we know he started in St. John&#8217;s Newfoundland and was stopped short in Thunder Bay when the cancer had spread to his lungs and he could no longer run.\u00a0 Until that point, he had been running the distance of one marathon per day for 143 days.\u00a0 This is an astounding feat given that one of his legs had been amputated due to cancer of the bone and he was running with the use of a fairly rudimentary (and certainly not comfortable) prosthetic limb.\u00a0 Terry Fox had a cancer called osteosarcoma. Now, before he was diagnosed with cancer in that that bone, he&#8217;d actually been in a in a vehicle accident and had sustained damage to that same leg.\u00a0 \u00a0When he was later diagnosed with cancer in that same leg, he thought it was quite the coincidence. He started speculating this, maybe during the healing of his leg, cancer had formed.\u00a0 During healing when there were rapid rates of mitosis, it may have been that DNA errors were created in regulatory genes that caused cells to become cancerous.\u00a0 Terry&#8217;s Marathon of Hope was stopped short and he died at age 22 as the cancer metastasized to his lungs.<\/p>\n<figure id=\"attachment_5824\" aria-describedby=\"caption-attachment-5824\" style=\"width: 300px\" class=\"wp-caption alignnone\"><a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/terry-fox-photo.png\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-5824 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/terry-fox-photo-300x180.png\" alt=\"Terry Fox\" width=\"300\" height=\"180\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/terry-fox-photo-300x180.png 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/terry-fox-photo-768x461.png 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/terry-fox-photo-65x39.png 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/terry-fox-photo-225x135.png 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/terry-fox-photo-350x210.png 350w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/terry-fox-photo.png 790w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><figcaption id=\"caption-attachment-5824\" class=\"wp-caption-text\">Figure 1.\u00a0 Terry Fox running in his Marathon of Hope, May 25, 1980. In 1980, the young Canadian athlete Terry Fox, who had grown up in British Columbia and had lost his right leg to cancer, embarked on an ambitious cross-country run using a prosthetic leg. His journey, known as the Marathon of Hope, was intended to raise funds and awareness for cancer research. The run began on April 12, 1980, in St. John\u2019s, Newfoundland, and was intended to conclude in Victoria, British Columbia. As Fox made his way from town to town across Canada, his fame grew exponentially. He set himself a grueling 26 mile (~42 km) daily regime, eventually covering over 3,339 miles (5,374 km) in 143 days. Having completed half of his projected journey, Fox ended his run near Thunder Bay, Ontario, on September 1. He died the following year at the age of 22. Photograph: The Terry Fox Foundation.<\/figcaption><\/figure>\n<h3><strong>Cancer is a Disease of the Genes?\u00a0<\/strong><\/h3>\n<p>It may seem odd that cancer is considered a genetic disease as it is <strong>rarely inherited<\/strong>, and more often is acquired through exposure to various mutagenic risk factors (some of which are mentioned above).\u00a0 Cancer is certainly a disease caused by <strong>gene mutations<\/strong>, specifically in regulatory genes required for cell cycling and\/or apoptosis as well as for ensuring proper and error-free DNA duplication.\u00a0 To date over 290 different gene mutations have been linked to cancer.<\/p>\n<h3><strong>What is the difference between a genetic disease, an inherited disease and a congenital disease?<\/strong><\/h3>\n<p>Although some cancers are <strong>inherited<\/strong> (e.g., retinoblastoma), most inherited diseases are not cancerous.\u00a0 For example, Cystic Fibrosis and Huntington&#8217;s Disease both occur when DNA mutations are inherited.\u00a0 In both of these cases the DNA mutations occur in genes that are involved other cellular processes that do cause problems, but do not result in cancer.<\/p>\n<p>Side note:\u00a0 Not all <strong>congenital diseases<\/strong> are inherited or genetic.\u00a0 Congenital is a term that translates to &#8220;born with&#8221;.\u00a0 For example, cerebral palsy is a congenital disease, though it is not genetic and is not inherited.\u00a0 Cerebral palsy is thought to occur when a brain lesion takes place either before or shortly after birth.<\/p>\n<div class=\"media-attributions clear\" prefix:cc=\"http:\/\/creativecommons.org\/ns#\" prefix:dc=\"http:\/\/purl.org\/dc\/terms\/\"><h2>Media Attributions<\/h2><ul><li about=\"https:\/\/openstax.org\/books\/biology-2e\/pages\/10-4-cancer-and-the-cell-cycle\"><a rel=\"cc:attributionURL\" href=\"https:\/\/openstax.org\/books\/biology-2e\/pages\/10-4-cancer-and-the-cell-cycle\" property=\"dc:title\">Cancer-Increased Cell Division and Decreased Apoptosis<\/a>  &copy;  Mary Ann Clark, Matthew Douglas, Jung Choi    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/\">CC BY-NC-SA (Attribution NonCommercial ShareAlike)<\/a> license<\/li><li about=\"https:\/\/commons.wikimedia.org\/wiki\/File:DNA_UV_mutation.svg\"><a rel=\"cc:attributionURL\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:DNA_UV_mutation.svg\" property=\"dc:title\">Pyrimidine Dimers DNA mutation caused by UV Radiation<\/a>  &copy;  By Mouagip - Own work based on: DNA UV mutation.gif by NASA\/David Herring, Public Domain, https:\/\/commons.wikimedia.org\/w\/index.php?curid=11367690    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/publicdomain\/mark\/1.0\/\">Public Domain<\/a> license<\/li><li about=\"https:\/\/ecampusontario.pressbooks.pub\/canadarthistories\/chapter\/terry-fox-memorial-2011\/\"><a rel=\"cc:attributionURL\" href=\"https:\/\/ecampusontario.pressbooks.pub\/canadarthistories\/chapter\/terry-fox-memorial-2011\/\" property=\"dc:title\">Terry Fox<\/a>  &copy;  Alena Buis; ecavaliere; Jen Kennedy; Johanna Amos; Sarah E.K. Smith; and Devon Smither    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/\">CC BY-NC-SA (Attribution NonCommercial ShareAlike)<\/a> license<\/li><\/ul><\/div>","protected":false},"author":1370,"menu_order":4,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"Pictures coming soon!","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-1090","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":35,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1090","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":15,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1090\/revisions"}],"predecessor-version":[{"id":6226,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1090\/revisions\/6226"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/35"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1090\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=1090"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=1090"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=1090"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=1090"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}