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The Hayflick limit is a concept in biogerontology that a human cell culture in vitro will only divide 48-50 times, on average. It is named after Dr. Leonard Hayflick. The Hayflick limit (or Hayflick phenomenon) is the number of times a normal human cell population will divide until cell division stops. Empirical evidence shows that the telomeres associated with each cell's DNA will get slightly shorter with each new cell division until they shorten to a critical length.

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  • Hayflick limit
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  • The Hayflick limit is a concept in biogerontology that a human cell culture in vitro will only divide 48-50 times, on average. It is named after Dr. Leonard Hayflick. The Hayflick limit (or Hayflick phenomenon) is the number of times a normal human cell population will divide until cell division stops. Empirical evidence shows that the telomeres associated with each cell's DNA will get slightly shorter with each new cell division until they shorten to a critical length.
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abstract
  • The Hayflick limit is a concept in biogerontology that a human cell culture in vitro will only divide 48-50 times, on average. It is named after Dr. Leonard Hayflick. The Hayflick limit (or Hayflick phenomenon) is the number of times a normal human cell population will divide until cell division stops. Empirical evidence shows that the telomeres associated with each cell's DNA will get slightly shorter with each new cell division until they shorten to a critical length. The concept of the Hayflick limit was advanced by American anatomist Leonard Hayflick in 1961, at the Wistar Institute in Philadelphia, Pennsylvania. Hayflick demonstrated that a population of normal human fetal cells in a cell culture will divide between 40 to 60 times. The population will then enter a senescence phase, which refutes the contention by Nobel laureate Alexis Carrel that normal cells are immortal. Each mitosis slightly shortens each of the telomeres on the DNA of the cells. Telomere shortening in humans eventually makes cell division impossible, and this aging of the cell population appears to correlate with the overall physical aging of the human body. This mechanism also appears to prevent genomic instability. Telomere shortening may also prevent the development of cancer in human aged cells by limiting the number of cell divisions. However, shortening of telomeres impairs immune function and thus might also increase susceptibility to cancer.
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