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lung cancer treatment
Its incidence in Chile has also increased progressively, which, added to the high rate of smoking in our country, make it possible that it will become a serious public health problem in the coming years. The main risk factor is cigarettes, so every effort should be made to discourage its consumption, exposure to arsenic seems to be an important factor in the North of the country. Multiple genetic alterations that would interact with cigarette carcinogens and a certain family predisposition for the development of lung cancer have been described. This cancer has a high lethality with overall survival of 16% at five years. The symptoms are nonspecific, so the diagnosis is generally late. Lung cancer is divided into Small Cell Lung Cancer (CPCP) representing 10-15% and Non-Small Cell Lung Cancer (NSCLC) representing 85-90%. CPCP is aggressive, with early metastases, with Chemotherapy being the treatment of choice. The CPNCP consists of several histological types, the most frequent being Adenocarcinoma, in this subtype mutations with a prognostic factor (EGFR, KRAS, ALK) have been described, incorporating in a standard molecular study.
Advances in diagnosis and staging have been made with the incorporation of EBUS, EUS, and PET / CT and adoption of the 7th TNM Classification of the IASLC (International Association for the Study of Lung Cancer), more accurate, and with better correlation with prognosis. in stages. Early diagnosis with low-dose chest CT has recently been shown to achieve a reduction in lung cancer mortality. Within treatment, advances in minimally invasive surgery currently allow performing video-assisted lobectomies with oncological results that are equivalent to open surgery, but with fewer complications, shorter hospitalizations, and early return to work. The use of resections in the early stages are also being evaluated.
Introduction
The number of cancers has been increasing progressively in the world. The probability of developing cancer is currently estimated to be worldwide, in both men and women, causing more than 1.3 million deaths a year. In the United States, it is estimated that in 2013 there will be 228,190 new cases of lung cancer, corresponding to 14% of all new cancers diagnosed in that country. The chance of developing lung cancer during life is estimated at 1 in 13 men and 1 in 16 women. In that country, lung cancer also represents the leading cause of death from cancer in both men and women, estimating for 2013, 159,480 deaths from this cause, which represents 27% of all cancer deaths. This means that more deaths from lung cancer occur annually than from breast, prostate, colon, and rectal cancers combined.
The dramatic increase in the incidence of lung cancer in the last 100 years is closely correlated with the increase in tobacco consumption and marketing and the mass production of cigarettes in the same period. This relationship is evident today, but it was not until 1939 that the first article in which tobacco was associated with lung cancer was published and only in 1964 in the report of the Surgeon General of the Public Health Service, it was established that the Cigarette smoking was the leading cause of lung cancer development. In addition to increased cigarette consumption, there has been a significant increase in life expectancy in the last century. Individuals live longer and are exposed to carcinogens such as cigarette smoke longer, which also explains the increase in the number of lung cancer cases observed in recent decades.
Lung cancer risk factors
85% of lung cancers are seen in smokers, with cigarette smoking being the main risk factor for lung cancer. The risk increases with the amount and duration of smoking and has a latency of 15 to 20 years to cigarette smoking. All types of tobacco use in addition to cigarettes are risk factors, including cigars, pipes, hookahs, among others.
In Europe and North America, exposure to radon, gas released from the soil and construction materials, would represent the second the most important cause of lung cancer development. Other risk factors are exposure to cigarette smoke (passive smoker), asbestos (especially in smokers), some metals such as arsenic, chromium and cadmium, some organic products, radiation, environmental pollution, smoke from diesel combustion, and paintings. Some occupational exposures have also been shown to increase the incidence of lung cancer, such as rubber manufacturing, paving, roofing, and chimney cleaning.
Among the diseases with the highest risk of developing lung cancer are cancers of the head and neck, also related to tobacco use in which the risk of developing lung cancer is approximately 4 times greater than that of the general population. Several lung diseases confer an increased risk of developing lung cancer. Especially relevant is COPD, which has a recognized risk of developing lung cancer, other lung diseases are patients with sequelae of Tuberculosis and patients with Silicosis.
Genetic disorders and lung cancer
Despite the carcinogenic effect of tobacco, many smokers do not develop lung cancer, and a percentage of people who have never smoked do. This translates the existence of complex interactions between environmental carcinogens and genetic factors, which have been slowly clarifying, evidencing a synergistic and not simply additive effect on the development of lung cancer.
Some of the genetic factors involved in the development of lung cancer are related to the ability to efficiently remove or detoxify different carcinogens and the ability to repair DNA. Polymorphisms in Phase I (activating) and in Phase II (detoxifying) enzymes can increase or decrease the carcinogenicity of tobacco derivatives. Similarly, gene polymorphisms that participate in cell cycle control such as CCND1, TP53, P21, and P73, increase the risk of developing lung cancer in smokers. However, there is great variability in the relative risk of these genetic alterations depending on smoking, racial, and ethnic factors. The genetic alterations most studied in recent years are mutations in p53, KRAS, and EGFR, as well as EML4-ALK translocation and alterations in ROS1. These genetic alterations have significant value as predictors of the response of personalized lung cancer therapy and will be discussed in greater detail later.
It has also been established that there is a higher incidence of lung cancer in family groups ( clustering ). Population studies carried out in the United States, Sweden, and Iceland, as well as a meta-analysis, have shown an increased risk of lung cancer when a relative has had this neoplasm, especially among smokers. The risk was higher the more members of a family had lung cancer.
All the described molecular and genetic alterations, their interactions, and especially their relationship with cigarette smoking are extremely complex.
The greater knowledge of them will allow identifying individuals with a higher risk of developing lung cancer, preventing their exposure to carcinogens, and carrying out specific screening programs. So far, however, cigarette smoking remains the main preventable risk factor.
Lung Cancer Classification
Lung cancer is divided into small cells (CPCP), which represents between 10 and 15% of the total, and non-small cell lung cancer (NSCLC), which represents the remaining 85 to 90%.
1. CPCP,
or oat cell lung cancer is also related to cigarette smoking. It generally occurs in advanced stages; approximately two-thirds of patients with CPCP have distant metastases and the other third extensive nodal involvement in the pulmonary, mediastinal, or supraclavicular hilus, which determines their general poor prognosis. Depending on its extension, it is generally classified as Extended or Localized Disease. Although the International Association for the Study of Lung Cancer (IASLC) recommends using the TNM classification. This aggressive behavior of the CPCP with early metastases determines its poor long-term survival, which is on average 10% at five years. Only occasionally, in small tumors without nodal or metastatic involvement, Surgery can be considered. In these patients with localized disease, survival can reach 14% at five years. The standard treatment for CPCP is chemotherapy plus chest radiotherapy in compromised areas. The most widely used chemotherapy scheme is Etoposide – Cisplatin. With this scheme, responses are obtained in 50-80% of patients. However, recurrence is frequent and prolonged survival scarce. Given the frequent and early involvement of the CNS, prophylactic cranial radiation is recommended, which reduces CNS recurrence and increases survival in patients who have had a good response to chemotherapy.
2. Non-Small
It is also an aggressive tumor with overall survival of approximately 16% at 5 years. Survival depends on the stage of diagnosis, generally being between 60 and 80% at five years in stage I, 55-60% in stage II, 20 to 40% in stages III, and 0 to 5%. Unfortunately, about 50% of patients metastasize at diagnosis, 20-30% have locally advanced disease, and only 25% present in the early stages. The main histological types are adenocarcinoma (40%), squamous cell carcinoma (25%), and large cell carcinoma (10%), which show some variability in their behavior and prognosis.
