Creative Bioarray

The Complete Guide to

Know The Relationship
Between Telomerase and
Tumor

contact@creative-bioarray.com
 e
gu
lo Brief Introduction
ta
Ca

Specific Information Related

to Tumor Production

How will cells control their

multiplication multiples

Conclusion
1 Brief Introduction
About Tumor Cells

Tumor is a kind of disease that faces various difficulties for

treating because our immune system can not recognize it,
and the tumor cell is a permanently dividing cell. Telomerase
is essential for the immortalization of tumor cells so that it
can serve as a good target for antineoplastic agents. If there
are drugs which are able to turn off telomerase in tumor
cells, the length of telomeres will gradually decrease as
tumor cells divide, mutations will occur and tumor cells will
become unstable. Experimental drug treatments have been
performed in mice, while some drugs entering the early
clinical trial phase.
More Specific Info on Tumor Cells
In normal human cells, telomere
shortening limits the grow ability of
cells, telomerase re-expression
plays an important role in cell
immortalization and carcinogenesis.
In determining telomerase
Therefore, some researchers think activity, it was found that more This situation has important
that cells with normal expression of than 90% of normal tissue cells clinical value for telomerase
telomerase activity will be easier to were negative for telomerase, activation, diagnosis and
turn into tumor cells. associating this enzyme with suppression.
the immortalization of the cells
and the tumor.
2 Information Related to
Tumor Production
Specific Information Related to
Tumor Production
30 trillion normal human cells make up a complex
and interdependent environment of common
management, mutual regulation. A cell proliferates
only when it receives growth stimulating signals
from other nearby cells and stops growing when it
receives an inhibitory signal.

This interaction allows each tissue to

maintain a certain size and shape to
suit the needs of the body.
 c er c ells,
a s t , c an
t r als
In con nore sign
ig trol
which rmally con llo w
t n o l y f o
th a
ra t i o n, o n
e ins ic
prolif i n t r
wn ia.
their o ation criter
er
prolif

They can e
ven move in
invade neig and
hboring tis
to such ma sues. Due
lignant tum
invade mor or cells
e and more
they will ca tis
use the dea sues,
body when th of
they interfe
the organs re with
and tissues
needs for s the body
ur vival.
 Some proto-
oncogene mutations
will interfere with
part of the signal
pathway in cells,
such as Ras protein,

Many of the proto-

oncogenes normally
function to transmit outside
stimuli to cells. When a
protooncogene mutation
affects an important growth
so that in vivo genes
stimulating signal, it will are also activated in
activate the silenced gene. the absence of
signals from outside
growth stimuli.
Inhibition of the external
In addition, the A large part of the tumor
signal is also can not be
cell cycle of cells in the p53 gene is
introduced into the cells
cancer cells is also missing or loss of function,
due to the signal
disturbed. which will lead p21 protein
cascade interference.
loses its ability to inhibit
the cyclin, CDK5 and their
complexes, thereby leaving
the cell cycle unrestricted.
Two methods tissues involved to control
cell proliferation and avoid cancer

cell apoptosis when important

components in the cell ar e
damaged or the control system
is dysregulated

the limit of cell multiplication.

3 How will cells control their
multiplication multiples
multiples?
Telomeres at the end of the chromosome act
If the cells have not undergone aging, a
as counters and start senescence and crisis
further shortening will eventually lead to a
at some point. The telomeres become
crisis, that is, telomeres that is too short will
slightly shorter in each S phase after
lead to chromosome fusion or break, causing
proliferation. While the length is less than a
fatal blow to the cells, thereby limiting cell
certain threshold, they will initiate the cell
proliferation.
into senescence mode.
4 Conclusion
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