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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 Production2

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 and invadeneighboring tissues. Due to suchmalignant tumor cells invademore and more tissues, they willcause the death of body whenthey interfere with the organs andtissues the body needs forsurvival.

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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16. Email: contact@creative-bioarray.com
Phone: 631-619-7922
URL: http://www.creative-bioarray.com/