Table 1 Genomic alterations in NSCLC

EGFR (Epidermal growth factor receptor)

7p11.2

Mutation

EGFR is a cell signaling, transmembrane protein intimately implicated in cell proliferation.

The occurrence is maximum in females and non-smokers, with LUAD histology, 90% of patients in LUAD.

miR-128b, miR-545-3p, and miR-494-3p

[15,16,17]

ALK (Anaplastic lymphoma kinase)

2p23.2-p23.1

Rearrangement

Gene productions are recognized to increase cell growth/proliferation and suppress apoptosis at baseline.

It was detected in 5–7% of NSCLC, mostly in never-smokers and approximately exclusively in LUAD.

miR-100-5p, and miR-200 C

[18, 19]

ROS1

6q22.1

Rearrangement

This gene increases proliferation and suppresses apoptosis.

It was detected in tumors, which are 1–2% of all NSCLCs. It preferentially impacts young persons, never-smokers with LUAD.

miR-760

[20]

KRAS

12p12.1

Mutations

The proto-oncogene generated was initially found to be a GTPase p21.

About 25% of smokers related to LUAD.

miR-181a-5p, miR-199b, miR-29b, let-7, and miR-21

[21,22,23,24]

RET

10q11.21

Rearrangement

A tyrosine kinase responds to growth factors and increases cell proliferation.

In 1–2% of lung LUAD.

miR-182

[25]

BRAF

7q34

Mutation

BRAF is a member of the Raf kinases, which modulate the

MAP kinase pathway.

BRAF mutations are identified in 1–4% of LUAD.

miR-21, and miR-130a-3p

[26, 27]

FGFR-1 (Fibroblast growth factor receptor-1)

8p11.23

Amplification

Have function in cell proliferation

Found in about 15–20% of LUSCs, and amplification is related to smoking and with worse overall survival.

Hsa-miR-16-1, miR‑497, and miR-214-3p

[28,29,30]

MET

7q31.2

Amplification

Encodes a protein production named the HGF receptor (HGFR) and its role in promoting tumor growth, development, and invasion in many cancers.

MET amplification is identified in 2–4% of untreated NSCLC.

miR-34a/c-5p, miR-449a/b, miR-206. and miR-182

[31,32,33]

DDR2 (Discoidin death receptor 2)

1q23.3

Mutation

Tyrosine kinase action and mutation of this gene in NSCLC are implicated in increased cell migration, development, and survival.

In 2.2–3.8% of LUSC smokers, in LUAD and LUSC patients, had one single type of KRAS mutation.

miR-30c, and miR-15a-5p

[34, 35]

PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)

3q26.32

Mutation

Lipid kinases are involved in the modulation of cell growth, development, and survival.

Occurs in less than 5% of NSCLCs.

miR-124-3p, miR-142-5p, and miR-183-5

[36,37,38]

AKT1 (AKT serine/threonine kinase 1)

14q32.33

Mutation

Proliferation, survival, migration, and invasion.

Great rates of intra-tumoral AKT2 in NSCLC and AKT1 in LUAD.

miR-99a, miR-9500, and miR-548 L

[39,40,41]

PTEN (phosphatase and tensin homolog)

10q23.31

Mutations

The tumor suppressor gene is an essential function in cell cycle development, apoptosis, growth, proliferation, and migration.

This gene protein expression is relatively usual in LUSC.

miR-10a, miR-21, and miR-20a

[42,43,44]