Editing Cell cycle (section)

== Role in tumor formation ==
A disregulation of the cell cycle components may lead to [[tumor]] formation.<ref>{{cite journal | vauthors = Champeris Tsaniras S, Kanellakis N, Symeonidou IE, Nikolopoulou P, Lygerou Z, Taraviras S | title = Licensing of DNA replication, cancer, pluripotency and differentiation: an interlinked world? | journal = Seminars in Cell & Developmental Biology | volume = 30 | pages = 174–180 | date = June 2014 | pmid = 24641889 | doi = 10.1016/j.semcdb.2014.03.013 | doi-access = free }}</ref> As mentioned above, when some genes like the cell cycle inhibitors, [[Retinoblastoma protein|RB]], [[p53]] etc. mutate, they may cause the cell to multiply uncontrollably, forming a tumor. Although the duration of cell cycle in tumor cells is equal to or longer than that of normal cell cycle, the proportion of cells that are in active cell division (versus quiescent cells in G<sub>0</sub> phase) in tumors is much higher than that in normal tissue.<ref name="Baserga_1965">{{cite journal | vauthors = Baserga R | title = The Relationship of the Cell Cycle to Tumor Growth and Control of Cell Division: A Review | journal = Cancer Research | volume = 25 | issue = 5 | pages = 581–595 | date = June 1965 | pmid = 14347544 | doi =  }}</ref> Thus there is a net increase in cell number as the number of cells that die by apoptosis or senescence remains the same.

The cells which are actively undergoing cell cycle are targeted in cancer therapy as the DNA is relatively exposed during cell division and hence susceptible to damage by [[Chemotherapy|drugs]] or [[Radiotherapy|radiation]]. This fact is made use of in cancer treatment; by a process known as [[debulking]], a significant mass of the tumor is removed which pushes a significant number of the remaining tumor cells from G<sub>0</sub> to G<sub>1</sub> phase (due to increased availability of nutrients, oxygen, growth factors etc.). Radiation or chemotherapy following the debulking procedure kills these cells which have newly entered the cell cycle.<ref name="Robbins"/>

The fastest cycling mammalian cells in culture, crypt cells in the intestinal epithelium, have a cycle time as short as 9 to 10 hours. Stem cells in resting mouse skin may have a cycle time of more than 200 hours. Most of this difference is due to the varying length of G<sub>1</sub>, the most variable phase of the cycle. M and S do not vary much.

In general, cells are most radiosensitive in late M and G<sub>2</sub> phases and most resistant in late S phase. For cells with a longer cell cycle time and a significantly long G<sub>1</sub> phase, there is a second peak of resistance late in G<sub>1</sub>. The pattern of resistance and sensitivity correlates with the level of sulfhydryl compounds in the cell. Sulfhydryls are natural substances that protect cells from radiation damage and tend to be at their highest levels in S and at their lowest near mitosis.

[[Homologous recombination]] (HR) is an accurate process for [[DNA repair|repairing DNA]] double-strand breaks.  HR is nearly absent in [[G1 phase]], is most active in [[S phase]], and declines in G<sub>2</sub>/M.<ref name="pmid18769152">{{cite journal | vauthors = Mao Z, Bozzella M, Seluanov A, Gorbunova V | title = DNA repair by nonhomologous end joining and homologous recombination during cell cycle in human cells | journal = Cell Cycle | volume = 7 | issue = 18 | pages = 2902–2906 | date = September 2008 | pmid = 18769152 | pmc = 2754209 | doi = 10.4161/cc.7.18.6679 }}</ref> [[Non-homologous end joining]], a less accurate and more mutagenic process for repairing double strand breaks, is active throughout the cell cycle.