In phosphorylated ERK1/2, thus demonstrated an increase in

In regards to figure 1, there were advanced
levels of EGFR distinguished in TNBC cells in comparison to non-TNBC cell line
MCF- 7, thus no express EGFR is shown. With regards to phosphorylated EGFR,
there is an increase of level only due to TNBC cell line. EGFR expression was
detected due to the highest and lowest levels in MDA MB 468 and SUM 1315 cell
lines. In TNBC cell line has a high amount of phosphorylated AKT and
phosphorylated ERK1/2, thus demonstrated an increase in comparison to MCF 7
cells. Distinctively AKT and ERK1/2 expression show a low TNBC cell line
compared to MCF 7 cells.


 Antibodies such as
MDA-MB-468 and SUM-1315 cell lines both inhibited proliferation after 20 to 30
% in comparison to untreated cells; thus no effect is shown in MDA-MB-231 and
HCC-1937 cell lines. An antibody concentration of 10 ?g/mL is shown to be used
to achieve a growth inhibitory as it stayed stable for higher density. The
figure shows a mechanism of resistance to anti-EGFR mAbs as MDA-MB-231, and
HCC-1937 cell lines appeared.

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Figure 2 demonstrates a dose-independent
manner from one EGFR-TKIs as it inhibited proliferation. Gefitinib and
erlotinib were more active on MDA-MBA-468 as it shows the differential effect
on figure 2. Furthermore, figure 2 shows the IC50 was not achieved as SUM-1315
cells were quite sensitive to erlotinib.











Table 1: shows monoclonal antibodies with combination of anti-EGFR and
single agent of erlotinib and gefitinib of its IC50 value 


Table 1 shows the summery of gefitinib and
erlotinib as one agent in amalgamation with cetuximab and panitumumab of the
half inhibitory concentration value. 
Table 1 also indicates MDA-MB-468 cell line of cetuximab ominously
increased the effect of cytotoxicity of gefitinib and erlotinib ranging from a
concentration of 1 to 20 ?M. Alternatively, the table shows there is an
increase of growth inhibitory in all level which is an effect of EGFR-TKIs;
thus this was caused due to SUM-1315 cell line and mAbs remarkably increasing
the growth inhibitory. Panitumumab ominously enhanced the effect of gefitinib
(5.9) and erlotinib (1.7) at all concentrations; thus similar values also show
with cetuximab.


3: In regards to
MDA-MB-468 cells after cetuximab and panitumumab treatment phosphorylated 2.5
fold down controlled ERK1/2 and five-fold, with regards to figure 3, EGFR-TKI
decreased the phosphorylation of ERK1/2 to 10 fold in comparison to untreated
cells. Furthermore, the phosphorylation of ERK1/2 is less efficient than
erlotinib due to the courses of mAbs and gefitinib blocked it in
the SUM-1315 cell line.  Compared to
untreated cells ERK1/2 was decreased by twofold and tenfold by gefitinib and
erlotinib. The ERK1/2 phosphorylation is suppressed due to the combination of
panitumumab or cetuximab.  The activation
status of RAS/MAPK pathway in regards to its effectiveness was associated with
anti-EGFR therapies seen on the cell viability. Alternatively, the results
propose inhibiting EGFR phosphorylation and reducing ERK1/2 activity respond to
TNBS cell lines to anti EGFR-targeted therapies.

In regards to figuring 4 and figure 5 the cell cycle
distribution was not affected by mAbs and neither did it effect HC 1937 cell
line and the apoptotic cells in MDA-MB-231. However, an anti-proliferation
effect was present as is shown in the result, thus in part, on induction of cell
cycle arrest at G1 phase and apoptosis.


3.0 Discussion

Cetuximab or panitumumab is not linked
with tumor expression of EGFR according to previous studies on mCRC that showed
the likelihood response. (Reference tumors
35–37). The cell cycle and the apoptotic profile
after treatment was consistent due to the anti EGFR therapies on TNBC cell of
growth inhibitory.


to other treatments, gefitinib possessed a more significant inhibitory effect
on cell cycle, thus including more significant levels of apoptosis. Alternatively
according to the results obtained it suggest that a combination of gefitinib
and anti-EGFR mAbs should be considered a suitable method for the dual
targeting of EGFR in TBC. (Reference)


The level of phosphorylated ERK1/2
was reduced due to most treatments reducing the activity of EGFR in the cell
line. However ERK1/2 inactivation is the central aspect of predicting response
to EGFR inhibitors. (Reference)


Baselga, et al
investigated the downstream of signaling of pathways of EGFR, et al. thus
suggested that anti- EGFR drug after treatment must serve as a marker of drug
response due to the down-regulated activity of ERK1/2. (Reference 19, 52).
Without a doubt, in regards to the result, mAbs and EGFR-TKIs did not bring
visible changes in phosphorylated-AKT levels in all cell lines tested.


The results are in acquiescent with
prior reports which showed the inhibition of reduction of ERK1/2 from EGFR
tyrosine kinase but show no phosphorylation AKT breast cancer patients with a
(Reference 19). Cell prevention of apoptosis and promotion of
proliferation can be detected by signaling pathways such as RAS/MAPK, according


According to several of other
research using a variety of breast cancer cells, (reference 58) suggested
that CDK2 is linked with reduction of cell viability after treatment of
erlotinib. Thus the author discovered that by expressing erlotinib in EGFR and
blocking CDK2 activity caused an increase of sensitivity in TNBC cell line (reference



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