**Author details**

*Oncogenes and Carcinogenesis*

type and mutant groups [8].

**3.3 Lung cancer**

drugs like glucagon-like peptide-1 (GLP-1) agonists, such as exenatide; dipeptidylpeptidase-4 inhibitors (DPP-4), such as sitagliptin; calcium channel blockers such as nifedipine, nicardipine, and diltiazem] can also contribute to the highly increasing incidence of PC throughout the world. On the other hand, gall stones, diabetes, and obesity are the major pathological factors associated with PC [27–29]. In a study by Slebos et al., mutations in KRAS codon 12 were found in 75% of the PC patients. However, there were no differences in blood PCB levels between the KRAS wild-

Lung cancer is the primary cause of cancer-related deaths worldwide. Active and passive smoking are the two of primary causes of lung cancer. Lung cancers are classified as small cell (non-epithelial) or non-small cell carcinomas (epithelialderived). Small cell carcinomas are highly malignant; has the ability to metastasize easily and chemotherapy is the choice of treatment. However, treatment of nonsmall cell cancer primarily involves surgical excision, supplemented by radiation or chemotherapy. Although this treatment method may provide partial or full recovery, it also increases the risk for concurrent diseases. Using anti-cancer drugs with

KRAS gene mutations are observed in 15–25% of all lung cancer cases. These mutations are more frequent in white populations than in Asian populations. About 25–50% of whites with lung cancer have KRAS gene mutations, whereas 5–15% of

In lung adenocarcinomas, both KRAS-activating mutations and in and EGFR mutations can be observed. KRAS appear to be mutually exclusive. Three different mutations in the KRAS gene have been associated with lung cancer [32]. Nearly all of the KRAS gene mutations associated with lung cancer change the amino acid glycine at position 12 or 13 (Gly12 or Gly13) or change the amino acid glutamine at position 61 (Gln61) in the K-Ras protein. These mutations cause a constantly activated KRAS, which directs the cells to proliferate in an uncontrolled way, and

Even though KRAS mutations were identified in non-small cell lung tumors more than 20 years ago, the clinical value of determining KRAS tumor status is recently gaining importance. Recent studies indicate that patients with mutant KRAS tumors fail to benefit from adjuvant chemotherapy and do not respond to EGFR inhibitors. There is a clear need for therapies specifically developed for patients with KRAS-mutant non-small cell lung cancers [34, 35]. KRAS gene mutations are much more common in long-term tobacco smokers with lung cancer when compared to nonsmokers. Lung cancers with KRAS gene mutations typically indicate a poor prognosis and are associated with resistance to several cancer

KRAS is a very important oncogene. K-Ras protein is upregulated in different cancers and can cause bad prognosis of the disease. However, KRAS mutations are not sometimes enough to initiate cancer. Therefore, along with KRAS mutations, several environmental chemicals and drugs may contribute to the cascade of events

It can be stated that in CRCs, PC, and lung cancer, KRAS mutations should be evaluated in clinics. On the other hand, the exposures of different environmental

"high efficacy and low-toxicity" is the priority goal in this field [30, 31].

Asians with lung cancer have KRAS gene mutations [14].

the high cellular proliferation leads to tumor formation [33].

**6**

treatments [33–35].

**4. Conclusion**

leading to cancer.

Pinar Erkekoglu Department of Toxicology, Faculty of Pharmacy, Hacettepe University, Ankara, Turkey

\*Address all correspondence to: erkekp@yahoo.com

© 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
