Research Trends in

MULTIDISCIPLINARY
RESEARCH
Volume - 17

Chief Editor
Dr. R. Jayakumar
Associate Professor, Siga College of Education, Villupuram, Tamil Nadu,
India

AkiNik Publications
New Delhi
Published By: AkiNik Publications

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 Contents

S. No Chapters Page No.

1. Role of Governor and President under Article – 356 01-12
(Mr. Amit)

2. Restoration Interventions of the Disturbed Coastal Forest

Ecosystems in Tanzania 13-30
(Elly Josephat Ligate)

3. Surplus Family Labour the Hidden Treasure 31-36

(SK Joshi and J Udgata)

4. Lung Cancer in Mexico 37-57

(Ana Laura Vega-Rodríguez, Alejandra Guadalupe Alcázar-Ramos,
Brenda Ugalde-Villanueva, Karla Liliana García-Mejía, Alma Delia
Bertadillo-Jilote, David Gustavo García-Gutiérrez, María del Pilar
Figueroa-Corona, Marco Antonio Meraz-Ríos, and Karla Isabel Lira-De
León)

5. Collection, Preservation and Dispatch of Samples for

Disease Diagnosis 59-71
(Rakesh Kumar Gupta, Debasish Niyogi and Satya Vrat Singh)

6. Scope and Significance of Multidisciplinary Research in

Ayurveda 73-90
(Dr. Niraj Srivastava and Dr. Varsha Saxena)

7. A Socio-Economic Survey at Lahowal under Dibrugarh

District, Assam 91-113
(Pinku Gohain and Achinta Saikia)

8. Antagonistic Mechanisms of Plant Growth Promoting

Rhizobacteria 115-130
(Dr. Y. Kavya)

9 Centres and Iconographic Representations of Vishnu in

Pre-Sankaradeva Assam 131-152
(Lakhinandan Bora)
 Chapter - 4
Lung Cancer in Mexico

Authors
Ana Laura Vega-Rodríguez
Maestría en Química Clínica Diagnóstica, Facultad de
Química, Universidad Autónoma de Querétaro, Querétaro
76017, México
Alejandra Guadalupe Alcázar-Ramos
Maestría en Química Clínica Diagnóstica, Facultad de
Química, Universidad Autónoma de Querétaro, Querétaro
76017, México
Brenda Ugalde-Villanueva
Maestría en Química Clínica Diagnóstica, Facultad de
Química, Universidad Autónoma de Querétaro, Querétaro
76017, México
Karla Liliana García-Mejía
Maestría en Química Clínica Diagnóstica, Facultad de
Química, Universidad Autónoma de Querétaro, Querétaro
76017, México
Alma Delia Bertadillo-Jilote
Maestría en Química Clínica Diagnóstica, Facultad de
Química, Universidad Autónoma de Querétaro, Querétaro
76017, México
David Gustavo García-Gutiérrez
Maestría en Química Clínica Diagnóstica, Facultad de
Química, Universidad Autónoma de Querétaro, Querétaro
76017, México

Page | 37
 Authors
María del Pilar Figueroa-Corona
Departamento de Biomedicina Molecular, Centro de
Investigación y de Estudios Avanzados del Instituto
Politécnico Nacional (CINVESTAV-IPN), Ciudad de México
07360, México
Marco Antonio Meraz-Ríos
Departamento de Biomedicina Molecular, Centro de
Investigación y de Estudios Avanzados del Instituto
Politécnico Nacional (CINVESTAV-IPN), Ciudad de México
07360, México
Karla Isabel Lira-De León
Dr. Karla I. Lira-De León, 52(442) 192-12-00, Cerro de Las
Campanas, s/n, Las Campanas, 76017 Santiago de Querétaro,
Qro, México

Page | 38
 Chapter - 4
Lung Cancer in Mexico
Ana Laura Vega-Rodríguez, Alejandra Guadalupe Alcázar-Ramos, Brenda Ugalde-
Villanueva, Karla Liliana García-Mejía, Alma Delia Bertadillo-Jilote, David Gustavo
García-Gutiérrez, María del Pilar Figueroa-Corona, Marco Antonio Meraz-Ríos, and
Karla Isabel Lira-De León

Abstract
In Mexico, lung cancer has the worst prognosis once is diagnosed, since
it is detected at very late stages with almost non effective treatment. One of
the risk factors associated to lung cancer. Is the tobacco consumption, which
has increased mainly in the adolescent´s population and young people, and
represents a serious public health problem. In addition to tobacco smoking, it
is very common for families in rural areas to cook with firewood, which has
been associated as an important risk factor as well. Urban areas have a
different scenario, where environmental pollution and exposure to pollutants
due occupational activity are the main associated risk factors. In addition to
this problem, Mexico currently has not established a program to achieve a
diagnosis and timely treatment for lung cancer. Therefore, it is necessary to
strengthen public policies that really achieve a change in exposure to these
risk factors that favor the development of tools against this deadly disease.
According to the above, the present work aims to describe the scenario of lung
cancer in Mexico, from its epidemiology to the main risk factors for both
tobacco smokers and non-smokers.
Key words: Lung cancer, Tobacco smokers, Never-smokers, Risk Factors.
1. Introduction
Lung cancer (LC) is one of the most lethal types of cancer worldwide,
since its diagnosis is carried out at late stages, therefore the prognosis is
reserved and the hope of survival is limited [1]. Lung cancer is a complex and
heterogeneous disease with two types of scenarios; those associated to tobacco
smokers and those with non-smokers. Where 80-90% of cases of LC and 82%
of deaths are related to smoking and the rest of the patients has an history of
never-smokers [2, 3]. Although the health damage caused by smoking is
currently known, smoking continues to increase, especially in developing

Page | 39
countries; and it is already considered a universal epidemic [4]. The LC begins
in cells of the bronchi, bronchioles and alveoli, once the epithelial cells of the
pulmonary parenchyma alter their genetic composition, either due to an acute
or chronic lung injury there is an increase potential to develop LC [5]. The
progression of LC will depend on the presence of genetic and epigenetic
changes in the altered cells, in addition to the interaction of these cells with
the cellular and extracellular matrix environment. These alterations cause the
erroneous expression of collagen, proteoglycans, laminins, proteases and
integrins in the microenvironment of the tumor, which forms a permissive
niche for the growth of the cancer cells [6]. Once that premalignant precursor
lesions are formed, they could become invasive, and lung epithelium may
undergo morphological changes like: hyperplasia, metaplasia, and dysplasia
to give rise to a Carcinoma in situ [7]. Based on cellular and histological
characteristics, there are two types of LC: small cell, responsible for 15% of
cases and 85% non-small cell (Figure 1), which at the same time is subdivided
into three subtypes: adenocarcinoma, squamous cell carcinoma and large cell
carcinoma (see Table 1) [8]. According to the predominant location,
adenocarcinoma is presumed to originate from distal airways, while squamous
cell carcinoma tumors develop from central airways [9].
Table 1: Histological classification of Lung cancer.

Type and frequency Clinical presentation

Small cell (small cells, small cells combined) 15% Central lymphadenopathy
Non-small cell lung cancer 85%: Heterogeneous
Large cell carcinoma 15% Peripheral
Squamous cell carcinoma 30% Centrally
Adenocarcinoma 40% Peripheral

Since LC in early stages is asymptomatic, patients who suffer from this

disease go to medical review at late stages, when they present symptoms such
as cough, dyspnea, dysphonia, hemoptysis and chest pain. All these symptoms
are characteristic of advanced stages (III or IV), with an average survival of
approximately 5 years [10]. In Mexico has been reported that tobacco smoking
cause 8.4% of the total deaths and the average number of current tobacco
smokers is 17.6% [11]. Therefore this review is focused on describe the scenario
of lung cancer in Mexico, and its association with active or passively tobacco
smoking.

Page | 40
 Fig 1: Major types of Lung cancer. Squamous cell carcinoma, adenocarcinoma and
large cell carcinoma, as part of a group called non-small cell lung carcinoma (more
frequent), to distinguish it from small cell carcinoma (less frequent).
2. Epidemiology of Tobacco smoking in Mexico
In Mexico, the first studies on tobacco smokers were derived from the
National addiction surveys (NAS) that were carried out in 1988. Where the
prevalence of smokers was known, and it was observed that the majority of
smokers were between 18 and 29 years of age [12]. Currently, tobacco smokers
includes children and adolescents and is a growing health problem. Among
the factors that have contributed to its consumption in these vulnerable groups
we can mention: the ease access to cigarettes, social pressure, and tobacco
promotion [13]. The NAS, carried out between 2010 and 2011, included a multi-
stage probabilistic design, which allowed to obtain national, urban-rural, and
regional representativeness data [14]. On the other hand, the statistics of the
National Health and Nutrition survey in 2012, show that the prevalence of
tobacco consumption is 20.6%, and in particular for men the consumption was
31.0% and in women 9.9% [15]. The NAS in general highlighted, in terms of
tobacco consumption, that 20.4% of the urban population between 12 and 65
years of age are active smokers, while in rural locations the proportion is only
11.3% [14]. In these studies, the Mexican population was characterized with
respect to tobacco consumption, with the following definitions [4]:
Active-smoker: person who declared that they had smoked at some time
in their life and smoked during the last year.
Ex-smoker: a person who declared that he had smoked at some time in
his life and stopped smoking more than a year ago.
Never-smoker: a person who declared that never smoked in life.

Page | 41
 In recent years, the disorders that can cause passive tobacco smokers have
been documented, where there is an involuntary smoker (non-smoker) who is
exposed to tobacco smoke from smokers when living with them [16].
According to data from GLOBOCAN, there are 7811 incidents that
correspond to LC cases in Mexico every year. In 2016 alone, 7044 deaths were
attributable to LC, making this the highest-mortality neoplastic disease in
Mexico [17].
Since smoking is a serious health problem, some smoking cessation
strategies have been implemented. However, the effectiveness of these
strategies are poor. The following surveys data were obtained: Active smokers
between 18 and 65 years of age were asked for information about quitting
smoking. About this, 16.1% answered that it would be difficult for them to
abstain from smoking in public places, and 56.9% of them declared to have
tried to quit smoking at some time. The several strategies in which they did so
were: suddenly stop smoking (66.7%); stop buying cigarettes (10.9%); replace
smoking with another activity (3.7%), and gradually decrease the number of
cigarettes (12.7%). Only 1.2% of the active smokers have undergone some
smoking cessation treatment [14, 18].
3. Tobacco smoking
Addiction to Nicotine present in tobacco, is the close cause of causing
tobacco smoking-induced diseases. Tobacco is made with the Nicotiana
tabacum leaf, subsequently mixed with different flavoring substances, and
exposed to air or artificial heat [19].
The combustion of tobacco causes two currents [20]:
• A mainstream by means of aspiration maneuver that the smoker
directs towards his own respiratory apparatus, passing from the oral
cavity directly to the lungs (contains 25% of the total carcinogens
such as Tar) [19].
• A secondary or lateral current that occurs when the cigarette is
spontaneously consumed, which is what the passive smoker inhales
(with the remaining 75% of products such as carbon monoxide and
Tar derivatives) [20].
Most cigarettes on the market contain 10 mg or more of nicotine, from
which 1 to 2 mg / cigarette is inhaled. In cigarette smoke is mainly acid salts,
so its absorption at the oral level is minimal; hence the need for the smoker to
take deep inhalations in order to absorb nicotine at the pulmonary level, also
dragging along with all the toxic substances present in the smoke. Nicotine

Page | 42
metabolism occurs mainly in the liver through cytochrome P-450, forming
metabolites without addictive capacity such as: cotinine and nicotine 1´-N-
oxide [13].
Tobacco smoke is composed of more than 4000 components, depending
on the characteristics such as taste, smell, among others [21], within all the
components that tobacco smoke contains in its different varieties, 60 of them
are carcinogens, which are divided into: aromatic hydrocarbons, N
nitrosamines, aromatic amines and inorganic components, these components
have the ability to enter the cell and form DNA adducts, whose errors are
resolved by tumor suppressor genes, but given the continuous exposure to
these substances, these DNA adducts are usually cumulative until they
generate mutations in the genes related to the cell cycle, also called oncogenes,
causing the onset of oncogenesis [22, 23].
Tobacco smoking is one of the main preventable causes of disease and
death in the world. The World Health Organization notes that 30% of adults
are smokers in the world population, and more than 3.5 million of these
smokers die each year [24].
4. Risk factors associated with tobacco smoking
It is important to highlight that smoking causes adverse consequences for
society, since it is related to health damages, medical care expenses,
productivity losses and premature death of both the smoker and unfortunately
those exposed to tobacco smoke [25, 26]. Smoking is associated with heart and
cerebrovascular diseases, chronic obstructive pulmonary disease (COPD),
lung cancer, and other diseases [27]. These diseases generate three types of costs:
direct (hospitalizations and medications), indirect (loss of productivity, family
care, cost of transportation to care, etc.); and intangible costs (pain and
suffering). For example; in the state of Querétaro (City in the central part of
México), where smoking is a serious health problem, since the prevalence in
the entity is above the national level, two people die daily due to smoking
associated diseases, with a total of 762 cases of death per year. It is worth
mentioning that the state health sector spent 76.7 million pesos in
hospitalization for patients with these diseases [28, 29]. Although it is well
known that a substantial reduction in tobacco consumption, the incidence of
tobacco-related diseases would decrease considerably, and this would bring
enormous benefits for the health, development and economic growth in the
country [16], in Mexico, however, the impact of the health policies
implemented is still far from desirable, and the commitments made by Mexico
in the international arena have been partially fulfilled [30–32].

Page | 43
 Currently, the LC is a leading cause of death in both men and women
worldwide. However, the risk of breast cancer or respiratory diseases is higher
in women than in men due to the characteristics of the body and the female
hormonal system. Smoker´s women are twice as likely to suffer from
cardiovascular disease; possibly because the tobacco´s smoke components
decrease estrogen body levels. It is observed that smoker´s women are 25%
more likely to suffer a coronary event than men. The National Institute on
Drug Abuse (NIDA) publish what women think about smoking, such as: that
light cigarettes are better than regular and do not affect them the same, they
smoke fewer cigarettes per day compared to men, tend to use those that are
low in nicotine and do not inhale as deeply as men. But there are several
studies where it has been found a big difference in the way smoking affects
men and women, for instance nicotine is an appetite suppressant and there are
studies that show that women are more sensitive to the effects of nicotine, this
puts women at greater risk to gain weight when trying to quit, since the
metabolism undergoes a slight decrease and a greater amount of calories is
ingested with a consequent greater risk of having a relapse due to anxiety [33,
34]
.
There are several characteristics which correlates smoking and LC. 1)
Start: The younger you start smoking, the earlier the onset of lung cancer may
occur; 2) Way of consumption: the filter reduces from 20% to 40% the
incidence of LC; 3) Duration/intensity of consumption: the risk becomes
exponential with the duration (month/year) combined with the intensity (10,
20, > 20 cigarettes / day) of consumption, in a linear manner [30].
In addition, the characteristics of the cigar that is ingested (such as the
type of filter, mentholated compounds, amount of nicotine, and others) could
be important as well, since these tend to increase the interaction between the
toxic elements of tobacco and the organism of the smoker, such is the case of
the light cigarettes whose nicotine content is lower, and the smoker consume
more cigarettes to reach the level of the desired effect, and the smoker makes
deeper inhalations, causing the toxic agent to reach more distal areas in the
lung where cancer develops. Is has been found that favored a peripheral
localization of adenocarcinomas in contrast to the focused localization of
squamous cancers [4].
Smoking can make a person difficult to breath even during moderate
exercise due to various factors that decrease respiratory efficiency in smokers
[35]
:
- Nicotine contracts the terminal bronchioles, which decreases the

Page | 44
 airflow that enters and leaves the lungs.
- The carbon monoxide in the smoke binds to hemoglobin and reduces
its oxygen carrying capacity.
- Smoke irritants increased secretion by the mucous membranes of the
bronchial tree and inflammation of the mucous lining, which
prevents airflow in and out of the lungs.
- Smoke irritants also inhibit ciliary movement and destroy cilia of the
epithelium and lining of the respiratory system.
- Over time, smoking leads to the destruction of elastic fibers in the
bronchioles and is the main cause of emphysema, these changes
cause the collapse of the bronchioles and air trapping in the alveoli
at the end of expiration, whose result is a less efficient gas exchange.
Tobacco smoke contains thousands of substances in vapor and particle
phases and at least 60 have been classified as carcinogenic. Tar exposure is
what leads to lung carcinoma, the total particles of cigarette smoke after
removing nicotine and water is called tar; which contains carcinogens
polycyclic aromatic hydrocarbons (PAH), azaarenes, N-nitrosamines,
aromatic amines, heterocyclic aromatic amines and aldehydes, in addition to
organic compounds such as 1-3 butadiene, ethyl carbamate; and inorganic
compounds such as arsenic, chromium, cadmium, nickel, hydrazine and
polonium-210 [36, 37].
Tobacco smoke also contains carbon monoxide (CO), a powerful toxin
that displaces oxygen from hemoglobin molecules. However, acutely, the
amount of CO in tobacco smoke can cause hypoxia and the body produces a
greater number of red blood cells to compensate [38].
To be carcinogenic, first, the compounds must be metabolically activated
by the cytochrome P450 enzymes and produce oxygenated compounds. These
oxygenated intermediates are transformed by the enzymes: glutathione S-
transferase, uridine-58-diphosphategucluronosyl transferase, sulphatases and
others. Some of the transformed products form adducts with the DNA of the
cells, that are mostly repaired by the DNA repair mechanisms of the cell, such
as: nucleotide excision or direct repair. Adducts that are not repaired could
affect important genes producing substitutions of G to T and G to A with
alteration of their expression and causing modifications in their function like
the p53 tumor supresor gene or mutations in the KRAS oncogenes [39].
Tar, also contains a mixture of free radical species such as quinones,
hydroquinones and semiquinones, each smoke contains approximately 1,015
free radicals; these free radicals cause redox recycling and produce superoxide

Page | 45
anions from molecular oxygen and also form hydrogen peroxide and hydroxyl
radical, which are highly reactive. The species create notches and breaks in
the DNA, and in combination with a DNA repair machinery altered,
carcinoma can be induced [37].
Oxidative stress is a damage caused when the antioxidant and the
elimination activity of free radicals in the body is not sufficient to cope with
the active oxidants produced by a harmful stimulant, in this case caused by
cigarette smoke. Oxidative stress involves macromolecular oxidative damage,
which induces protein denaturation, DNA damage and lipid peroxidation and
interferes with the normal metabolic activity of the body, which leads to the
onset and / or development of diseases. It has been confirmed that oxidative
stress is involved in cancer. Reactive oxygen species (ROS) constitute the
majority of active oxides and represent more than 95% of the total oxides.
ROS are involved in the appearance and development of malignant tumors
through the induction of DNA damage and genetic mutations, inhibition of
apoptosis and promotion of proliferation, invasion and metastasis of malignant
cells [40].
4.1 Biomarkers to determine exposure to tobacco smoke
In order to assess the status of a smoker and thus be able to measure
exposure to tobacco smoke even passively, the metabolism of these substances
within the body is used. In this regard, the use of different methods to
determine concentrations of these substances such as: carbon monoxide in
exhaled air (average life time of 2 to 5 hours), thiocyanate (average life time
of 10 to 14 days) and less frequently, carboxyhemoglobin (variable half-life),
nicotine (half-life of less than 2 hours) and its main metabolite: cotinine (half-
life of 19 hours), has been used [41].
The most used biomarker of nicotine intake is Cotinine, which can be
measured in blood, urine, saliva, hair and nails. Cotinine is obtained after
metabolizing nicotine by CYP2A6 in the liver and then eliminated mainly in
the urine [42, 43]. The current optimal cut-off point for plasma cotinine to
distinguish active smokers from non-smokers in the general US population it
is 3 ng/mL [44]. While in the case of passive smokers, values between 0.31 and
1.99 ng / mL have been identified [45]. However, nicotine metabolism varies
according to individuals, since the CYP2A6 gene usually has genetic variants
that produce enzymes with different characteristics such as, slowly
catabolizing activity, and in some cases causing the person to be more prone
to nicotine addiction since their metabolism is slower than normal and require
less intake for the same effect [46].

Page | 46
4.2 Added risk factors in Tobacco smokers
In addition to tobacco smoking, there are other known risk factors that
include age, family history, diet, physical activity, asbestos exposure,
radiation exposure, air pollution, presence of other acquired lung diseases and
genetic factors. Contaminant exposures in the workplace are known to cause
LC, such as: arsenic, chromium, cadmium and nickel. The risk factors confer
a relative risk (RR) for LC and are dose and duration dependent, and some
carcinogens act synergistically when combined with tobacco smoke such as
asbestos [47]. There is substantial evidence of the relationship between the
factors and their RR, such as: active-smoker (20), ex-smoker (9), passive-
smoker (1.3), environmental exposures; asbestos and radon (3), comorbidities;
human immunodeficiency virus (HIV) infection (2-11), idiopathic pulmonary
fibrosis (7), COPD (2-3.1), other; history of thoracic radiotherapy (5.9),
chemotherapy History (4.2) and family history of LC (2) [48].
Air pollution
Air pollution is a diverse mixture of pollutants originated from
anthropogenic and natural sources, is comprised of particulate matters, gases
(carbon monoxide, ozone), organic compounds (PAH, resin acids), metals
(lead, vanadium, and nickel), microbes, and others [5]. Air pollution is divided
into ambient air pollution and household air pollution, and is a global
environmental health risk that affects the populations all over the world [5].
Familial history
The occurrence of LC in non-smokers with a familial history of LC. An
approach based on familial association studies have been used to discover LC
associated genes with high penetrance and low-frequency, like: genes
involved in carcinogen metabolism, nucleotide excision repair, base excision
repair and cell cycle control appears to have a role in developing LC [49].
Comorbidities; respiratory disease: a chronic inflammation of the lungs,
because: COPD, tuberculosis, pneumonia or asthma, are risk factors for LC
development. This chronic immune response damages lung tissues, enhance
the rate of cell division and increase possibility of DNA damage. Infectious
diseases: HIV due to the history of inflammatory diseases that the patient may
have, mainly in the airway [48].
Frequent chemical or mineral exposure (occupational): coal products,
chloromethyl ethers, beryllium, mustard gas, cadmium, silica, vinyl chloride,
nickel compounds and chromium compounds. Principally, these compounds
mediates generation of ROS that also produced chronic inflammatory
response, DNA damage, and mutations [37].

Page | 47
 Life style: cholesterol levels tend to be high in intracellular cancer cells
and cholesterol is needed for cancer progression. A diet high in cholesterol
might be indicative of a lifestyle prone to health-related problems such as
cardiovascular diseases and cancer [50].
Mexico has a big pollution problem in the most populated cities like;
Mexicali, Toluca, Mexico City, Monterrey, Pachuca, Salamanca, León, to
name a few. In the report called 2018 World Air Quality Report it was found
that these cities exceeded the limit of particulate matters (2.5), recommended
by the World Health Organization that is 0 to 10 μg/m³ [51, 52]. Although, the
50% of the Mexican population is never-smoker, around 30.3% of people who
have never smoked, reported being exposed to environmental tobacco smoke,
so they can be considered as passive-smokers [14].
In Mexico, patients with LC had a history of wood-smoke exposure,
instead of high consumption of tobacco-smoke, with the presence of higher
Epithelial Growth Factor Receptor (EGFR) mutation frequency (34%) and
lower KRAS-mutation frequency (15.9%) [53].
5. Diagnosis of Lung Cancer
Because, in the early stages of LC there is not symptoms and the diagnosis
in the patients is done at late stages, the prognosis is bad [10]. The diagnosis
involves staging the LC to describe its size, position and whether it has spread.
A number / letter system is used to describe the stages from “I” through “IV”,
according to the TNM (Tumor size, Lymph Node, Metastasis) System
neoplasm staging method, developed by the American Joint Committee on
Cancer in collaboration with the International Union Against Cancer. A
patient with a lower stadium of progression has better prognosis [9].
In Mexico, stage I-II lung cancer patients are almost anecdotic, and 98%
to 99% of patients are diagnosed within the late-stages [17].
The diagnostic evaluation includes tissue diagnosis. Experienced doctors
can diagnose the type of lung cancer according to the clinical presentation and
chest x-ray, but a tissue sample is essential to optimize the diagnosis and plan
the treatment. There is a wide variety of diagnostic methods available, the
procedure chosen depends on the type, location and size of the tumor;
comorbidities and accessibility of metastasis. In general, the least invasive
method possible should be used [47].
5.1 Non-invasive procedures auxillary for diagnosis
Chest x-ray: they often reflect the invasion of anatomical structures
adjacent to the lung and often help in the decision to surgical treatment; it can

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be decisive to determine the degree of invasion and simplify the staging
process [54].
Computed tomography of the chest (CT): with respect to the primary
tumor, it allows to obtain detailed information on the size, location, anatomical
relationships with neighboring structures and can detect very small nodules
that are not detectable with the chest x- ray; Computed tomography is a two-
dimensional representation of a three-dimensional sectional section,
composed of pixels and voxels [21].
Positron emission tomography (PET): based on the greater metabolic
activity of neoplastic cells, it provides information on tumor biology, but has
lower spatial resolution than CT, however in the mediastinal assessment, PET
is more effective than CT, highlighting that it also has a high sensitivity to
detect distant metastases [48].
5.2 No-surgical invasive procedures auxillary for diagnosis
Transbronchial needle aspiration (TBNA): is a flexible bronchoscopic
technique used to obtain tissue samples from mediastinal lymph nodes or
peribronchial locations. The diagnostic efficacy only approximates the
ultrasound-oriented puncture in the subcarinic station, in the rest its
performance is lower (58% vs. 84%) [55].
Respiratory endoscopic ultrasound (EBUS): it has high diagnostic
accuracy for mediastinal lymph node staging, even in nodes smaller than 1 cm
[56]
EBUS-TBNA is now widely accepted as a first-step procedure for
confirmation of suspicious nodal disease in patients with lung cancer [57].
Endoscopic ultrasound (EUS): In lung cancer, EUS is emerging as an
accurate, nonsurgical alternative to staging the mediastinum through EUS
fine-needle aspiration. This method, coupled with fine needle aspiration
puncture (EUS-PAAF) also allows to detect subdiaphragmatic metastases, as
well as assess the presence of mediastinal invasion by the tumor, with much
more precision than the techniques radiological [58].
The combination of EBUS-PAAF and EUS-PAAF allows
complementary access to all mediastinal ganglionic stations, with the
exception of the left upper lobe [21, 54].
In Mexico, the most commonly used diagnostic methods are: sputum
cytology, bronchial lavage, bronchial brushing, biopsies obtained by
bronchoscopy, fine needle aspiration biopsy and surgical biopsy [59]. Recently,
in the National Institute of Medical Sciences and Nutrition Salvador Zubirán
analyzes of liquid biopsies are performed for the diagnosis of LC; which
consists of the detection of tumor DNA in blood samples [60].

Page | 49
 Recently, the approach to the development of cancer diagnostic
techniques has shifted towards biomarkers due to various advantages such as
effective detection at a very low concentration of biomarkers, cut-off points
are well defined, multiple biomarkers can be used for detection, and the
process is faster and more profitable. In Mexico for the proper classification
of LC, pathological assessment and molecular diagnosis; they allow us to
determine the extension, lineage, the origin of the primary and the associated
genetic alterations (see Table 2) [61, 62].
Table 2: Immunohistochemistry panel and molecular biomarkers for Lung Cancer
diagnosis in Mexico.

Immunohistochemistry antibody Molecular Biomarker

TTF-1 (Adenocarcinoma) EGFR (Mutation)
P40 (Squamous cell carcinoma) ALK (Rearrangement)
CK7 (Small Cell) ROS1 (Rearrangement)
CK5/6 (Squamous cell carcinoma) PDL1 (Amplification)
Neuroendocrine markers (Small Cell) BRAF (Mutation)

5.3 Never-smokers
Lung cancer in never smokers and/or women were mostly
adenocarcinoma of the lung whereas in smoker´s male, squamous cell
carcinoma was dominant [37]. In addition, it has been demonstrated that tumor
samples from tobacco smokers had more number of point mutations than
tumor samples from non-smokers [63].
6. Lung Cancer Treatment
After a diagnosis, patients with a stage I and II, according to the TNM-
type lung cancer are treated with surgical resection, and recommending
complementary chemotherapy which is customized according to the
characteristics of the localized tumor; in the case of patients with stage IIIA
they have unfavorable final results when they are only treated with resection,
so from this point they must refer to protocols of multiple modalities that
include both chemotherapies and radiotherapies to improve survival,
including patients in stage IIIB in which in addition to resection, they have
multiple modalities treatment, and it is possible that they can be cured. Finally,
stage IV patients are treated with chemotherapies or palliative measures based
on symptoms. In the case of microcytic carcinoma, good prognostic responses
to chemotherapy are given; However, when the cancer reappears, the response
to drugs decreases and most of the patients die [64, 65].
In terms of therapeutic strategies, patients in Mexico have access to

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surgery; however, most patients who are candidates for surgery are attended
by a cardiothoracic surgeon, rather than by a thoracic oncology specialist [17].
7. Conclusion
Mexico needs to establish more effective health programs to be able to
arrive at an opportune diagnosis of LC, this has to be accompanied by an easy
access for its treatment when the diagnosis of LC has been confirmed, and
improve the prognosis and possibility of the patient survival. It is essential to
establish effective prevention programs that reduce the interaction of the
people with the risk factors of the disease; such as the reduction of
environmental pollution, either from tobacco smoke or from the pollution.
Particularly in rural areas where families use wood or burning fuels for
cooking.
Conflict of interests
The authors declare that they have no real or potential conflict of interest
with this article.
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