Targeted Therapy for Non-Small Cell Lung Cancer: Mechanisms of Resistance

This article discusses targeted therapy for non-small cell lung cancer, including the use of epidermal growth factor receptor inhibitors and their side effects. It also explores the mechanisms of resistance to targeted therapy.

Target therapy

Table of Contents
TITLE..............................................................................................................................................1
EXPLANATION.............................................................................................................................1
REFERENCES................................................................................................................................2

TITLE
“Target therapy for the non-small lung cancer and their mechanism that develop resistance”
EXPLANATION
The targeted therapy is defined as the treatment which is drive with the cancer specific gene,
proteins or the tissue environment which help to contribute the cancer growth and survival. The
treatment is helpful to inhibit the growth and spread of cancer cell and limit the damage to
healthy cells (Jünger and et. al., 2021). In this, some of the lung cancer, abnormal protein which
is found unusual large amount of cancer cell. It helps the doctor to check each patient with their
effective way towards the treatment. The target therapy for the NSCLC is epidermal growth
factor receptor inhibitor (Phallen and et. al., 2019). It is found that the mechanism of EGFR
inhibitor is that they block EGFR which may be effective for the preventing the growth of lung
cancer when the cancer cell has EGFR mutation. The medication is based on the oral
administration. The side effect which is evaluated of EGFR usually include acne and diarrhoea
(Aggarwal and et. al., 2019).
The epidermal growth factor of receptor show the family of receptor named tyrosine
including EGFR, HER2/erbB2 and the HER3/erbB3 that is a target for the antitumor strategies.
Moreover, the enhance EGFR used to copy the number which is associated with the improved
survival in the non-small cell cancer patient (Karachaliou and et. al., 2018). The raise in the
expression of mutant and wild type EGFR molecule have molecular determinant towards the
gefitinib. In this, the relation between EGFR phosphorylation and the sensitivity of drug in the
cell of cancer. The discussion of antiangiogenic effect of gefitinib in relation with EGFR
activation and the phosphatidylinositol 3 kinase/Akt activation in vascular endothelial cells
(Bradley and et. al., 2020).
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REFERENCES
Books and Journals
Aggarwal and et. al., 2019. Clinical implications of plasma-based genotyping with the delivery
of personalized therapy in metastatic non–small cell lung cancer. JAMA oncology, 5(2),
pp.173-180.
Bradley and et. al., 2020. Long-term results of NRG oncology RTOG 0617: standard-versus
high-dose chemoradiotherapy with or without cetuximab for unresectable stage III non–
small-cell lung cancer. Journal of Clinical Oncology, 38(7), p.706.
Jünger and et. al., 2021. Fully Automated MR Detection and Segmentation of Brain Metastases
in Non‐small Cell Lung Cancer Using Deep Learning. Journal of Magnetic Resonance
Imaging.
Karachaliou and et. al., 2018. Interferon gamma, an important marker of response to immune
checkpoint blockade in non-small cell lung cancer and melanoma patients. Therapeutic
advances in medical oncology, 10, p.1758834017749748.
Phallen and et. al., 2019. Early noninvasive detection of response to targeted therapy in non–
small cell lung cancer. Cancer research, 79(6), pp.1204-1213.
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