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 In regards to figure1, there were higher levels of EGFR detected in TNBC cells in comparison to nonTNBC cell line MCF- 7, thus no express EGFR is shown.

With regards tophosphorylated 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 468and SUM 1315 cell lines. In TNBC cell line a high quantity of phosphorylatedAKT 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 toMCF 7 cells.  Antibodies such as MDA-MB-468 and SUM-1315 cell lines bothinhibited proliferation after 20 to 30 % in comparison to untreated cells, thusno effect is shown in MDA-MB-231 and HCC-1937 cell lines. An antibodyconcentration of 10 ?g/mL is shown to be used to achieve a growth inhibitory asit stayed stable for higher concentration. The figure shows a mechanism ofresistance to anti-EGFR mAbs as MDA-MB-231 and HCC-1937 cell lines appeared.  Figure2  Figure 2 demonstrates a dose independent manner from one EGFR-TKIsas it inhibited proliferation.

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Gefitinib and erlotinib was more active onMDA-MBA-468 as it shows differential effect on figure 2. Furthermore figure 2shows the IC50 was not achieved as SUM-1315 cells was quite sensitive toerlotinib.    Table 1: shows monoclonal antibodies with combination of antiEGFR and single agent of erlotinib and gefitinib of its IC50 value  Table 1 shows the summery of gefitinib anderlotinib as one agent in amalgamation with centuximab and panitumumab of thehalf inhibitory concentration value.

  Table1 also shows MDA-MB-468 cell line of cetuximab ominously increased the effectof cytotoxicity of gefitinib and erlotinib ranging from concentration of 1 to20 ?M.Alternatively the table shows there is an increase of growth inhibitory in allconcentration which is an effect of EGFR-TKIs, thus this was caused due toSUM-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 aftercetuximab and panitumumab treatment phosphorylated ERK1/2 was down controlledby 2.5 fold and 5 fold. According to figure 3,EGFR-TKI reduced the phosphorylation of ERK1/2 to 10 fold in comparison tountreated cells. Furthermore the phosphorylation of ERK1/2 is lesseffective than erlotinib due to the courses of mAbs and gefitinib blocked it inSUM-1315 cell line.  Compared tountreated cells ERK1/2 was decreased by 2 fold and 10 fold by gefitinib anderlotinib. The ERK1/2 phosphorylation is suppressed due to the combination ofpanitumumab or cetuximab.

  The activationstatus of RAS/MAPK pathway in regards to its effectiveness was associated toanti-EGFR therapies seen on the cell viability. Alternatively the resultspropose inhibiting EGFR phosphorylation and decreasing ERK1/2 activity respondto TNBS cell lines to anti EGFR-targeted therapies. In regards to figure 4 and figure 5 thecell cycle distribution was not effected by mAbs and neither did it effect HC1937 cell line and the apoptotic cells in MDA-MB-231. However ananti-proliferation effect was present as it shown in the result, thus in part, oninduction of cell cycle arrest at G1 phase and apoptosis.

 3.0 DiscussionCetuximab or panitumumab is not linkedwith tumour expression of EGFR according to previous studies on mCRC thatshowed the likelihood response. (Reference tumors 35–37).

Thecell cycle and the apoptotic profile after treatment was consistent due to theanti EGFR therapies on TNBC cell of growth inhibitory. Compared to other treatments, gefitinib possessed agreater inhibitory effect on cell cyle, thus including greater levels ofapoptosis. Alternatively according to the results obtained it suggest that acombination of gefitinib and anti-EGFR mAbs should be considered a suitablemethod for the dual targeting of EGFR in TBC. (Reference)  The level of phosphorylated ERK1/2was reduced due to most treatments reducing the activity of EGFR in the cellline.

However ERK1/2 inactivation is the main aspect of predicting response toEGFR inhibitors. (Reference) The downstream of signaling ofpathways of EGFR was investigated byBaselga, et al. thus suggested that anti- EGFR drug after treatment must serveas a marker of drug response due to the down regulated activity of ERK1/2. (Reference 19, 52). Without a doubt, inregards to the result, mAbs and EGFR-TKIs did not bring visible changes inphosphorylated-AKT levels in all cell lines tested.

 Theresults are in acquiescent with prior reports which showed the inhibition of reductionof ERK1/2 from EGFR tyrosine kinase, but does not show no phosphorylation AKTbreast cancer patients with tumour. (Reference19). Cell prevention of apoptosis and promotion of proliferation can be detectedby signaling pathways such as RAS/MAPK, according to (53)   According to several of other researchusing variety of breast cancer cells, (reference58) suggested that CDK2 is linked with reduction of cell viability aftertreatment of erlotinib. Thus the author discovered that by expressing erlotinibin EGFR and blocking CDK2 activity caused an increase of sensitivity in TNBCcell line (reference 58)

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