Lung mainly in regulation of cell division, (molecular.,

Lung cancer is a process that involves DNA adaptation
which alters normal cells into malignant cells (Larsen, J., et al., 2011). It
is predominantly acknowledged that molecular mutation in proto-oncogenes or
tumor suppressor genes can result to cancer. Although previous studies have
focused on the diagnosis and treatment of lung cancer, the percentage of survival
(5 years) for patients requires improvement. Lung cancer is one of the dominating
causes of cancer- associated mortality. Because of the poor clinical results, substantial
research into the processes of pathogenesis of this disease is increasing. Due
to advances in technology and scientific research done in the past, researchers
have gain scientific knowledge regarding therapeutic target related to molecular
biology and pathogenesis of lung cancer. Scientists have recognized several matters
that can contribute to tumor progression and cell growth (Pendharkar, D., et
al., 2013). This review highlights some of the significant molecular
configuration of lung cancer, diagnostic, therapeutic target, and its clinical
implications. 

 

 

Types of
lung Cancer

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Lung
cancer is classified into two main types: non-small cell lung cancer (NSCL) and
small cell lung cancer (SCLC) accounting to 85 percent and 15 percent of all
lung cancers, respectively. NSCLC is clustered into three subtypes:
adenocarcinoma, squamous cell carcinoma, and large cell lung carcinoma. It is
the second common cancer in both gender. Mortality rate of lung cancer is
increasing, recurrence rate is high, and  it is usually detected at the late stage. In addition
to that, lung cancer does not show signs and symptoms during the initial stage.

SCLC
develops rapidly and metastasize to other tissues, usually to the liver, brain,
bones and adrenal glands. Survival rate is usually one year after diagnosis of
cancer (American., anon; Larsen, J., et al., 2011; Langevin, S.,).

 

 

Molecular
etiology of lung cancer

 

Lung cancer develops due to multiple chromosomal and
epigenetic adaptations affecting apoptosis and cell proliferation (tumor
suppressor genes and oncogenes). Tumor suppressor genes that are associated in
lung cancer carcinogenesis are also linked with prognosis (Davis, M., et al., 2014).
Tumor suppressor genes are commonly distorted in the early period of lung cancer
(Yunxi, J., et al., 2017).

RAS is directly involved
and function mainly in regulation of cell division, (molecular., anon) and also
the commonly altered proteins. It is the fundamental mediators for signal transduction and cell multiplication,
comprising K-RAS,
H-RAS, and N-RAS. Activation of downstream signaling pathways (PI3K and MAPK-
mitogen-activated protein kinase) would result in mutation. This would cause KRAS altered tumors independent
of EGFR signaling, hence, making it resistant to EGFR TKIs (Larsen, J., et al.,
2011). In order for the RAS to
be activated, it has to bind with guanosine triphophate (GTP). On the other hand, it is deactivated by
GTPase -activating protein (GAP) by breaking down guanosine triphosphate to
guanosine diphosphate (GDP). Alterations at or around the GTP-binding domain of
RAS gene inhibits the deactivation of GTP, thus causing in uninterrupted RAS
activity (Singh, C., et al., 2014).  Mutation occur due to exchange in
position of amino acid 12,13 or 61 (Zappa, C., et al 2016).

HER-2 protein is a growth factor receptor belonging to the tyrosine kinases
group comprising of EGFR/ERBB1, HER2/ERBB2/NEU, HER3/ERBB3, and
HER4/ERBB4.  Insertion in exon 20 leads
to kinase activity and heightened signaling by means of downstream pathways. This mechanism will promote
tumorigenicity and pathogenesis. HER2 alterations
are discovered in approximately 2–4% of NSCLC cases, develop generally in adenocarcinomas
of never smokers females (Roh, M., et al., 2014).