PTEN “believes” the growth factor is bind though

PTEN genes involves in the
regulation of cell division by controlling cell multiplication in controlled
manner, hence, mutation would result to uncontrolled cell multiplication. Research
established that this enzyme conserves the cell’s genetic information, and
regulates migration, adhesion and angiogenesis (molecular., anon).

EGFR gene feeds directions for producing a small chemical, the epidermal growth factor receptor, which are generated by a cell and
bind to other protein (ligand) on the same cell or outside the cell – like
fitting of a key into locks. The attachment of the ligand to the epidermal
growth receptor will create a chemical reaction inside the cell. This will
trigger activation of signal pathways promoting controlled cell growth and
proliferation. In cancer, the mutated gene “believes” the growth factor is bind
though it is actually not attached. As a result, the tumor cell proliferates
uncontrollably. F (Kobayashi, K., et al., 2013). Alteration usually happen in
exon 18-21, but 90% of deletion and point alteration take place in exon 19 and
L858R, respectively (Zappa, C., et al 2016).

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P53 regulates cell cycle, initiates apoptosis and preserve genome integrity,
also works as a master growth regulatory switch (Singh, C., et al., 2014). Alterations mainly suggest G to T substitution caused by bulky DNA adducts
(Massion, P., et al., 2003). P53 gene will affect tumor-suppression functioning resulting to uncontrolled cellular
proliferation. P53 was the
frequently mutated protein in lung cancer in both SCLCs and NSCLCs, approximately 100 % and 90 %, respectively. P53 genes has the capacity to
transform by binding with normal P53 and then inactivate itself (Singh, C., et
al., 2014; Larsen, J., et al., 2011).

Anaplastic Lymphoma Kinase (ALK) is a growth factor receptor that can be seen in cancer cells.
Generally, it can be found in adult’s brain tissue and researched has
established that it is vital receptor in fetal development. In the course of
cell mutation, intron 10 will merge with intron 13 and “turn it on” resulting
in cancer multiplication (Roh, M. 2014; Eldridge, L. 2017).

BRAF
is a serine/ threonine kinase molecular pathway that is responsible for the
regulation of cell multiplication. It can be found on the upper part of the MEK
and ERK signalling cascade. BRAF mutation will stimulate MEK and ERK
resulting to cancer cell activation. (Guanghui, C., et al.,).

FGFR1 is one of the commonest amplified genetic
factor in human malignancies. No recognized targeted therapeutic agents for
SQCs. Research suggest that FGFR
inhibitors will result to considerable tumor reduction in size, therefore, it could possibly be an advantageous
therapeutic option in FGFR1 amplification (Okimoto, R., et al., 2014).

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