{"id":37,"date":"2023-05-23T19:14:46","date_gmt":"2023-05-23T23:14:46","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&p=37"},"modified":"2026-01-03T16:16:38","modified_gmt":"2026-01-03T21:16:38","slug":"section-1-neoplasia","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/section-1-neoplasia\/","title":{"raw":"Review of Cell Cycling, DNA duplication, Cell Differentiation and Errors that can lead to Cancer","rendered":"Review of Cell Cycling, DNA duplication, Cell Differentiation and Errors that can lead to Cancer"},"content":{"raw":"

Review of Cell Cycling and DNA duplication<\/strong><\/h3>\r\nCell cycling<\/strong> in humans begins right away, starting with a fertilized egg.\u00a0 Undoubtedly you don't remember when you were this young, however, your first act as a fertilized egg was to grow larger in size and then get divide from 1 cell into 2 identical cells.\u00a0 This process is termed cell cycling.\u00a0 During cell cycling a cell becomes larger, duplicates its organelles and DNA and then divides into two identical daughter cells.\u00a0 This process of cell duplication is also sometimes called cell division<\/strong>, or cell proliferation<\/strong> or simply mitosis.<\/strong>\r\n\r\nThe steps of cell cycling are all equally important. The process begins in Interphase and there are three distinct stages within Interphase: G1, S<\/strong> and G2.<\/strong>\u00a0 In G1,<\/strong> the cell is growing in size and is duplicating its organelles.\u00a0 In S phase<\/strong>, DNA duplication occurs and in G2,<\/strong> the cell grows a bit more.\u00a0 After interphase is complete, the cell enters Mitosis.<\/strong>\u00a0 Within mitosis the enlarged cell divides into two cells<\/strong>, with half of its organelles and one set of DNA ending up in each daughter cell.\r\n

Review of Cell Differentiation<\/strong><\/h3>\r\nAs the fertilized egg grows, and repeatedly goes through cell cycling<\/strong>, a ball of identical cells called a blastocyst is created.\u00a0 At this point in time cells begin to mature and differentiate<\/strong> slightly to form 3 unique cell lineages (endoderm, mesoderm, and ectoderm).\u00a0 Within each of these cell types, cells continue to go through cell cycling and the embryo gets larger and larger in total size.\u00a0 Eventually these cells will become even further differentiated forming lineages for all 200 cell types of the human body (e.g. epithelial cells, cardiomyocytes, hepatocytes, etc.).\u00a0 Organs will form with unique sets of cell types becoming more and more functional.\u00a0 Wtihin each organ and tissue, some daughter cells (termed stem cells<\/strong>) continue to cell cycle, producing more cells, allowing the embryo to get larger, while other daughter cells exit<\/strong> the cell cycle and full mature or differentiate.\u00a0 These fully mature cells can no longer cell cycle and divide, and instead express specific proteins and enzymes to become more and more functional.\u00a0 This process continues through all stages of development from embryo to fetus to newborn to child to teenager.\u00a0 Even as a full-size adult, many tissues contain stem cells that divide in order to allow for the replacement of mature cells that get old and die.\u00a0 However most cells have exited the cell cycle and have fully differentiated to ensure that each organ and tissue is functional.\r\n\r\n \r\n\r\nCellular Review of Cellular proliferation and differentiation begin with a fertilized egg.\r\nDuring embryogenesis, the fertilized egg undergoes mitosis, leading to cell division.\r\nCells differentiate into various types, such as epithelial, connective, muscle, and neural tissue.\r\nStem cells undergo mitosis to produce daughter cells, which may differentiate into functional cells.\r\nDuring mitosis, organelles double, and DNA duplication occurs during the S phase of the cell cycle.\r\nEnzymes check DNA for errors during duplication, triggering apoptosis if mutations are found.\r\nTelomeres, end caps of chromosomes, shorten with each cell division, acting as a safety net to limit division.\r\nTelomere shortening helps prevent excessive divisions, reducing the risk of mutations and cancer development.\r\nApoptosis is triggered if telomeres reach a certain length, preventing further cell division and potential cancerous growth\r\n\r\n \r\n\r\n[caption id=\"attachment_972\" align=\"aligncenter\" width=\"800\"]\"Control<\/a> Control of the Cell Cycle[\/caption]\r\n\r\n \r\n\r\n \r\n

DNA mutations and Cancer<\/strong><\/h3>\r\nUnfortunately during S phase, as DNA is duplicated there is a chance for errors<\/strong> in sequencing together the correct strands of nucleotides.\u00a0 \u00a0Luckily there are several enzymes that check the DNA for errors during duplication<\/strong> and will trigger apoptosis<\/strong> if mutations<\/strong> are found that can not be fixed.\u00a0 It is known that mutations that occur in DNA (depending on the location) can cause cancer.<\/strong>\u00a0 It is also known that inevitably DNA errors do occur during duplication just due to the shear number of times DNA is duplicated, not to mention the number of nucleotides within each of the 23 pairs of chromosomes.\u00a0 It may seem obvious that the more DNA duplication events there are, the more risk there is for DNA errors to occur.\u00a0 Therefore a person's age<\/strong> becomes a risk factor for DNA mutations (and the possibility that these mutations may give rise to cancer).\u00a0 One can also imagine that if any of the enzymes responsible for checking DNA for errors<\/strong> in S phase is damaged or mutated or absent, that again person has an increased risk of accumulating mutations and therefore susceptibility to cancer.\r\n\r\n \r\n

Role of Telomeres and Telomerase in Cancer<\/strong><\/h3>\r\nTelomeres,<\/strong> the end caps of chromosomes, which are maintained through childhood and adolescence through the enzymatic action of telomerase<\/strong> which continues to add telomere to the ends of chromosome.\u00a0 Telomerase is inactivated in adulthood and the telomeres begin to shorten with each cell division, acting as a safety net to limit division.\u00a0 At a certain length, a critical point is reached, and the cell becomes dormant<\/strong> or dies.<\/strong>\u00a0 This telomere shortening helps prevent excessive divisions, reducing the risk of mutations and cancer development.\u00a0 Additionally, at a certain age the cell has likely become less functional or dysfunctional,<\/strong> potentially accumulating waste<\/strong> products or abnormalities<\/strong> and it would become detrimental to the body if it wasn't inactivated or removed.\u00a0 In tissue that is regenerative, old cells can be replaced through the division of tissue-specific stem cells.\u00a0 In cells that die when telomeres reach a certain length, apoptosis<\/strong> is triggered and macrophages engulf and recycle their components.\u00a0 Interestingly it has been found that in 90% of cancers, telomerase has been re-activated in the cancerous cells (which helps them to become immortal - continually adding telomere length and thereby permitting continual cell cycling).","rendered":"

Review of Cell Cycling and DNA duplication<\/strong><\/h3>\n

Cell cycling<\/strong> in humans begins right away, starting with a fertilized egg.\u00a0 Undoubtedly you don’t remember when you were this young, however, your first act as a fertilized egg was to grow larger in size and then get divide from 1 cell into 2 identical cells.\u00a0 This process is termed cell cycling.\u00a0 During cell cycling a cell becomes larger, duplicates its organelles and DNA and then divides into two identical daughter cells.\u00a0 This process of cell duplication is also sometimes called cell division<\/strong>, or cell proliferation<\/strong> or simply mitosis.<\/strong><\/p>\n

The steps of cell cycling are all equally important. The process begins in Interphase and there are three distinct stages within Interphase: G1, S<\/strong> and G2.<\/strong>\u00a0 In G1,<\/strong> the cell is growing in size and is duplicating its organelles.\u00a0 In S phase<\/strong>, DNA duplication occurs and in G2,<\/strong> the cell grows a bit more.\u00a0 After interphase is complete, the cell enters Mitosis.<\/strong>\u00a0 Within mitosis the enlarged cell divides into two cells<\/strong>, with half of its organelles and one set of DNA ending up in each daughter cell.<\/p>\n

Review of Cell Differentiation<\/strong><\/h3>\n

As the fertilized egg grows, and repeatedly goes through cell cycling<\/strong>, a ball of identical cells called a blastocyst is created.\u00a0 At this point in time cells begin to mature and differentiate<\/strong> slightly to form 3 unique cell lineages (endoderm, mesoderm, and ectoderm).\u00a0 Within each of these cell types, cells continue to go through cell cycling and the embryo gets larger and larger in total size.\u00a0 Eventually these cells will become even further differentiated forming lineages for all 200 cell types of the human body (e.g. epithelial cells, cardiomyocytes, hepatocytes, etc.).\u00a0 Organs will form with unique sets of cell types becoming more and more functional.\u00a0 Wtihin each organ and tissue, some daughter cells (termed stem cells<\/strong>) continue to cell cycle, producing more cells, allowing the embryo to get larger, while other daughter cells exit<\/strong> the cell cycle and full mature or differentiate.\u00a0 These fully mature cells can no longer cell cycle and divide, and instead express specific proteins and enzymes to become more and more functional.\u00a0 This process continues through all stages of development from embryo to fetus to newborn to child to teenager.\u00a0 Even as a full-size adult, many tissues contain stem cells that divide in order to allow for the replacement of mature cells that get old and die.\u00a0 However most cells have exited the cell cycle and have fully differentiated to ensure that each organ and tissue is functional.<\/p>\n

 <\/p>\n

Cellular Review of Cellular proliferation and differentiation begin with a fertilized egg.
\nDuring embryogenesis, the fertilized egg undergoes mitosis, leading to cell division.
\nCells differentiate into various types, such as epithelial, connective, muscle, and neural tissue.
\nStem cells undergo mitosis to produce daughter cells, which may differentiate into functional cells.
\nDuring mitosis, organelles double, and DNA duplication occurs during the S phase of the cell cycle.
\nEnzymes check DNA for errors during duplication, triggering apoptosis if mutations are found.
\nTelomeres, end caps of chromosomes, shorten with each cell division, acting as a safety net to limit division.
\nTelomere shortening helps prevent excessive divisions, reducing the risk of mutations and cancer development.
\nApoptosis is triggered if telomeres reach a certain length, preventing further cell division and potential cancerous growth<\/p>\n

 <\/p>\n

\"Control<\/a>
Control of the Cell Cycle<\/figcaption><\/figure>\n

 <\/p>\n

 <\/p>\n

DNA mutations and Cancer<\/strong><\/h3>\n

Unfortunately during S phase, as DNA is duplicated there is a chance for errors<\/strong> in sequencing together the correct strands of nucleotides.\u00a0 \u00a0Luckily there are several enzymes that check the DNA for errors during duplication<\/strong> and will trigger apoptosis<\/strong> if mutations<\/strong> are found that can not be fixed.\u00a0 It is known that mutations that occur in DNA (depending on the location) can cause cancer.<\/strong>\u00a0 It is also known that inevitably DNA errors do occur during duplication just due to the shear number of times DNA is duplicated, not to mention the number of nucleotides within each of the 23 pairs of chromosomes.\u00a0 It may seem obvious that the more DNA duplication events there are, the more risk there is for DNA errors to occur.\u00a0 Therefore a person’s age<\/strong> becomes a risk factor for DNA mutations (and the possibility that these mutations may give rise to cancer).\u00a0 One can also imagine that if any of the enzymes responsible for checking DNA for errors<\/strong> in S phase is damaged or mutated or absent, that again person has an increased risk of accumulating mutations and therefore susceptibility to cancer.<\/p>\n

 <\/p>\n

Role of Telomeres and Telomerase in Cancer<\/strong><\/h3>\n

Telomeres,<\/strong> the end caps of chromosomes, which are maintained through childhood and adolescence through the enzymatic action of telomerase<\/strong> which continues to add telomere to the ends of chromosome.\u00a0 Telomerase is inactivated in adulthood and the telomeres begin to shorten with each cell division, acting as a safety net to limit division.\u00a0 At a certain length, a critical point is reached, and the cell becomes dormant<\/strong> or dies.<\/strong>\u00a0 This telomere shortening helps prevent excessive divisions, reducing the risk of mutations and cancer development.\u00a0 Additionally, at a certain age the cell has likely become less functional or dysfunctional,<\/strong> potentially accumulating waste<\/strong> products or abnormalities<\/strong> and it would become detrimental to the body if it wasn’t inactivated or removed.\u00a0 In tissue that is regenerative, old cells can be replaced through the division of tissue-specific stem cells.\u00a0 In cells that die when telomeres reach a certain length, apoptosis<\/strong> is triggered and macrophages engulf and recycle their components.\u00a0 Interestingly it has been found that in 90% of cancers, telomerase has been re-activated in the cancerous cells (which helps them to become immortal – continually adding telomere length and thereby permitting continual cell cycling).<\/p>\n

Media Attributions<\/h2>