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Sunday, March 24, 2013

Aging and Cancer cells vs. Stem cells


On pgs 183-189, Dr. Moalem explains how humans have genetic controls for aging. Cells have evolved to reproduce under a limit. Cells start to die off after reaching this limit and aging starts to take its toll. Cancer, on the other hand, involves cells that avoid this reproducing limit and become immortal cells. This relates to Big Idea 1: The process of evolution drives the diversity and unity of life.

The Hayflick limit is an example of an aging mechanism used by cells.
Using pgs 183-189, define the Hayflick limit explain how normal cells have evolved in relation to aging. Cancer cells on the other hand, are able seemingly able to reproduce infinitely with the use of telomerase. Using information from earlier units and pgs 183-189, explain how telomerase helps avoid this evolutionary reproduction limit, and why cancer cells are deadly. Finally, stem cells, like cancer cells, use telomerase to become immortal. Using pgs 188-189 and further research online, explain why stem cells can be beneficial despite the fact that they reproduce outside the Hayflick limit.

Submitted by Weilly Tong (wtong4@students.d125.org)

2 comments:

  1. The Hayflick limit allows cells to "only divide a fixed number of times before they up and quit... In humans the limit is around fifty-two to sixty" (185). After a normal cell has divided to a number around the Hayflick limit, the cell is programmed to undergo apoptosis, cell death, due to the shortening of its telomere region.

    Shortening of telomeres occurs in mitosis. During mitosis, genetic material is duplicated using DNA polymerases. At the very ends of the lagging strand, DNA polymerase is unable to duplicate a small section at very end of the telomeres, resulting in the next generation being slightly shorter.

    With Big Idea 1 (The process of evolution drives the diversity and unity of life), we can see that the Hayflick limit, which is a factor that contributes to aging, stayed with eukaryotes despite being damaging in the long run. This is because in the short run, it allowed the organism to survive long enough to reproduce. Otherwise, it's much more likely that an organism would contract cancer and have it spread quickly, which lowers the reproductive fitness of that organism. As Dr. Moalem says on page 189, "The flip side to the Hayflick limit, of course--compromise, compromise--is aging."

    In cancer cells, telomerase allows them to bypass the Hayflick limit. Telomerase results from a mutation that activates them in cancerous cells. It lengthens the telomeric region of the cancer cells, preventing the shortening that leads to apoptosis and making the cancer cell almost immortal. Cancer cells that can divide themselves indefinitely become very deadly to the organism.

    However, stem cells use "telomerase to fix their telomeres the same way that some cancer cells do" (188-189). They are beneficial, unlike cancer cells, because they are undifferentiated. "They have the potential to become anything and they never run out of steam" (189). With further advances, researchers will be able to grow them in vitro and give them the right chemical signals to have them differentiate into the desired cells, such as cells that make up organs for organ transplantation. This was something that Sam Rhine touched upon in his Genetic Update Conference. Stem cells hold great potential for their future medical uses.

    Austin Hua (auhua4@students.d125.org)

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  2. According to pages 183-189, the Hayflick limit is a concept that states the existence of a “limit on cellular reproduction” upon which cells “up and quit” dividing (Moalem 185). This limit is around 52-60 and Moalem states that many scientists “believe cancer prevention is the ‘reason’ cells have evolved with a limit on the number of times they can reproduce” (Moalem 189). From an evolutionary standpoint, the short term prevention of cancer has benefit that outweigh the long term effects of aging that are the flipside to the Hayflick limit.
    Normal cells have evolved to be related to telomeres, which dictate the lifespan of a normal cell. As we have discussed in Unit 4 this year, telomeres protect the ends of chromosomes from degradation. Since after each cell division the DNA strand gets shorter and shorter, eventually the telomeres will degrade completely and DNA will be damaged, causing apoptosis, or cell death, as Austin mentioned. Telomerase helps avoid this evolutionary reproduction limit by lengthening the telomeres at the ends of chromosomes generally specifically to cancerous cells, so they can reproduce indefinitely. This is extremely life-threatening because scientists are finding it very hard to control the rapid cell division of cancerous cells making cancer a huge threat to the global population, relating to Big Idea 1:The process of evolution drives the diversity and unity of life (however in this case in a very negative manner). The do this by adding TTAGGG repeats to the telomere end (3’), creating an “immortal cell”, only found in stem cells and cancer cells.
    Stem cells can be beneficial despite the fact that they reproduce outside the Hayflick limit because they are self cells, therefore the barriers of the immune system won’t attack them as foreign. Currently stem cells are being used for stem cell transplants after high doses of chemo and radiation therapy to kill cancerous cells, in order to foster growth of new, healthy cells. Mini allogeinic transplants are also beneficial to older patients because stem cells provide new blood cells that their body systems couldn’t otherwise produce enough of.

    http://www.cancer.org/treatment/treatmentsandsideeffects/treatmenttypes/bonemarrowandperipheralbloodstemcelltransplant/stem-cell-transplant-types-of-transplant

    (Stephanie Li steli4@students.d125.org)

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