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.

1. The Complete Guide to
Know The Relationship
Between Telomerase and
Tumor
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2. Catalogue
Conclusion
How will cells control their
multiplication multiples
Specific Information Related
to Tumor Production
Brief Introduction

3. Brief Introduction
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4. 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.

5. More Specific Info on Tumor Cells
In determining telomerase
activity, it was found that more
than 90% of normal tissue cells
were negative for telomerase,
associating this enzyme with
the immortalization of the cells
and the tumor.
Therefore, some researchers think
that cells with normal expression of
telomerase activity will be easier to
turn into tumor cells.
This situation has important
clinical value for telomerase
activation, diagnosis and
suppression.
In normal human cells, telomere
shortening limits the grow ability of
cells, telomerase re-expression
plays an important role in cell
immortalization and carcinogenesis.

6. Information Related to
Tumor Production
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7. 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.

8. In contrast, cancer cells,
which ignore signals
that normally control
proliferation, only follow
their own intrinsic
proliferation criteria.
They can even move in andinvade neighboring tissues. Dueto such malignant tumor cellsinvade more and more tissues,they will cause the death ofbody when they interfere withthe organs and tissues the bodyneeds for survival.

9. Many of the proto-
oncogenes normally
function to transmit outside
stimuli to cells. When a
protooncogene mutation
affects an important growth
stimulating signal, it will
activate the silenced gene.
Some proto-
oncogene mutations
will interfere with
part of the signal
pathway in cells,
such as Ras protein,
so that in vivo genes
are also activated in
the absence of
signals from outside
growth stimuli.

10. A large part of the tumor
cells in the p53 gene is
missing or loss of function,
which will lead p21 protein
loses its ability to inhibit
the cyclin, CDK5 and their
complexes, thereby leaving
the cell cycle unrestricted.
Inhibition of the external
signal is also can not be
introduced into the cells
due to the signal
cascade interference.
In addition, the
cell cycle of
cancer cells is also
disturbed.

11. Two methods tissues involved to control
cell proliferation and avoid cancer
cell apoptosis when important
components in the cell are
damaged or the control system
is dysregulated
the limit of cell multiplication.

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

14. Conclusion
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