In mAbs extremely increasing the growth inhibitory. Panitumumab

 In
regards to figure 1, there were higher levels of EGFR detected 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 observed due to the highest and lowest levels in
MDA MB 468 and SUM 1315 cell lines. In TNBC cell line a high quantity of
phosphorylated AKT and phosphorylated ERK1/2 show an increase compared to MCF 7
cells. Distinctively AKT and ERK1/2 expression shows a low TNBC cell line
compared to MCF 7 cellsAntibodies
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 stay stable for higher
concentration. The figure shows a mechanism of resistance to anti-EGFR
mAbs as MDA-MB-231 and HCC-1937 cell lines appeared. Figure 2 demonstrates a
dose independent manner from one EGFR-TKIs as it inhibited proliferation. Gefitinib
and erlotinib was more active on MDA-MBA-468 as it shows differential effect on
figure 2. Furthermore figure 2 shows the IC50 was not achieved as SUM-1315
cells was quite sensitive to erlotinibTable
1 shows the summery of gefitinib and erlotinib as one agent in amalgamation
with centuximab and panitumumab of the half inhibitory concentration
value.  Table 1 also shows MDA-MB-468
cell line of cetuximab ominously increased the effect of cytotoxicity of
gefitinib and erlotinib ranging from concentration of 1 to 20 ?M. Alternatively the table shows there is an increase of
growth inhibitory in all concentration which is an effect of EGFR-TKIs, thus
this was caused due to SUM-1315 cell line and mAbs extremely increasing the
growth inhibitory. Panitumumab ominously increased the effect of gefitinib (5.9)
and erlotinib (1.7) at all concentrations, thus similar values also shows with
cetuximab. Figure
3: In regards to MDA-MB-468 cells after cetuximab and panitumumab treatment
phosphorylated ERK1/2 was down controlled by 2.5 fold and 5 fold. According to figure 3, EGFR-TKI reduced the
phosphorylation of ERK1/2 to 10 fold in comparison to untreated cells.
Furthermore the phosphorylation of ERK1/2 is less effective than erlotinib due
to the courses of mAbs and gefitinib blocked it in SUM-1315 cell line.  Compared to untreated cells ERK1/2 was
decreased by 2 fold and 10 fold 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 to anti-EGFR
therapies seen on the cell viability. Alternatively
the results propose inhibiting EGFR phosphorylation and decreasing ERK1/2
activity respond to TNBS cell lines to anti EGFR-targeted therapies. 

In regards to figure 4 and figure 5 the cell
cycle distribution was not effected 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 it shown in the result, thus in part, on induction of
cell cycle arrest at G1 phase and apoptosis.Cetuximab
or panitumumab is not linked with tumour 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. Compared to
other treatments, gefitinib possessed a greater inhibitory effect on cell cyle,
thus including greater levels of apoptosis. Alternatively according to the
results obtained it suggest that a combination of gefitinib and anti-EGFR mAbs
should be considered an 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 main
aspect of predicting response to EGFR inhibitors. (Reference) 

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The
downstream of signaling of pathways of EGFR was investigated by Baselga, 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.