Presentation about lung cancer, form, types, classification, treatment. A lot of anatomical and histological pictures accompanied with small and precised informations about every type of lung cancer.

1. Lung Cancer
BY FOTSO BENNIS MOUNIR
MEDICAL STUDENT AT BELARUSIAN STATE MEDICAL UNIVERSITY
FACULTY OF GENERAL MEDICINE

2. ANATOMICAL OVERVIEW OF THE
PULMONARY REGION

5. General Overview
 Lung Cancer is the most prominent type of cancer nowadays.
 It is responsible for approximately 1/3 of all cancer-related deaths.
 Lung cancer risk is related to life style, sex, ethnicity and other factors.
 Among men, African Americans had the highest incidence of lung cancer
risk ( approximately 7.5 % ) , whereas Swedes had the lowest cumulative
risk (approximately 2 % ) .
 Among women, cumulative lung cancer risk was highest in African
Americans (approximately 3 .5 % ) , whereas French and Korean women
had very low cumulative risks (approximately 1% )

8. Lung Cancer Risk Factors
We can list several risks factors to the development of lung cancer such as :
 Smoking (1st and 2nd hand)
 Genetics
 Radon and Asbestos Exposure
 Environmental Factors

10. SMOKING
Smoking is known to increase the risk of cancer. About 80% of lung cancer occurs in
smokers of in those who recently stopped smoking.
The risk of lung cancer development is estimated 60 times higher in heavy smokers than
in non-smokers.
Although, less prominent, the risk of lung cancer in 2nd hand smokers is approximately
twice bigger than in non-smokers.
Cessation of smoking decreases the risk of lung cancer but it may never return to the
baseline levels, even with regular practice of exercise.
Not all people exposed to smoke develop cancer. This is because mutagenic effect of
carcinogens are modified by genetic variants.
Specific and highly polymorphic p-450 monooxygenase enzyme has an increased
capacity to activate the procarcinogens in smoke.

15. GENETIC FACTORS
Mutations occur in the pulmonary epithelial cells. Some of which may be found in the
bronchial epithelium of smoker without lung cancer.
Large area of pulmonary mucosa have been preconditioned by carcinogens found in tobacco
to predispose it towards development of cancer.
Known as « field defect », or « field cancerization », it is important in progression into cancer
like observed by Vogelstein et al. who pointed out that more than half of the somatic
mutations identified in tumors occured in a field defect.
As genetic factors we have
 Oncogenes : Activation of oncogenes or inactivation of tumor suppressing genes increase
the risk of lung cancer development. Mutations in the K-ras proto-oncogene are
responsible for 10–30% of lung adenocarcinoma.

16. GENETIC FACTORS (Cont.)
 Chromosomal Damage : Damage to chromosome can lead to impairment or destruction
of some genes, especially tumor suppressing genes. Damage to chromosomes 3p, 5q, 13q
and 17p are common in small-cell lung carcinoma. The p53 tumor suppressor gene,
located on chromosome 17p is affected in 60-75% of cases.
 Mutation in Epidermal Growth Factor Receptor (EGFR) : It usually leads to non-small-cell
lung cancer since EGFR is responsible for regulation of
proliferation, apoptosis, angiogenesis, and tumor invasion.
 Genetic polymorphisms : It increases the risk of cancer development. It concerns
polymorphisms in genes coding for interleukin-1, cytochrome P450, apoptosis promoters
(caspase-8), DNA repair molecules (XRCC1).

17. p

18. RADON & ASBESTOS EXPOSURE
Asbestos is a set of six naturally occurring silicate minerals which are long thin fibrous
crystals composed of fibrils that can be released by abrasion. Prolonged inhalation of
asbestos fibers can cause serious and fatal illnesses including lung cancer, mesothelioma and
asbestosis. Exposure to asbestos is associated with all major histological types of lung
carcinoma (adenocarcinoma, squamous cell carcinoma, large-cell carcinoma and small-cell
carcinoma). The latency period between exposure and development of lung cancer is 20 to
30 years. It is estimated that 3%-8% of all lung cancers are related to asbestos.
Radon is a chemical element with symbol Rn. It is a radioactive, colorless, odorless, tasteless
noble gas, occurring naturally as a decay product of radium. While radon is the second most
frequent cause of lung cancer, it is the number one cause among non-smokers, according to
EPA estimates. Radon was primarily used to treat cancer but have been found to increase
rate of illness.

19. Relative risk of lung cancer mortality by cumulative exposure to radon decay products (in
WLM), and fitted adjusted linear ERR model, from the combined data from 11 cohorts of
underground hard rock miners with the exposure limited to <400 WLM (Lubin et al., 1995).
Error bars show the 95% CI for each exposure group

21. ENVIRONMENTAL FACTORS
We can list
 Arsenic
 Chromium
 Nickel
 Diesel
 Bis(chloromethyl) ether
 Methyl ether
 Ionizing radiations (X-rays, Gamma-rays)
 Mustard Gas
 Mineral Oils.

22. SYMPTOMS OF LUNG CANCER
 Chest pain
 Wheezing
 Fatigue
 Loss of appetite
 Continuous cough
 Coughing up blood
 Shortness of breathe

23. TYPES OF LUNG CANCER
We can list
 Non-Small-Cell Carcinoma (NSCC) :
1. Most Common type (80-85% of cases)
2. Grows slower.
3. Subdivided into : Adenocarcinoma, Squamous cell carcinoma, Large cell carcinoma
 Small-Cell Carcinoma (SCC) :
1. Spreads more quickly and aggressively
2. About 15% of cases
3. Mostly in heavy smokers

24. ADENOCARCINOMA
Adenocarcinomas can be subdivided into more typical pulmonary adenocarcinomas with
papillary, acinar and tubular differentiation, or rare bronchoalveolar carcinoma, also termed
adenocarcinoma in situ, characterized by a distinctive growth of tumor cells along the lining
of alveolar walls. A subset of adenocarcinomas show extensive mucin production and are
termed mucinous or colloid carcinomas. The typical adenocarcinomas of the lung show
differences in degree of pleomorphism, cellular atypism, rate of mitotic figures and
formation of glandular structures, all which is used as criteria for determining the
differentiation grade (well, moderate or poor).

25. Adenocarcinoma

26. Poorly differentiated Adrenocarcinoma

27. Moderately differentiated Adrenocarcinoma

28. Well differentiated Adrenocarcinoma

29. SQUAMOUS CELL CARCINOMA
Squamous cell carcinoma is suggested to originate from metaplastic squamous epithelia in
the bronchial tree. It is defined by a variable degree of squamous differentiation, such as
keratinization or intercellular bridging. The degree of squamous differentiation provides the
basis for determining if the carcinoma is well, moderately or poorly differentiated.
Currently, four variants (papillary, small-cell, clear-cell, and basaloid) of squamous-cell
carcinoma of the lung are recognized. Of these variants, there is some evidence that the
basaloid and poorly differentiated small-cell variants may have worse prognoses than
"conventional" squamous-cell carcinomas. The papillary variant occurs more frequently as a
primarily superficial, endobronchial lesion, with a modestly better prognosis.

30. Squamous Cell Carcinoma

32. LARGE CELL CARCINOMA
Large cell carcinomas of the lung show undifferentiated morphology and are characterized
as tumors growing in sheets of relatively large and pleomorphic cells, lacking clear-cut
features of differentiation towards either adenocarcinoma or squamous cell carcinoma.
It is a heterogeneous group of undifferentiated malignant neoplasms that lack the cytologic
and architectural features of small cell carcinoma and glandular or squamous differentiation.
In most series, LCC's comprise between 5% and 10% of all lung cancers.

33. This large cell
carcinoma at autopsy
shows a large
multilobulated tumor
adjacent to the hilum.
A metastatically
involved lymph node
is present next to the
bronchus.

34. The corresponding
surgical resection shows
neoplastic cells with
abundant pale
eosinophilic cytoplasm
and a surrounding
infiltrate of
inflammatory cells
which can also be seen
among the tumor cells
in the fine needle
aspirate specimen. A
histologic section shows
a proliferation of
atypical cells along the
alveolar walls

35. SMALL-CELL CARCINOMA
Small cell carcinoma represents the end of the spectrum of poorly differentiated
neuroendocrine tumors and is a highly aggressive tumor with an extremely poor clinical
outcome independent of stage. Signs of neuroendocrine differentiation can be difficult to
visualize and the diagnosis is mainly based on morphological appearance. These tumors are
characterized by the proliferation of primitive-appearing relatively small tumor cells of about
double or triple the size of an ordinary lymphocyte. The tumor grows in haphazardly
arranged sheets of a homogeneous population of tumor cells separated by thin fibrous
septa. Necrosis is extensive and a common feature of these tumors

36. Small Cell Carcinoma

38. DIAGNOSIS AND TREATMENT
Methods of diagnosis include :
 X-Ray
 CT Scan
 PET Scan
 Biopsy
Methods of treatment include
 Surgery
 Chemotherapy
 Radiation therapy

39. Reading a Chest Xray

40. Reading a CT Scan

42. PET Scan Anatomy
spine
Spinal cord
ribs

43. Xray versus CT versus PET scan

44. PET/CT Scan showing lung cancer in three different planes

46. TREATMENT FOR NSCC
Stage Description Treatment Options
Stage I Tumor of any size is found only in the
lung
Surgery
Stage II Tumor has spread to lymph nodes
associated with the lung
Surgery
Stage III a Tumor has spread to the lymph nodes
in the tracheal area, including chest
wall and diaphragm
Chemotherapy followed
by radiation or surgery
Stage III b Tumor has spread to the lymph nodes
on the opposite lung or in the neck
Combination of
chemotherapy and
radiation
Stage IV Tumor has spread beyond the chest Chemotherapy only

48. TREATMENT FOR SCC
Limited stage :
 The cancer is localized in one specific area of the chest affecting nearby lymph nodes.
 It is treated with radiation therapy and chemotherapy
Extensive stage :
 Common stage for about 70% of the case, the tumor spread out of the lungs.
 It is treated by chemotherapy.

49. SOURCES
 "Lung Cancer" by Robert J Miller, MD, Medical Director at Wellspring Oncology
 "Lung Carcinoma" by Vivek D. Jamnik, First year M.Sc.Nursing, G.C.O.N Jalgaon
 "Lung Cancer" by Emily Bruce
 "An Overview of Epidemiology, Etiology and Classification of Lung Caner" by Dr. Shah Ashiqur
Rahman Ashiq Choudhury, Phase-A Resident, Pulmonology, BSMMU
 https://histologydrawings.blogspot.com.by/2014/02/respiratory-system.html
 http://ajplung.physiology.org/content/292/4/L984
 www.proteinatlas.org/learn/dictionary/cancer/lung+cancer+5/detail+1
 http://pathhsw5m54.ucsf.edu/case22/image223.html
 https://en.wikipedia.org/wiki/Neoplasm
 http://www.dfiles.me/asbestos-lung-histology.html
 https://en.wikipedia.org/wiki/Asbestos
 https://en.wikipedia.org/wiki/Asbestos-related_diseases
 https://en.wikipedia.org/wiki/Radon
 https://en.wikipedia.org/wiki/Squamous-cell_carcinoma_of_the_lung
 https://en.wikipedia.org/wiki/Large-cell_lung_carcinoma