2. LUNG TUMORS
Primary : Benign: Hamartoma
Malignant :
95 % are Bronchogenic Carcinoma
Extremely common
Age 55-65, M:F = 2:1
Incidence is ↓in males, ↑in females
Commonest cause of cancer related death
Majority are related to smoking
Bad prognosis (5-year survival < 15%)
5% are Bronchial carcinoids, Mesenchymal tumors, Lymphoid
tumors and others
Secondary: very common
3. Classification of malignant epithelial lung
tumors :
Until recently, carcinomas of the lung were classified into two
broad groups: small cell lung cancer (SCLC) and non–small cell
lung cancer (NSCLC).
SMALL CELL LUNG CANCER: SCLC
Small Cell Carcinoma
NON SMALL CELL LUNG CANCER: NSCLC
Squamous Cell Carcinoma
Adenocarcinoma
Large Cell Carcinoma
Note: Combined patterns are possible
4. This classification has been recently replaced by
a 2015 World Health Organization classification
Histologic Classification of Malignant Epithelial
Lung Tumors (2015 WHO Classification, Simplified
Version)
Adenocarcinoma
Acinar, papillary, micropapillary, solid, lepidic predominant,
mucinous subtypes
Squamous cell carcinoma
Large cell carcinoma
Neuroendocrine carcinoma
Small cell carcinoma
Large cell neuroendocrine carcinoma
Carcinoid tumor
Mixed carcinomas
Adenosquamous carcinoma
Combined small cell carcinoma
Other unusual morphologic variants
Sarcomatoid carcinoma
Spindle cell carcinoma
Giant cell carcinoma
5. Etiology
1- Cigarette smoking – risk
Contain numerous carcinogens (Polycyclic Hydrocarbons )
Up to 90% squamous & small cell CA occur in smokers
Correlation between smoking in pack per years & lung CA
Passive smoking
Effect of carcinogen is genetically conditioned
6. Etiology
2 - Genetic Factors:
Step wise accumulation of genetic mutations triggered by
carcinogens
Earliest is inactivation of suppressor gene on chromosome 3P
Later mutations in P53 & K- RAS …etc
Activating mutations in EGFR & K-RAS in
adenocarcinoma
RB mutation in Small Cell Carcinoma
P 16/ CDKN2A inactivation in NSCLC
7. Etiology
3- Environmental Hazards :
Asbestos workers
Uranium workers
Exposure to radiation
Nickel , arsenic , chromate….etc
4- Scarring in lung tissue
( Scar Cancer ) usually adenocarcinoma
8. Diagnostic techniques for lung cancer
1- Chest X ray, CT, …..etc
2- Sputum Cytology & bronchial wash
3- Bronchial biopsy: Biopsy taken by bronchoscope
4- Transbronchial biopsy: forceps down bronchoscope into
lung parenchyma to take a biopsy.
5- Transcutaneous needle biopsy
6 -Open lung biopsy
10. Gross appearance of most types :
Central
Thickening mucosa
Later may show irregular whitish warty lesion ulceration
Infiltration of wall of bronchus into lung
Hemorrhage & necrosis may be seen
Peripheral:
Consolidated rounded lesion
13. 1- SQUAMOUS CELL CA :
Male> female, > 90% in smokers
Usually central location, Warty ± cavitation
May present with HYPERCALCEMIA
Precursor Lesion:
Squamous metaplasia Dysplasia
Carcinoma in Situ Squamous cell CA
Histology :Various degrees of squamous differentiation ±
Keratin formation
Prognosis better than Small Cell CA
15. Squamous cell carcinoma with nests of polygonal cells with pink
cytoplasm and distinct cell borders. The nuclei are hyperchromatic
and angular.
16. 2- ADENOCARCINOMA :
Commonest in females
Least associated with smoking
Usually peripheral but may be central
Growth is slower than squamous but widely metastasize
Types include :
A- Usual bronchial derived ( 80%) ± mucin.
May be:
Acinar
Papillary
Solid
17. Adenocarcinoma of the lung.
The glandular structures formed by this neoplasm are
consistent with a moderately differentiated
adenocarcinoma
18. Multifocal diffuse or localized nodule .
Peripheral location with diameter of 3 cm or less
May present as pneumonic consolidation
Growth along alveolar walls without destruction of walls
(non-invasive)
Prognosis is better than usual adenocarcinoma.
B- Bronchioloalveolar CA/
Adenocarcinoma in situ
19. Adenocarcinoma in situ/Bronchioalveolar Carcinoma
composed of columnar cells that proliferate along the framework
of alveolar septae. The neoplastic cells are well-differentiated with
no destruction of alveolar architecture or stromal invasion.
20. Precursor Lesions in Adenocarcinoma:
? Presence of Bronchioalveolar Alveolar Stem Cells (BASC)
expansion after lung injury
Atypical Adenomatous Hyperplasia (AAH) →
Adenacarcinoma in situ/ Bronchioalveolar CA →
Adenocarcinoma
AAH has same 3P deletion & K-RAS mutation similar to CA
21. 3- LARGE CELL ANAPLASTIC CARCINOMA :
Poorly differentiated tumors
Difficult to type, may need special immunostains.
Incidence is about ( 10-15 % )
Probably poorly differentiated Squamous Cell CA or
Adenocarcinoma
Prognosis is poor
22. 4- SMALL CELL CARCINOMA (SCLC)
Male > Female , > 90% in smokers
Arise from neuroendocrine cells
Central mass
Most aggressive, necrosis, metastasize early
Most frequent type with ectopic hormones
Cytology: Crush artefact, nuclear molding
Histology : Small blue cells (Oat Cell CA), mitosis++,
necrosis++
23. Small cell anaplastic (oat cell) carcinoma
Arising centrally in this lung and spreading extensively
(soft, lobulated, white to tan appearance)
24. Spread of lung cancer :
1- Local extension: pleura, pericardium & mediastinum, nerves
& vessels
2- Lymph node metastases: regional L.N., bronchial, tracheal
and mediastinal
3- Distant metastases: Adrenal (> 50% ), Liver, Brain, bone …
25. Staging of Lung CA
BASED ON TNM STAGING SYSTEM :
Stage I = T1 N0 M0 (tumor <3cm.)
Stage II = T2 N1 M0 ( tumor 3cm.)
Stage III = T3 N1 M0 ( tumor involving chest wall,
mediastinum, contralateral nodes….etc.)
Stage IV = Any T, any N, M1
26. T1 Tumor <3 cm without pleural or main stem bronchus involvement
T2 Tumor >3 cm or involvement of main stem bronchus 2 cm from carina, visceral pleural
involvement, or lobar atelectasis
T3 Tumor with involvement of chest wall (including superior sulcus tumors), diaphragm,
mediastinal pleura, pericardium, main stem bronchus 2 cm from carina, or entire lung
atelectasis
T4 Tumor with invasion of mediastinum, heart, great vessels, trachea, esophagus, vertebral
body, or carina or with a malignant pleural effusion
N0 No demonstrable metastasis to regional lymph nodes
N1 Ipsilateral hilar or peribronchial nodal involvement
N2 Metastasis to ipsilateral mediastinal or subcarinal lymph nodes
N3 Metastasis to contralateral mediastinal or hilar lymph nodes, ipsilateral or contralateral
scalene, or supraclavicular lymph nodes
M0 No (known) distant metastasis
M1 Distant metastasis present
TNM, Lung
27. Paraneoplastic Syndrome
Present in 10% of tumors, most in SCLC
Ectopic hormone production :
ADH , ACTH, Gonadotrophic H….in SCLC
PTH →↑ Calcium in Squamous cell CA
Migratory thrombophlebitis, DIC in AdenoCA
Digital clubbing, hypertrophic osteoarthropathy
Neuromuscular disorders …etc in SCLC
28. Carcinoid Tumor: (Low grade neuroendocrine Ca.)
Younger age than CA , 5% of lung tumors
Arise from neuroendocrine Kulchitsky cells lining bronchi
Most arise in bronchial wall, fill lumen or extend into lung
Histology: Typical Carcinoid : Uniform small round cells, absent
mitoses, arranged in nests & cords
Atypical Carcinoid : Show mitoses, necrosis, atypia
Clinical course:
Obstruction & atelectasis, Infection
Most cases are hormonally inactive, but few produce the Carcinoid
syndrome (characterized by intermittent attacks of diarrhea, flushing,
and cyanosis)
Surgery curative in most cases
About 30 % may metastasize to lymph nodes ± distant metastases
31. Continuous assessment
What type of lung cancer fits this description? The tumour
cells originate from neuroendocrine (Kulchitsky) cells. It is
associated with smoking and is centrally located along the
bronchial airways. There is an association with
paraneoplastic syndromes, for example Cushing’s.
a. Adenocarcinoma
b. Carcinoid tumour
c. Squamous cell carcinoma
d. Small cell carcinoma