Female non-smokers face a much higher risk of death from lung cancer over the last few years. Many causes explain why lung cancer rates have skyrocketed among the women non-smokers. The increase in mortality risk from lung cancer in female never-smokers can be due to causes including environmental tobacco smoke, radon(a radioactive gas found in nature in soil and rocks)asbestos, outdoor and indoor air pollution. This literature study has shown that in addition to these cases it is likely that genetic factors have the potential to cause lung cancer in the female nonsmoking population. There is also evidence that the infection of HPV virus can increase the risk of lung cancer but this varies significantly depending on geography. This means that even though HPV vaccination can, in theory, reduce the chances of developing lung cancer, future research attention is needed to address whether an HPV vaccine can effectively aim in the prevention of the occurrence of lung cancer.
Lung cancer is the predominant cancer-related cause globally. Amongst all different cancer types, it has had the least improvement of long-term survival rate. Historically, men have had the highest prevalence of lung cancer; nevertheless, the rate of lung cancer in women is under rising. Unfortunately, women are starting to smoke, whereas men are giving up smoking. Even though the vast majority of lung cancer cases are related to tobacco, more and more non-smokers are diagnosed with this deadly disease. It is important to note that 25% of the people who are diagnosed with lung cancer are never-smokers. Studies show that lung cancer differs biologically among men and women. The most common cancer in women is adenocarcinoma while in men, it is squamous cell carcinoma, which causes more symptoms and therefore it is easier to diagnose. In the U.S. and Europe, the incidence rates of people who have never smoked is higher in women than in men- 20% approximately of women with lung cancer have never smoked unlike to 2–6% of nonsmoking men. (Helland and Brustugun 2009). Lung cancer has become a concern for both genders due to a recent drastic increase in cigarette smoking. Therefore, for diagnostic evaluation and treatment of lung cancer, it is vital that the risk factors in never smokers are identified. This research will study the etiological factors that bear the responsibility for increasing the incidence of lung cancer in the female never smokers. To answer this question, the genetic predisposition to lung cancer in women will be explored. Next, the association between Human Papilloma Virus haplotypes and lung cancer development in female never-smokers will be looked at.
Lung cancer risk factors in never-smoking women
In general, cancers develop when the normal processes, which keep people healthy and alive by making new cells, go wrong. Carcinogenic chemicals, ultraviolet radiation, and viruses can all harm the DNA in cells causing a cancerous malfunction. However, in many cancers, there is not an identifiable external risk and this may be the case for some of the non-smoking people who get lung cancer. There are numerous factors linked up with the risk of developing lung cancer in never smokers such as second-hand smoke, radon, asbestos, other occupational causes, indoor and outdoor air pollution, and genetic factors.
Genetic profiling in lung cancer
The genetic makeup influences the chance of getting lung cancer in nonsmoking women. Females are more likely to be presented with genetic components connected to lung cancer risk. There is a correlation between p53 mutation risk and tobacco consumption; mutations are thus rarer in non-smoking females (10–47%) than in smoking women (26–71%). Another genetic factor that may appear to play a role in the pathogenesis of lung cancer in for women is the epidermal growth factor (EFGR), a protein found at a greater rate on the surface of lung cancer. EGFR mutations are identified more frequently in the female, especially with Asian ethnicity who have adenocarcinoma histology and particularly in women who have never smoked. (Helland and Brustugun 2009)HER2 is another type of EGFR mutation and it appears to be more frequent in never-smoking women with adenocarcinomas. The EML4-ALK fusion tyrosine kinase is a rearrangement in the chromosomes that leads to the activation of the tyrosine kinase and it is resulting in unopposed cell proliferation found in 3–11% of younger nonsmoking patients with adenocarcinomas. (Helland and Brustugun 2009). Moreover, KRAS mutations are encountered in 20–30% of NSCLC cases, mostly in adenocarcinomas and even though they are more frequently found in female smokers, they may be presented in never smokers a well. (Helland and Brustugun 2009)
The association between Human Papilloma Virus and lung cancer
Besides genetic factors, it has been proposed that the Human Papilloma Virus is probably related to lung neoplasms. Studies comparing female smokers among East Asian patients who had lung cancer have shown dramatic growth in the expression of HPV haplotypes in pulmonary squamous cells and connection in the development of this disease. Human Papillomavirus (HPV) is a carcinogen substance which is known to cause head and neck cancer in never-smoking populations. In one study it was found that women of Taiwanese origin
were more likely to be diagnosed with lung cancer under the condition that they had been exposed to HPV; HPV infections rates were encountered in 43–49% of adenocarcinomas cases in comparison with 24–29% of squamous cell carcinomas. (North and Christiani 2013). There are two proposed explanation for the development of HPV infection in lung tissue. The first proposed mechanism postulates that cervical infection results in the circulation of the virus and subsequently in systemic dissemination including pulmonary tissue. A second hypothesis suggests that the high risk of oral and genital contact results in oral HPV contagions, which leads to lung squamous cell infection. (North and Christiani 2013)
Areas of research
Apart from the above advances in targeted therapies, the selection of lung cancer treatment remains still challenge. Further research to assess the existence of HPV in lung cancer cells needs to be conducted given that it has been established success with the protection of HPV vaccines against cervical cancer. The difference in the expression of specific genetic mutations paves the way for molecularly-oriented therapy, which may help in the decrease of the side effects and as well as improve the overall survival.
While tobacco smoke is the leading cancer-related cause, not all cases of lung cancer occur in people who smoke. Even though not every non-smoker who suffers from lung cancer will have a risk factor that has great responsibility for developing the disease, numerous conditions and circumstances have been found that will increase a non-smoker’s incidence rate of getting this cancer. Aside from second-hand smoke, other factors such as radon, asbestos, other occupational exposure, and outdoor air pollution would be considered core contributors to the risk of developing lung cancer. Around 50% of never-smoking women show molecular mutations that might be treated at present or in the future through targeted therapies compared to 10% of smoking female patients. (Helland and Brustugun 2009)
Female never smokers are more susceptible to lung cancer than male. Both genders share the same risk factors, the greatest of which is second-hand tobacco smoke. But among nonsmokers, more women than men have been linked to a high incidence of the disease. Aside from secondhand smoke, there are other factors like radon (a naturally occurring gas) or asbestos and certain other airborne chemical contaminants which can increase a person’s chance of getting lung cancer. Additionally, the pathogenesis of the disease may be clarified by genetic and hormonal causes. For instance, the kind of mutation in p53 or KRAS alters with tobacco smoking status in females. Although there has been detection of HPV virus in lung cancer cells, the importance of finding HPV in lung cancer cells isn’t still known or understood.