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7/30/2019 Morphological Variants of Lung Cancer
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Morphological variants of Lung Cancer- Squamous cell carcinoma- Adenocarcinoma- Small Lung Cell Carcinoma (SLCC)- Carcinoid airway cancer
Stats- Leading cause of death- Men > women- Trend is increasing in women now- Peak incidence in 50s and 60s
Eitiology
- Tobacco smoke mutations- Proportional to duration, amount &
quality of smoking & deep inhaling.- 90% are smokers and 10% are non
smokers- 20 fold risk if >40cigarettes per day
- >100 fold combined with Asbestos,coal, radon, etc.
Smoke carcinogens.- Initiators Benzo-pyrenes- Promoters Phenol derivatives- Radioactive substances Polonium,
C14, K40- Overall: damage p53 and KRAS etc.
Overall causes:- Smoking*
- Occupational exposure:- Asbestosis, Nickel, chromates, mustardgas, arsenic coal-tar distillation.
- Fibrosis/scaring- TB, Pneumoconiosis, honeycomb lung
Ad.ca.- Radioactive gases
- Radon, Atomic bomb survivors.
Clinical Features:- Weight loss Cytokines.. IL6, IL8, PIF.- Cough Bronchus, obstruction,
necrosis.
- Haemoptysis Invasion, less stroma,necrosis.
ComplicationsLocal:
- Obstruction- Effusion- Pneumonia* lipid, other.- Bronchiectasis- Atelectasis lung collapse- Haemoptysis- COPD (risk)
Systemic: (paraneo symptoms)- Cachexia- Paraneoplastic syndrome- Clubbing- Pulm. Osteoarthropathy.- Bone pain
- CNS dysfunction
Bronchogenic Ca (95%)
Small cell ca. SCC 15-20%(oat cell ca)
Non Small cell NSCC 80%
Squamous cell carcinoma 20-30%
Adeno carcinoma(+Broncho-alveolar)30-40%
Large cell anaplasticcarcinoma (rare)
BronchialCarcinoidTumor (5%)
MiscellaneousTumors
(angio(sarco)ma,fibro(sarco)ma, etc) (
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SCC NSCC- early spread- NO surgery- Responds to
chemo
- Late spread localized- Staging & Surgery - OK- Does not respond to
chemo.
Pathogenesis
Cdewqd
Investigations- Imaging X-Ray, US, MRI, CT, PET- Cytology sputum, Bronchial lavage- Bronchoscopy- Biopsy Needle, excision- Tumor markers.
- Staging investigations: History, exam & CT scan chest &
abdomen
Complete blood count &differential
Serum chemistry Liver, Kidney,
Electro. & Ca+
Pulm.FT & Mediastinoscopy for
surgery.
PET Scan.
Multiple Mutations..oncogene activationcancer.
KK--RasRasCC--mycmyc
p53p53
Irritation Carcinogens Initiation Promotion Ca.
KK--RasRas
MetaplasiaDysplasia Neoplasia
Normal Hyperplasia Metaplasia
Dysplasia Mild Severe Dysplasia Malignancy
Cilia
Goblet cell
Nucleus
Loss of Cilia
& Columnar cells
Cell death.
Stratified Squamous
Epithelium (metaplasia)
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Lung cancer AP view
Lung cancer Lateral view
CT squamous cell carcinoma (NSCC
bronchogenic) central location
Adenocarcinoma peripheral (unlike squamous)
Squamous Cell Carcinoma (NSCC)- M>W
- Highly associated with smoking- Most arise near the hilum, and big bronchi
(CENTRAL) LARGE AIRWAYSMicro- Dysplasia and carcinoma in situ- Thickening and irregularity of the
bronchial mucosa may be seen with abronchoscope
- Prominent keratin production andintercellularbridges
Macro- Often have prominent necrosis and may
cavitate- Tend to spread locally and metastasize
later than other patterns
Central near hilum + cavitate
Origin in main bronchus
Spread
ClearMargin
Smoke
rslung
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Cavitation in squamous cell carcinoma
Microscopy
IF PINK SQUAMOUS CELL KERATIN!!!
CYTOLOGY (above) rest = microscopy
Keratin pearls large nests of Keratin
Note: pink (keratinized) cancer cells (dysplastic)
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Adenocarcinoma- Less associated with smoking than
squamous or small cell carcinomas, butmost
- 75% patients have a history of smoking
- Most common type of lung cancer inwomen and nonsmokers!
Gross- Peripherally located; may be associated
with a scarMicro
- Gland formation mucus- more well differentiated- Columnar or cuboidal cells with
pleomorphic nuclei, often large nucleoli- 80% contain mucin (MUCUS)Cytology- Round/ oval/cuboidal cells
- Blue!- Prominent nucleiExamin with needle biopsy as in periphery oflung! SMALL AIRWAYS
Peripheral adenocarcinoma
Peripheral Adeno
Peripheral adeno a non-smoker woman!
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Cytology
- Cuboidal cells
- Glandular shapes/ formation- BLUE! colour
- Glands- Lumen filled with mucin- Vacuolated
Glandular, cuboildal, mucus
Bronchoalveolar- A subtype of adenocarcinoma- peripherally located - arise in terminal
bronchioles or alveoli- Show appearance on CXR like
pneumonia extensive invasion of lung- Any age, both sexes equally.
Morphology:- Multiple diffuse nodules more like
pneumonia- Columnar-to-cuboidal epithelial cells that
line up along alveolar septa withoutdestruction.
- tall columnar to cuboidal epithelial cells(differentiation along linesof mucin-secreting bronchiolar cells, Clara cells,and/or type II pneumocytes)
- Malignant cells grow along septal wall ofalveoli without invading them
Clinical- Cough, hemoptysis, and pain, but
atelectasis and emphysema areinfrequent.
- Metastases are not widely disseminatedand do not occur early;
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- Overall survival rate is approximately25%.
Note:- Adenocarcinoma can progress to this- Cancer cells IN the alveoli (the cells that line
up along alveolar)- Show bronchopneumonia like diffuse
consolidation (NOT the tumour but theinflammatory response causes this)
-
The tumor cells diffusely infiltrate the alveolar
spaces mimicking a pneumonic process
Malignant cells grow along alveolar septumwithout disturbing it
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Atypical adenomatous hyperplasia(AAH):
o A form of Adenocarcinomao Cytologic atypia is less marked
o Typically
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Bronchogenic Mesothelioma (pleural)
Small Cell Lung Carcinoma (SCLC)- >95% smokers- centrally located masses near hilum
- invade/extension into the lung
parenchyma early spread to hilar
and medistinal lymph nodes- Aggressive and invasive metastatis
widespread
Paraneoplastic syndrome- These tumors are derived from
neuroendocrine cells of the lung =they express a variety ofneuroendocrine markers
- SLCC secrete neuroendocrinal paraneoplastic syndromes
Macroscopic- LARGE central airways- 70% of cases present as perihilar
mass- Extensive lymph node metastases are
common- Typically peribronchial; endobronchial
lesions are uncommon
- neuroendocrine differentiation
Microscopic
- SMALL cells- Round to fusiform shape (look like
lymphocytes) reduced cytoplasm +large relative hyperchromatic neuclei(nuclei>cytoplasm)
- Salt/ pepper granulated chromatin- nuclear molding; faint or absent
nucleoli; scant cytoplasm- Extensive necrosis
Three histologic categories:o Small cell
o Mixed small cell/large cell
o Combined small cell/adeno- or
squamous cell Carcinoma
SCLC affecting the hilar lymph nodes +bronchus
Infiltration pattern around major bronchus - Irregular border
- Spread along bronchus lymph nodes
Infiltration pattern around bronchusNote: black spots in lung = smokers lung
11
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SCC some bronchiactiac changes
Large nuclei compared to cytoplasmRound small cells
Cytology
Oat cells SCC- BAL bronchio-alveolar lavage fluid.- Gets sample of cells with brush during
bronchoscopy and stained for visualization
- Small Cell Barely any cytoplasm andmostly purple nucleus (cells are bigger thanlymphocytes)
Large nuclei
Looks like inflammatory cells
Carcinoid Tumours
Overview
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Bronchial Carcinoid Tumour:
Note: Benign gross appearance. Round cell clusters.
(Neuroendocrine cells)
- Slow growing, malignant tumour offrom cells of the neuroendocrinesystem.
- 1% to 5% of all lung tumors- Mainly occur in individuals