LWBK1006-02 LWW-Govindan-Review November 24, 2011 11:18
Chapter 2•Molecular Biology of Cancer Part 2 25ANSWERS
Answer 2.1. The answer is C.
Mitosis is divided into prophase, prometaphase, metaphase, anaphase,
and telophase. Most of the internal membranous components of the cell
are dissembled and dispersed in prophase. Prometaphase prepares the
cell for metaphase by forming bivalent attachments to the spindle driving
them to the cellular equator. Paired chromatids align along the spindle
during metaphase, followed by anaphase where sister chromatids pull to
opposite poles. During telophase, prophase is reversed. Mitosis is com-
pleted by daughter cells separating during cytokinesis.Answer 2.2. The answer is B.
Cyclins are the required positive regulatory subunits of CDKs. B-type
cyclins, along with CDK1, are responsible for getting cells into and
through mitosis. Cyclin B1 accumulates during S and G2 phase and then
is degraded at the metaphase–anaphase transition.Answer 2.3. The answer is A.
After phosphorylation of the T loop, there is an increase in CDK-cyclin
contacts and changes in the binding site. Proteins from the INK4 (p15,
p16, p18, and p19), Cip/Kip (p21Cip1, p27Kip1, and p57Kip2), and Rb
(p107 and p130) families all act as inhibitors of CDKs. Function of CDKs
is dependent on cellular availability of cyclins for them to have enzymatic
activity. Last, nuclear import/export regulation further regulates the activ-
ity of CDKs.Answer 2.4. The answer is B.
Accumulation of cyclins E and A via transcriptional induction and inter-
action with CDK2 allows for entry into S phase from G1 and is regulated
by proteins from the Cip/Kip family. Cyclin B-CDK1 similarly accumu-
lates allowing for the transition into M phase from G2. Entry into M
phase is signaled by the dephosphorylation of T15 and Y15 resulting in
the activation of CDK1. Activation of CDK1 and binding of CDC20 to
APC/C is the trigger for which sister chromatids separate and move to
opposite poles during anaphase.Answer 2.5. The answer is D.
Positive cell-cycle machinery is dismantled after the reduction of CDKs
and cyclins. Cell-cycle exit is also usually associated with a transient
increase in the number of CDK inhibitors, such as those from the INK4,
Cip/Kip, and Rb protein families. Cells in quiescence also have a reduced
rate of protein synthesis. Protein synthesis is largely dependent on growth
factors and mitogens activating the cell through the mitogen-activated
protein kinase/extracellular signaling-regulated kinase pathway and the
phosphoinositide 3 (PI3) kinase/AKT pathway.