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The Cell Cycle,Cancer !!
THE CELL CYCLE AND CANCER
A disease caused by severe disruption of the mechanisms that
normally controlled the cell cycle.
DIFFERENCE BETWEEN CANCER CELL AND NORMAL
CELL
There are some differences in between cancer cell and the
normal cell. These cells behave differently than normal cell
in the body. Many of these differences are related to cell
division.
1. Cancer cell can multiply in culture without any growth
factor where as normal cells needs growth factor in
culture for multiplication.
2. Normal cell show contact inhibition. Because of this,
they form a single layer on the bottom of a culture
dish. Cancer cells, in contrast, keep dividing and pile
on top of each other in lumpy layers.
3. Normal cells divide poorly if they are floating in
liquid or soft gel, a property called anchorage
dependence. Cancer cells lose anchorage dependence and
grow fine in liquid or gel.
4. Cancer cells are called as “immortal”. They can grow and
divide in culture for long periods of time, years or
even decades. Normal cells only divide a certain number
of times in culture before they stop dividing and
eventually die.
5. Cancer cells are also different from normal cell in ways
that are not directly cell cycle related. This
difference helps them to grow, divide and form
tumors.For instance cancer cells may not undergo
programmed cell death or apoptosis, under conditions
that would trigger this process in normal cell.
6. Cancer cell also gain the ability to migrate from the
initial site of a tumor to other part of the body. This
process is known as metastasis.
CELL CYCLE REGULATORS AND CANCER
Different types of cancer involve different types of mutation
and each individual tumor has a unique genome and set of
genetic alteration. Positive regulators may be over activated
(become oncogenic) while negative regulators, also called
tumor suppressor may be inactivated.
ONCOGENES
Positive regulators that move the cell cycle forward may be
overactive cancer. A growth factor receptor may send signals
even when growth factors are not there, or a cyclin may be
expressed at abnormally high levels. These overactive forms of
genes are called oncogenes and the normal forms of genes are
called as proto oncogenes.
Mutation that turns proto oncogenes into oncogenes can take
variety of different forms. Some change the amino acid
sequence of the protein, altering its shape and trapping it in
an ‘always on’ state. Other involve amplification, in which a
cell acquires extra copies of a gene (errors in DNA
replication or repair).the extra copies of the gene result in
higher levels of protein, which drive increased or
inappropriate cell cycle progression.
Many of the proteins that transmit growth factor signals are
encoded by proto oncogenes. Normally these proteins drive cell
cycle progression only when growth factors are available. In
this simplified growth factor signalling pathway, the growth
factor receptor, the G protein Ras and the signalling enzyme
Raf are encoded by proto oncogenes. This overactive form of
proteins is commonly found in cancer cell.oncogenic Ras
mutations are found in an estimated 90% of pancreatic cancer.
TUMOR SUPPRESSORS
Negative regulators that block cell cycle progression may be
less active in cancer cells.
Tumor suppressor genes are family of normal genes that
instruct cells to produce proteins that restrains cell growth
and division. Sence,tumor suppressor genes code for proteins
that slow down cell growth and division, the loss of such
proteins allows a cell to grow and divide in an uncontrolled
fashion.
One of the most important tumor suppressors is tumor protein
p 53 , which plays a key role in the cellular response to DNA
damage. It acts primarily at the G1 checkpoint, where it blocks
cell cycle progression in response to damaged DNA and other
unfavourable conditions.
When a cell DNA is damaged, a sensor protein activates p53,
which
halts the cell cycle at G1 checkpoint by triggering production
of a protein called Cdk inhibitor. This inhibitor binds to
cyclin Cdk complexes and inactivates them, preventing the cell
from moving into S phase.
53
If the damaged is successfully fixed, p will release the cell
allowing to continue through the cell cycle. If the damage is
not fixable, p53 will play a final role, triggering apoptosis
(programmed cell death) so that damaged DNA is not passed on.
When p53 is defected a cell with damaged DNA may proceed with
cell division rather than pausing the cell cycle, attempting
DNA repairs or undergoing apoptosis. The daughter cells
produced in such a division are likely to inherit mutations
due to the unpaired DNA of the mother cell. Over generation,
cells with faulty p53 tend to rapidly accumulate mutations, some
of which may convert proto oncogenes to oncogenes or inactive
other tumor suppressor and thus lead to the development of
cancer.
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