lung and pleural tumours

Question 1

aetiology?

Answer 1

 Smoking:
• Epidemiological: Cumulative dose
• Pathology: Premalignant change common
• Toxins: Benzopyrene, nitrosamines, nickel,
cadmium, vinyl chloride
 Genetic susceptibility
 Industrial hazards:
• Radiation: (Hiroshima, Uranium)
• Asbestos:
• Nickel, Arsenic, Beryllium, silica
 Air Pollution:
• Radon gas, domestic coal fires, diesel fumes
 Lung Fibrosis: IPF (CFA/UIP) – 14X RR

Question 2

pathology?

Answer 2

Pathology important in staging
• Frozen section; mediastinoscopy
• Resection: size, pleural + nodal
involvement, atelectasis, metastases,
malignant effusion

Question 3

benign?

Answer 3

papilloma

adenoma

Question 4

malignant?

Answer 4

Squamous carcinoma
Variants:Papillary, Clear cell, Small cell, Basaloid

Small cell carcinoma
Variant:Combined

Adenocarcinoma
Variants: Papillary, Bronchioalveolar,Solid carcinoma with
mucus, Mixed, Foetal type, Mucinous (colloid), Mucinous
cystadenoma, Signet ring cell, Clear cell

Large cell carcinoma
Variants: Neuroendocrine,BasaloidLymphoepithelioma-like,
Clear cell,Rhabdoid

Adenosquamous carcinoma

Pleomorphic, sarcomatoid carcinoma

Question 5

macroscopoic appearances?

Answer 5

 Usually around hilus of lung (75%
occur in 1, 2, 3 bronchi)
 intraluminal mass
 intraparenchymal mass

Question 6

metastasis?

Answer 6

Distant metastasis sites include
adrenal (50%), liver (40%), brain
(20%), bone(20%)

Question 7

SCC

Answer 7

M>F, Smokers+++
 Often central, hilar masses- larger than
other lung cancers, but spread later.
 50% show signs of bronchial obstruction,
cavitate / necrosis.
 Keratin production, intercellular bridges
characteristic
  Calcium caused by PTH related protein

 80% Male. 98% smokers.
 Typically central.
 Histology:Small hyperchromatic cells,mits++,
fine chromatin pattern (neuroendocrine)
 ICC: keratin+ve. neuroendocrine markers e.g.
neuron- specific enolase,chromogranin,CD56
 EM: scattered dense core secretory granules.
May secrete hormones (ACTH, 5HT, ADH, HCG,
PTH)
 Poor prognosis: <2% 5year survival.

Question 8

adenocarcinoma?

Answer 8

50% of all tumours in females ( in
prevalence. M=F)
 non-smokers Often peripheral, can
involve pleura. Usually poorly defined
 Many associated with a scar
 Gland formation, papillae, mucin, but
wide range of patterns (see
classification)

Question 9

bronchioloalveolar carcinoma?

Answer 9

 Variant of adenocarcinoma, occurs in
terminal brochioalveolar regions.
Represents between 1% of all lung
cancers. M=F.
 Reclassified in 1999 WHO
 Peripheral, multiple nodules may coalesce
to produce a pneumonia-like
consolidation.
 Histology-distinct
 5 year survival- excellent.

Question 10

large cell carcinoma?

Answer 10

 Pleomorphic tumours without definite
evidence of squamous or glandular
differentiation (often diagnosis of
exclusion).
 Probably poorly differentiated variant of
other tumour types.
 Large, polygonal cells, vesicular nuclei.
 Variants: Giant cell carcinoma, Clear cell
carcinoma, Spindle cell carcinoma.

Question 11

EGFR

Answer 11

 Important to distinguish between
adenocarcinoma and squamous cell
carcinoma.
 Subset of adenocarcinomas contain
EGFR mutations.
 These tumours are responsive to
tyrosine kinase inhibitors such as
erlotinib (Iressa).

Question 12

subtyping?

Answer 12

 Mucin histochemistry (Diastase PAS)
 Adenocarcinoma
 Immunohistochemistry
 TTF – 1+ Adenoca. Small cell ca (NOT SQ.CA)
 CK 5/6+ Squamous ca.
 P63+ Squamous ca.

Question 13

carcinoid tumour (type of adenocarcinoma)

Answer 13

 Formerly known as bronchial adenomas.
Account for <5% of 1 lung tumours.
Derived from neuroendocrine cells of
bronchial tree.
 Younger <40years.
 M=F.
 No association with smoking.
 Usually divided into 2 types
• Typical
• Atypical

Question 14

central carcinoid?

Answer 14

 Commonest. Usually adults.
 Slow growing solitary mass. Usually <3cm. Collar
button lesion (penetrates bronchial wall to fan
out). Polypoid. Vascularity++
 Small uniform cells with central nuclei. Grows in
compact nests, cords, solid pattern.
 Chromogranin +ve, Synaptophysin +ve.
 Dense core granules on EM. May be hormonally
silent or secrete ACTH.
 Regional LN+ in 5%. Distant mets rare.
 70-80% 5 year survival.

Question 15

atypical carcinoid?

Answer 15

 Can be central or peripheral but with
increased mitoses,
nuclear hyperchromasia, or
necrosis.
 LN mets in 60%
 60% 5 yr survival

Question 16

uncommon tyumours?

Answer 16

 Adenosquamous carcinoma
 Salivary gland type carcinoma
• Mucoepidermoid
• Adenoid cystic
• Pleomorphic adenoma
 Mesenchymal tumours (0.1%)
 Malignant lymphoma

Question 17

malignant mesothelioma?

Answer 17

 90% associated with asbestos exposure.
 Chronic asbestos exposure carries a 2-3% risk of
mesothelioma;
 Risk is not increased by smoking
 Amphibole asbestos most carcinogenic.
 Long latency between exposure and tumour (25-
45years).
 Multiple grey/white, ill defined nodules- may grow
extensively to fill pleura cavity and encase the lung.
Pleural effusion present.
 Prognosis poor 50% 1year survival. Very few survive
2 years.

Question 18

malignant mesothelioma?

Answer 18

 Histological Subtypes:
• Epithelial:
• Sarcomatoid:
• Mixed: Combination of first two.

Question 19

distinguish pleural mesothelioma from pulmonary adenocarcinoma?

Answer 19

 Histological stains:
 Immunohistochemistry:
• MM usually Calretinin, Thrombomodulin,
Cytokeratin5/6+ve
• Adenocarcinoma - CEA, Leu MI, Ber-EP4 +ve
 Electron Microscopy: Mesothelial cells have
long, slender villi.