PULMONARY TUMORS

Kathryna Lesley T. Ayro

INTRODUCTION
Majority are malignant
Currently:
o Most frequently diagnosed
major cancer
o Most common cause of
cancer mortality
Carcinogenic effects of cigarette
smoke
o Lung cancer incidence and
mortality
o Prevalence of various
histologic types
ETIOLOGY
Cigarette smoke
o Frequency:
Amount of daily
smoking tendency to
inhale
Duration of smoking
habit
o 10-60 fold greater risk
o Women are more
susceptible
o P53 mutations
Industrial hazards
o High dose ionizing radiation
o Uranium
o Asbestos
Air pollution
o Radon- indoor air pollution
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Molecular genetics
o Dominant genetics
C-MYC, KRAS, EGFR,
C-MET and c-KIT
o Deletion of inactivated
tumor suppressor genes
P53, RB1, p16
(INK4a)
Chromosome 3p
FHIT, RASSF1A
Telomerase activity
is increased
o Small cell carcinoma
C-KIT- over
expressed, rarely
mutated
MYCN
MYCL
P53
RB
BCL2
3p
o Non small cell carcinoma
EFGR
KRAS
P53
P16INIK4a
LKB1, PTEN, TSC (mTOR pathway)
o Activation of signal
transduction molecules
AKT
Phosphatidylinositol3-kinase
ERK1/2
STAT5
Paxillin

Precursor lesions
Squamous dysplasia
CIS
Atypical
adenomatous
hyperplasia
Diffuse idiopathic
neuroendocrine cell
hyperplasia

Histologic Classification of Malignant

Epithelial Lung Tumors
Squamous cell carcinoma
Small-cell carcinoma
Combined small-cell carcinoma
Adenocarcinoma
Acinar; papillary,
bronchioloalveolar, solid, mixed
subtypes
Large-cell carcinoma
Large-cell neuroendocrine
carcinoma
Adenosquamous carcinoma
Carcinomas with pleomorphic,
sarcomatoid, or sarcomatous
elements
Carcinoid tumor
Typical, atypical
Carcinomas of salivary gland type
Unclassified carcinoma

MORPHOLOGY
Central/hilus of the lung
o Small cell carcinoma
o Squamous cell carcinoma
Peripheral

Adenocarcinomas

SQUAMOUS CELL CARCINOMA

Males
Smoking history
p53 mutations

LARGE CELL CARCINOMA

ADENOCARCINOMA

females
non smokers
peripherally located
small than SCCA
grow slowly but with early and
wider metastasis
may be associated with scarring
KRAS mutations
Pure or mixed
Patterns:
o Acinar
o Papillary
o Bronchioalveolar
o Solid with mucin production

Undifferentiated
Lacks cytologic differentiation
SMALL CELL CARCINOMA

Bronchioalveolar carcinoma
Terminal bronchioalveolar region
Single to multipla small nodules
o Pneumonia-like
consolidation
Does not involve major bronchi
Emphysema and atelectasis are
not common
Subtypes:
o Mucinous

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Mucin secreting clara

cells and type 2
pneumocytes
Aerogenous spread
Non mucinous

Highly malignant
Cigarette smoking
Major bronchi and peripheral lung
No known pre invasive phase
Most aggressive
Widely metastasizing
Associated with ectopic hormone
production
P53 and RB gene
Sheets of cells
Cells with scant cytoplasm
Molded nuclei
Uniform fine chromatin
absent nucleoli
>10mitoses/10 HPF
Necrosis (not shown)
Few dense- cored granules by EM

CARCINOID TUMOR

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Younger patients
Equal sex incidence
Low grade
Typical or atypical
Features:

Intraluminal growth
Metastasize
Elaborate vasoactive
amines
Ribbon or sheet architecture
Polygonal cells
Moderate cytoplasm
Regular nuclei
Finely stippled chromatin
Small nucleoli
Delicate capillary stroma
<2mitoses/ 10 HPF
Chromogranin +
By EM, many dense-colored,
membrane- bound granules are
found in the cytoplasm (arrows).
o
o
o

ATYPICAL CARCINOID
Ribbon or sheet architecture
Nuclei resemble carcinoid tumors
but show hyperchromatism, some
irregularity in shape
Moderate cytoplasm
Focal necrosis (left)
2-10 mitoses/HPF
HAMARTOMA
Benign neoplasm
Well circumscribed
Composed of mixture of cartilage,
fat, and fibromyxoid tissue
Sharply circumscribed and
surrounded by normal lung
(bottom)
Cartilage lies to the right

 Lobules of fibromyxoid tissue to

the left are covered by nonneoplastic respiratory epithelium
(arrow).

Pleural
effusion
Hoarseness

PARANEOPLASTIC SYNDROMES
The hormones or hormone-like factors
elaborated include:

ADH
ACTH
PTH
Calcitonin
Gonadotropins
Serotonin

Pancoast tumors
o Apical lung cancers
Superior pulmonary
sulcus
Invade neural
structures
Severe pain in
ulnar nerve
distribution
Horners syndrome
Enophthalmus
Ptosis
Miosis
Anhidrosis
Local Effects of Lung Tumor Spread
Clinical
Pathologic Basis
Feature
Pneumonia,
Tumor obstruction of
abscess,
airway
lobar

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collapse
Lipoid
pneumonia

Dysphagia
Diaphragm
paralysis
Rib
destruction
SVC
syndrome
Horner
syndrome
Pericarditis,
tamponade

Tumor obstruction;
accumulation of cellular
lipid in foamy
macrophages
Tumor spread into pleura
Recurrent laryngeal
nerve invasion
Esophageal invasion
Phrenic nerve invasion
Chest wall invasion
SVC compression by
tumor
Sympathetic ganglia
invasion
Pericardial involvement

International Staging System for Lung

Cancer
T1
Tumor <3 cm without pleural or
main stem bronchus
involvement (T1a, <2 cm; T1b,
23 cm)
T2
Tumor 37 cm or involvement of
main stem bronchus 2 cm from
carina, visceral pleural involvement,
or lobar atelectasis (T2a, 35 cm;
T2b, 57 cm)
T3
Tumor >7 cm or one with
involvement of chest wall (including
superior sulcus tumors), diaphragm,
mediastinal pleura, pericardium,
main stem bronchus 2 cm from
carina, or entire lung atelectasis, or
separate tumor nodule(s) in the

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same lobe
Tumor with invasion of mediastinum,
heart, great vessels, trachea,
esophagus, vertebral body, or carina
or separate tumor nodules in a
different ipsilateral lobe
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 distant metastasis
M1 Distant metastasis (M1a, separate
tumor nodule in contralateral lobe or
pleural nodules or malignant pleural
effusion; M1b, distant metastasis)
STAGE GROUPING
Stage Ia
T1
N0
M0
Stage Ib
T2
N0
M0
Stage IIa
T1
N1
M0
Stage IIb
T2
N1
M0
T3
N0
M0
Stage IIIa
T13
N2
M0
T3
N1
M0
Stage IIIb
Any T
N3
M0
T3
N2
M0
T4
Any N
M0
Stage IV
Any T
Any N
M1
T4

PLEURAL EFFUSION
Occurs in:

Increased hydrostatic pressure, as in

congestive heart failure

Increased vascular permeability, as

in pneumonia
Decreased osmotic pressure, as in
nephrotic syndrome
Increased intrapleural negative
pressure, as in atelectasis
Decreased lymphatic drainage, as in
mediastinal carcinomatosis

Condition

Type of
fluid
Inflammatory
Serofibrin Serofibrin
ous
ous
pleuritis
exudate
Suppurati Pus
ve
pleuritis
(empyem
a)
Hemorrha Bloody
gic
exudate
pleuritis
Non inflammatory
Hydrothor Transudat

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ax
Hemothor
ax

e
Blood

Chylothor
ax

Chyle
(lymoh)

Ruptured aortic
aneurysm,
trauma
Tumor obstruction
of normal
lymphatics

MALIGNANT MESOTHELIOMA

PNEUMOTHORAX

Common
associations
Inflammation in
adjacent lung
Collagen vascular
dse
Suppurative
infection in
adjacent lung

Air/ gas in pleural cavities

Spontaneous, traumatic, therapeutic

PLEURAL TUMORS

Primary VS secondary
Secondary- more common
o Metastatic tumors

SOLITARY FIBROUS TUMOR

Tumor

CHF

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BENIGN
Localized
Not related to asbestos exposure
Gross:
o Solid tumor with occasional
cysts filled with viscid fluid

Microscopic:
o Whorls of reticulin and
collagen fibers
o CD34+, cytkeratin-

Arise from visceral or parietal pleura

Asbestos exposure
o Require 25-45 years of
exposure
o Poorer prognosis for patients
who also smoke
Markers of asbestos exposure
o Asbestos bodies
o Asbestos plaque
Morphology
o Widespread pleural
involvement
o Extensive pleural effusion
Microscopic
Types:
o Sarcomatoid
o Epithelial
o mixed
e.valerio