Debate and discussion of any biological questions not pertaining to a particular topic.
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General questions about how cancer affects the cell cycle...
1) Does cancer actually speed up the individual phases of mitosis (prophase, metaphase, anaphase, telophase) ... ie metaphase occurs 100x sooner following prophase in a cancer cell compared to a normal cell? or does cancer just increase the number of times mitosis as a whole is performed?
2) Also, it seems that cyclins and cdks play a great role in cancer cells. From my understanding, the cyclin and/or cdk becomes defective and is used too much, causing mitosis to repeat without stop. Is this correct?
3) If I am correct in (2), is there a specific phase in the cell cycle where these cancer inducing cyclins and cdks are found? Are these cyclins and cdks only found in the interphase? Only in G1? Only in mitosis? Throughout all of interphase and mitosis? Only in G2? etc etc
If cancer affects the cell cycle it will be that it has mutated the proteins that keep it tightly regulated. Whether or not it speeds up the individual cell phases of the cycle I do not know, but if the regulatory proteins are mutated to be permanently activated/"on" then it will proceed thru the cell cycle at optimal speeds, and continuously, without waiting to make sure all the DNA is proper, or the chromatin has segregated appropriately, or whether the cell's external signaling even needs to proceed with its synthesis (uncontrolled cell growth).
Cyclin-CDK complexes are all thru out the mammalian cell cycle:
Mid-G1 cyclin CDKs -
Cyclin D-CDK4, Cyclin D-CDK6
(complexes form in mid G1 phase and peak at the restriction point, then taper off at S phase)
Late-G1 cyclin CDK -
(complexes starts right after the restriction point, peaks at the beginning of S phase, then tapers off at the mid S phase)
S-phase cyclin-CDK -
(begins and ends with the S phase, very distinct)
Mitotic cyclin-CDKs -
Cyclin A-CDK1, Cyclin B-CDK1
(complexes start at the end of S phase, peak during mitosis, and abruptly ends at G1 phase)
All of these complexes are regulated by multiple proteins (i.e. p53 for inhibition, or Cdc25A and APC/C-Cdc20 for activation),that could be sites for mutation that could contribute to cancer.
http://bcs.whfreeman.com/lodish6e/pages ... 000|99000|
2 posts • Page 1 of 1
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