LUNG CANCER

• Affects 94,000 males and 78,000 females

LUNG CANCER
(UPDATED 2009)
Rommel D. Bayot, MD, FPCP, FPCCP
Philippine Heart Center
FEU-NRMF Medical Center
(US), 86% die w/in 5 yrs of diagnosis
• Leading cause of cancer death in both men
and women in all races
• Incidence peaks between 55 and 65 yrs old
• Accounts for 31% of all cancer deaths in
men and 25% have disease spread to
regional lymph nodes & > 55% have distant
metastases

LUNG CANCER LUNG CANCER

• WHO classification :
• 5- year survival rate 1. Squamous or epidermoid carcinoma
2. Small cell (or oat cell) carcinoma
- local disease: 50%
3. Adenocarcinoma (including
- with regional disease: 20% bronchioalveolar)
- overall: 14% 4. Large cell (or large cell anaplastic)
carcinoma
5. Others: Undifferentiated Carcinoma, Carcinoid,
Bronchial Gland Tumors (Adenoid Cystic Carcinoma.
Mucoepidermoid Tumors)

LUNG CANCER Non-small cell CA

• Histologic Classification:
1. Small cell carcinoma- at presentation, have already
spread such that surgery is unlikely to be curative
- usu. present as central masses w/ endobronchial
growth
- managed by chemotherapy with or w/o
radiotherapy
2. Non-small cell varieties (Squamous, adenocarcinoma,
large cell, bronchioalveolar, and mixed versions)
• Found to be localized at the time of presentation-
may be cured with either surgery or radiotherapy
• Do not respond as well to chemotherapy as small cell
CA
• 90% of patients w/ lung CA of all histologic types are
current or former smokers
• ADENOCARCINOMA- most common lung CA arising
in non smokers, in women, in young patients (< 45
yrs)
• ADENOCARCINOMA- have replaced squamous cell
CA as the most frequent histologic subtype for all
sexes and races combined

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 Non small cell CA
• In non-smokers with adenoCA, the possibility of
other primary sites should be considered
• Squamous and small cell CA usu present as central
masses w/ endobronchial growth
• Adenocarcinomas and large cell CA tend to present
as peripheral nodules or masses, frequently with
pleural involvement
• Squamous and large cell CA cavitate in 10-20% of
cases
Biology of Lung CA
• Lung Cancer is the leading cause of death in
industrialized countries
• Squamous carcinoma: Conversion of normal
bronchial epithelium by oncogenic triggering
• Adenocarcinoma: development from a
premalignant precursor lesion
(Atypical Adenomatous Hyperplasia)
Hallmarks of Human Cancer Cells
• Chromosomal alterations
• Chromosomal instability
• Tumor suppressors
• Alterations in DNA methylation
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Biology of Lung Cancer
Lung CA
• Molecular Biologic Studies
– Overt cancers carry multiple genetic and
epigenetic alterations
• Epidemiologic Studies
– Most cases of primary lung cancer: caused by
smoking
– Carcinogens in smoke: induce multiple genetic
alterations through DNA adducts
Chromosomal Alterations
• Critical molecular events
– Inactivation of tumor suppressor genes
– Activation of dominant oncogenes
• Lung cancers share similar chromosomal
changes/ histologic type specific characteristic
alterations
 Chromosomal Losses Chromosomal Gains
• Non Small Cell Lung Ca • Non Small Cell Lung Ca
–3p, 8p, 9p, 13q, 17p –1q, 3q, 5p, 8q

• Small Cell Lung Ca • Small Cell lung Ca

–3p, 4q, 5q, 8p, 10q 13q, 17p –3q, 5p, 8q

Tumor Suppression Knudson Hypothesis

• 2 events • An individual with an inherited predisposition
– Deletion of a large chromosomal DNA segment of to cancer inherits one normal and one mutant
one allele tumor suppressor gene
– Smaller mutation or epigenetic inactivation of the • A non-predisposed individual must acquire
other allele somatic mutations in both the maternal and
• Tumor Suppressor Gene paternal suppressor gene alleles to initiate
– Genes whose reduced function can lead to tumor formation
neoplastic change

Alterations in DNA Methylation p53/ MDM2/ p14ARF Pathway

• Cytosine-Guanosine (CpG) dinucleotide
– Contained in promoter regions
– Protected from methylation in normal cells
– Methylation associated with loss of expression of
the particular gene; aternative mechanism for loss
of tumor suppressor gene function
– 9p21, 13q14, 17p13
• P53 Tumor Suppressor Gene
– Guardian of the genome; safeguard against
genetic instability
– Activated p53 may participate directly in DNA
repair via induction of p53R2
– Activated p53 transactivates genes that may
impose cell cycle arrest in G1 and G2
– Smoking induces p53 mutations

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 p53/ MDM2/ p14ARF Pathway
– Correlates with poor prognosis after surgical • p14ARF
treatment of lung cancers, especially in stage I
cancers. – Exerts growth inhibition by inhibiting the
• MDM2 ubiquitin E3 ligase activity of MDM2
– Ubiquitin E3 ligase; oncogene – Deletion may promote tumor-promoting
– Interacts with p53 and targets the p53 protein for activity of oncogenes
degradation
– Paradoxically in association with a favorable
prognosis

Retinoblastoma Proteins
• p16INK4A
– Maintains RB in phosphorylated state
– Exerts tumor suppressor activity only in the
presence of wild-type RB
– p16INK4A-RB: critical regulator of cell cycle
progression
– Alterations in RB detected in 90% of SCLCs
• Transforming Growth Factor - β
– Inhibits cell proliferation of normal epithelial cells,
including bronchial and peripheral lung epithelial
cells, thru inductions of CDK inhibitors
• Cell Cycle Check Points
– Induce arrests/ delay of cell cycle progression;
provide time for DNA repair

Epidemiology of Lung CA
• Most Lung CA are caused by carcinogens and
tumor promoters ingested via cigarette smoking
• Relative risk of developing lung CA is ↑ 13x by
active smoking & 1.5x by long term passive
Epidemiology of Lung Cancer smoking
• Lung CA death rate is related to the total cigarette
pack years ( risk is ↑60-70x for smoking 2
packs/day for 20 yrs compared to non smoker)
• Risk of dev lung CA decreases with cessation of
smoking but may never return to nonsmoker level

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 Epidemiology of Lung CA
• Increase in lung CA rate in women is
associated with rise in cigarette smoking
• Women have a higher relative risk per given
exposure than men (↑1.5 x) likely due to
higher susceptibility to tobacco carcinogens in
women
Epidemiology of Lung CA
• Human occupational causes
– Arsenic, Asbestos, Chromates, Chloromethyl
ethers, Nickel, Polycyclic Aromatic hydrocarbons,
Radon progeny
• Outdoor air pollutants
– Combustion-related carcinogens
• Indoor air pollution
– Asbestos, Radon, Cigarette smoke, Fumes from
cooking stoves
•* Older age groups
– Rates continue to increase in both sexes
– Rates of increase decelerating more significantly
in men
• Younger age groups
– Rates decreasing; decreases more pronounced for
men
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* Epidemiology of Lung CA
• The present pandemic of lung cancer followed
the introduction of cigarettes
• Role of carcinogens in disease causation
• First identified occupational respiratory
carcinogen: Radon
* Patterns of Occurrence
Temporal Trends
• Differing epidemic patterns in men and
women
• Epidemic among women followed that of men
• Lung Cancer: most frequent cause of female
cancer mortality
Epidemiology of Lung CA
Race and Ethnicity
– Rates similar among African American and white
women
– Rates 50% higher among African American men
than among white men
– Mortality rates:
Hispanics, Native Americans,
Asians/ Pacific Islanders > African
Americans and non Hispanic whites
 Epidemiology of Lung CA
Geographic Patterns
– Most common in developed countries
– North America, Europe > Africa, South America
– Rates tend to be highest in urban areas; costal
areas
Occurrence by Histologic Type
– Adenocarcinoma: now the most common
histologic type; most common type in females
– Squamous Cell: more common type in males
than females
– Increasing rates of Adenocarcinoma:
• Changes in cigarette smoking behavior
• Features of cigarettes
A Carcinogenic Pathway
• AAH → small, focal BAC → invasive AdenoCa
• Atypical Adenomatous Hyperplasia (AAH)–
most common precursor to Adenocarcinoma
• Bronchio-Alveolar CA (BAC) – low prevalence;
includes AAH as precursor step
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Occurrence by Histologic Type
– Dose-response relationship (number of cigarettes
smoked) steepest for Small Cell Undifferentiated
Carcinoma
– Chloromethyl ethers, Radon exposure exhibit
specificity for Small Cell Lung Cancer
Epidemiology of Lung CA
• Changes in cigarette characteristics
– Puff volume increased
• Change in deposition patterns (peripheral airways
and alveoli)
– Nitrate levels in tobacco smoke increased
• Nitrogen oxide production increased
• Increased dose of Nitrosamine 4-
(methylnitrosamino)-1-(3-pyridyl)-1-butanone
(NNK)
*Etiology of Lung Cancer
• Exposure to etiologic (or protective) agents
• Individual susceptibility to these agents
Environmental and Occupational Agents
• Compared to never smokers, smokers have a
20-fold increase in lung cancer risk
• Risk increases with duration of smoking and
number of cigarettes smoked per day
• Stronger effect of duration of smoking than
amount smoked per day
• Smoking Cessation
– Risk decreases among those who quit smoking
compared to those who continue
• The Changing Cigarette
– Unfiltered → filtered cigarettes
• Cellulose acetate, charcoal
– “Light” or “mild” labels
– Cigarette tar: condensable residue of cigarette
smoke
• Those smoking > 22 mg had the highest risk, after
adjustment for smoking amount and for age of
starting of smoke
– Lee:
• Risk reduction estimated for smokers of filter vs
nonfilter cigarettes (decades ago)
– Changes in cigarette design and
manufacturing over the last 50 years had not
benefited public health
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Environmental and Occupational Agents
• Tripling the number of cigarettes smoked per
day was estimated to triple the risk; tripling
the duration of smoking was estimated to
increase the risk 100x
• Starting at younger age have a greater
likelihood of becoming heavier smokers and
remaining smokers
– Bross and Gibson:
• Filter cigarettes provided some reduction for
lung cancer risk
– Hammond and colleagues:
• Lung cancer risk and tar yield of products
– Low yield (<17.6 mg/ cigarette)
– Intermediate
– High yield (25.8 – 35.7 mg/ cigarette)
• Passive smoking/ environmental tobacco
smoke/ secondhand smoke
– Nonsmoking spouses married to smokers were
30% likely to develop lung cancer
– More weakly associated with lung cancer than is
active smoking; lower doses of carcinogen
– There is NO threshold for tobacco carcinogenesis
• Diet
– Specific micronutrients may have anti
carcinogenic activity – Alcohol drinking*
– Tomatoes, cruciferous vegetables • Highest consumption categories associated
• Reduces risk with increased risk
– β - carotene
• Increased risk
– Lower BMI
– Vitamin C • Increased lung cancer risk relative to heavier
• Protective association persons
– Vitamin A – Concomitant effects of smoking (?)
• Studies yield null findings

Occupational Carcinogens for Lung CA

• Environmental exposures Proven Suspected

Arsenic Acrylonitrile
– Occupational exposures
Asbestos Beryllium
– Asbestos Bis(chloromdethyl)ether Vinyl chloride
– Radiation Chromium Silica
– Air pollution Mustard gas Iron ore

• Atmospheric air pollution Nickel Wood dust

• Indoor air pollution Polycyclic aromatic hydrocarbon

Ionizing radiation

Asbestos * Radiation

• Fibrous, naturally occuring silicate material • Types of Radiation

• Peak incidence occur 30 -35 years after initial – Low Linear Energy Transfer (LET)
exposure • X-rays
• γ-rays
• In combination with smoking, act • Associated with higher risk when exposure occur at
synergistically to increase lung cancer risk higher dose rate
– Mechanism: – High Linear Energy Transfer (LET)
• Alter deposition pattern in the lung • Neutrons
• Enhance retention of asbestos fibers • Radon
• Nonthreshold dose-response relationship

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 Air Pollution Host Factors
• Atmospheric Air Pollution • Genetic susceptibility
• Polycyclic aromatic hydrocarbons, arsenic, – History of lung cancer predicts increased risk;
nickel, chromium mendelian codominant autosomal gene
• Indoor Air Pollution – Genetic factors may be more important at
– Most important indoor air pollutants in younger ages; association stronger in ages 40 – 59
never smokers: years than older persons
• Passive smoking
• Radon
• Others: asbestos, unprocessed solid fuels

Scheme linking nicotine addiction and lung cancer via

tobacco smoke carcinogens and their induction of
multiple mutations in critical genes
• HIV and Lung Cancer
Persistence – Greater than 2 fold increased risk
Cigarette miscoding
smoking
Metabolic
activation Mutations and other – Predominance of non small cell lung ca
nicotine Changes: RAS, MYC,
• Adenocarcinoma
PAH, NNK and DNA Lung
addiction Other carcinogens adducts p53, p16, RB, FHIT, Cancer
And other critical genes
Metabolic
• Squamous cell
Repair
– Most are males
detoxification

Excretion Normal DNA Apoptosis

– Median age of 45 years or less

• HIV and Lung Cancer • Acquired Lung Diseases and Lung Ca *

– Potential reasons for the increased risk: – Diseases that obstruct airflow
• HIV acting as viral carcinogen • COPD
• Defective immune surveillance – Diseases that restrict lung capacity
• Recurrent opportunistic infections and • Pneumoconioses
parenchymal lung inflammations leading to • Presence of silicosis is associated with an
inflammatory foci and scar carcinomas increased risk

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 • Screening for Lung cancer

Bronchogenic Carcinoma – There is no role for screening for lung

cancer, even in high risk individuals
American Cancer Society
US Preventive Services Task Force

Presenting Symptoms of Bronchogenic

Carcinoma
– Sputum cytology, chest radiograph
Symptoms Percentage of Patients
– LD - CT
• The thinner the slice, the more noncalcified Cough 45 – 75%
nodules are detected Weight loss 8 – 68%
• Consistently detected NSCLC as stage IA in 60 – Dyspnea 37 – 58%
90% of cases; major improvement in 5-year
survival Hemoptysis 27 – 57%
Chest pain 27 – 49%
Hoarseness 2 – 18%

Clinical manifestations
• Peripheral growth of primary tumor may
cause:
1. pain from pleural or chest wall involvement
(malignant pleural effusion)
2. cough
3. dyspnea
4. symptoms of lung abscess resulting from
tumor cavitation

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 Clinical manifestations
• Central or endobronchial growth of primary
tumor may cause:
1. Cough
2. Hemoptysis
3. Wheeze and stridor
4. Dyspnea
5. Post-obstructive pneumonitis (fever and
productive cough)

Pancoast’s (Superior Sulcus Tumor) Paraneoplastic Syndromes In Lung CA

Syndrome Syndrome Histologic Type

• Results from local extension of a tumor (usually Squamous Endocrine and Metabolic Cushing syndrome Small cell CA
cell CA) growing in the apex of the lung SIADH Small cell CA
• Involve the 8th cervical, 1st and 2nd thoracic nerves Hypercalcemia Squamous cell CA
• Present with shoulder pain that cha. radiates in the ulnar Gynecomastia Large cell CA
distribution of the arm
Connective tissue Clubbing & hypertrophic Squamous cell, adenoCA,
• Often with radiologic destruction of the 1st and 2nd ribs
pulmonary large cell
• Other problems of regional spread: osteoarthropathy
- Superior vena cava syndrome from vascular obstruction Neuromuscular Peripheral neuropathy Small cell CA
- Precordial and cardiac extension w/ tamponade Subacute cerebeller Small cell CA
- Arrhythmia or cardiac failure degeneration,
- Lymphatic obstruction with pleural effusion Myasthenia (Eaton- Small cell CA
- Lymphangitic spread through the lungs with hypoxemia and Lambert),
dyspnea Dermatomyositis
All

Paraneoplastic Syndromes In Lung CA

Cardiovascular Thrombophlebitis Adenocarcinoma

Non-bacterial
verrucous endocarditis

Hematologic Anemia All Staging of Primary Tumor

DIC
Eosinophilia
Thrombocytosis
Cutaneous Acanthosis All
nigricans
Erythema gyratum

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Primary Tumor TNM Staging for NSCLC
Tx Primary tumor cannot be assessed, or tumor proven by the
Primary Tumor TNM Staging
presence of malignant cells in sputum or bronchial washing but
not visualized by imaging or bronchoscopy
T0 No evidence of primary tumor T3 Tumor >7 cm; or directly invading chest wall, diaphragm,
phrenic nerve, mediastinal pleura, or
T1 Tumor = 3cm surrounded by lung or visceral pleura, not more Parietal pericardium
proximal to the lobar bronchus Or tumor in the main bronchus ,< 2 cm distal to the
carina;
T1a Tumor = 2 cm
Or atelectasis, obstructive pneumonitis of entire lung;
T1b Tumor > 2cm but = 3cm Or separate tumor nodules of same lobe

T2 Tumor with any of the following features:

T4 Tumor of any size with invasion of the heart, gret vessels,
* > 3 cm but = 7 cm in greatest dimension
trachea, recurrent laryngeal nerve, esophagus, vertebral
* involves main bronchus > 2 cm distal to the carina body, or carina; or separate tumor nodules in a different
* involves the visceral pleura ipsilateral lobe
* assoc with atelectasis or obstructive pneumonitis that
extends to the hilar region but does not involve entire lung
T2a Tumor > 3 cm but = 5 cm
T2b Tumor > 5 cm but = 7 cm

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 Staging of Mediastinal
Lymph Nodes

*Computed Tomography

• Use of spiral or multisection CT, thin (5-mm)

sections with IV contrast material.
• Normal-sized nodes may contain metastases
and nodes may be enlarged due to
inflammatory causes although they contain no
malignant cells.
• The short axis diameter is the most reliable
measurement of lymph node size on CT scans.
A short axis diameter of greater than 10 mm is
abnormal regardless of the nodal station

* NODAL ASSESSMENT:CT Normal Size (Diameter) of Thoracic

LNS
• LYMPH NODE DIAMETER OF 1.0 CM IS USED TO
DISTINGUISH NORMAL FROM ABNORMAL
• Anterior Mediastinum < 6 mm
• SHORT AXIS DIAMETER OF NODE IS USED
• Aortopuimonary Window < 15 mm
• SHORT AXIS MEDIASTINAL NODE CORRELATES MOST
CLOSELY WITH THE ACTUAL NODE DIAMETER • Hilar < 10 mm
• UPPER LIMIT OF 1.5 CMS IS USUALLY USED FOR
NODES IN THE SUBCARINAL REGION
• Subcarinal < 10 mm
• Para-aortic < 7 mm

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 Regional Lymph Node
• N0 - No lymph nodes involved
• N1 - Ipsilateral bronchopulmonary or perihilar ,
intrapulmonary nodes
• N2 - Ipsilateral mediastinal nodes or ligament
involved
– Upper Paratracheal & Lower Paratracheal Nodes
– Pretracheal and Retrotracheal Nodes
– Aortic and Aortic Window Nodes
– Para-aortic Nodes
– Para-esophageal Nodes
– Pulmonary Ligament
– Subcarinal Nodes
• N3 - contralateral mediastinal or hilar nodes involved
(see or any scalene or supraclavicular nodes involved

Staging of Distant
Metastases

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 Metastatic Involvement
• M0 - No metastases
• M1a – separate tumor nodules in a
contralateral lobe;tumor w/ pleural
nodules; malignant pleural dissemination
• M1b- distant metastasis

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 TNM Staging of Non-small Cell CA
STAGE TNM subset
IA T1a,b, N0 M0
IB T2a N0 M0
T1a,b N1 M0
IIA
T2a N1 M0
T2b N0 M0

T2b N1 M0
IIB
T3 N0 M0
T3 N1 M0
T1-3 N2 M0
IIIA
T4 N0,1 M0

T4 N2 M0
IIIB
T1-4 N3 M0

IV Any T, any N, M1a,b

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 Staging of Small Cell CA
• Limited Stage
- confined to one hemithorax and regional
lymph nodes (including mediastinal
contralateral hilar, and ipsilateral
supraclavicular nodes
- Advanced stage
- with involvement of contralateral
hemithorax

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Summary of Treatment Approach
to Patients with Lung Cancer
Stages IA, IB, IIA, IIB, and some IIIA NSC CA
-Surgical resection for stages IA, IB, IIA, and IIB
-Surgical resection with complete-mediastinal lymph
node dissection and consideration of neoadjuvant
CRx for stage IIIA disease with "minimal N2
involvement" (discovered at thoracotomy or
mediastinoscopy)
-Postoperative RT for patients found to have N2
disease if no neoadjuvant CRx given
-Discussion of risks/benefits of adjuvant CRx with
individual patients
-Curative potential RT for "nonoperable" patients
Treatment modalities
Stages IIIA "advanced, bulky, clinically evident
N2 disease" (discovered preoperatively) and
IIIB disease that can be included in a
tolerable RT port:
• Curative potential RT + CRx if performance
status and general medical condition are
reasonable; otherwise, RT alone
• Consider neoadjuvant CRx and surgical
resection for IIIA disease with advanced N2
involvement
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Major contraindications to Curative surgery:
• Extrathoracic metastases
• Superior vena cava syndrome
• Vocal cord and phrenic nerve paralysis
• Malignant pleural effusion
• Cardiac tamponade
• Tumor w/in 2 cm from the carina
• Metastasis to supraclavicular lymph node
• Contralateral mediastinal node metastasis
• Involvement of main pulmonary artery
Treatment modalities
Stage IIIA with selected types of stage T3 tumors:
• Tumors with chest wall invasion (T3): en bloc
resection of tumor with involved chest wall and
consideration of postoperative RT
• Superior sulcus (Pancoast's) (T3) tumors:
preoperative RT (30-45 Gy) followed by en bloc
resection of involved lung and chest wall with
consideration of postoperative RT or intraoperative
brachytherapy
• Proximal airway involvement (<2 cm from carina)
without mediastinal nodes: sleeve resection if
possible preserving distal normal lung or
pneumonectomy
Treatment modalities
Stage IIIB disease with carinal invasion (T4) but
without N2 involvement:
• Consider pneumonectomy with tracheal
sleeve resection with direct reanastomosis to
contralateral mainstem bronchus
 Treatment modalities
Stage IV and more advanced IIIB disease:
• RT to symptomatic local sites
• CRx for ambulatory patients
• Chest tube drainage of large malignant pleural
effusions
• Consider resection of primary tumor and metastasis
for isolated brain or adrenal metastases
Treatment modalities
SMALL CELL LUNG CANCER
• RT for brain metastases, spinal cord compression,
weight-bearing lytic bony lesions, symptomatic local
lesions (nerve paralyses, obstructed airway,
hemoptysis, intrathoracic large venous obstruction,
in non-small cell lung cancer and in small cell cancer
not responding to CRx)
• Appropriate diagnosis and treatment of other
medical problems and supportive care during CRx
• Encouragement to stop smoking
• Entrance into clinical trial, if eligible

Non-small Cell CA Staging for Small Cell Lung Ca

• Early stage Lung Cancer • Limited Disease (LD)
– Stage I and II – Limited to one hemithorax
• surgical disease
• Supraclavicular and mediastinal
• Locally Advanced Lung Cancer lymphadenopathy
– Stage IIIA and B – Chemotherapy + radiotherapy
• Chemotherapy + radiotherapy
• Extensive Disease (ED)
• Metastatic Disease
– Stage IV
– Any disease outside of the hemithorax
• chemotherapy – Chemotherapy

Solitary Pulmonary Nodule Solitary Pulmonary Nodule

• An X-ray density completely surrounded by
normal aerated lung, with circumscribed
margins of any shape, ususually 1-6 cm in
greatest diameter
• Approx 35% in adults are malignant (primary
lung CA)
• <1% are malignant in non-smokers under 35
years old
• Risk factors in favor of malignancy:
1. History of cigarette smoking
2. age =35 yrs, relatively large lesion
3. lack of calcification
4. chest symptoms- asso. atelectasis,
pneumonitis, or adenopathy
5. growth of the lesion revealed by
comparison with old CXR

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 Solitary Pulmonary Nodule
• Radiographic criteria which reliably predict a
benign nature of solitary pulmonary nodule:
1. lack of growth over a period of > 2 yrs
2. characteristic patterns of calcification:
a. dense nidus
The End
b. multiple punctate foci God Bless!
c. “bull’s-eye” calcification- (granuloma)
d. “popcorn ball” calcification-
(hamartoma)

KDE, 2009

TNM Staging of Non-small Cell CA

STAGE TNM subset
IA T1a,b, N0 M0
IB T2a N0 M0
T1a,b N1 M0
IIA
T2a N1 M0
T2b N0 M0

T2b N1 M0
IIB
T3 N0 M0
T3 N1 M0
T1-3 N2 M0
IIIA
T4 N0,1 M0

T4 N2 M0
IIIB
T1-4 N3 M0

IV Any T, any N, M1a,b

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Primary Tumor TNM Staging for NSCLC
Tx Primary tumor cannot be assessed, or tumor proven by the
presence of malignant cells in sputum or bronchial washing but
not visualized by imaging or bronchoscopy
T0 No evidence of primary tumor

T1 Tumor = 3cm surrounded by lung or visceral pleura, not more

proximal to the lobar bronchus
T1a Tumor = 2 cm
T1b Tumor > 2cm but = 3cm

T2 Tumor with any of the following features:

* > 3 cm but = 7 cm in greatest dimension
* involves main bronchus > 2 cm distal to the carina
* involves the visceral pleura
* assoc with atelectasis or obstructive pneumonitis that
extends to the hilar region but does not involve entire lung
T2a Tumor > 3 cm but = 5 cm
T2b Tumor > 5 cm but = 7 cm

Primary Tumor TNM Staging

T3 Tumor >7 cm; or directly invading chest wall, diaphragm,

phrenic nerve, mediastinal pleura, or
Parietal pericardium
Or tumor in the main bronchus ,< 2 cm distal to the
carina;
Or atelectasis, obstructive pneumonitis of entire lung;
Or separate tumor nodules of same lobe

T4 Tumor of any size with invasion of the heart, gret vessels,

trachea, recurrent laryngeal nerve, esophagus, vertebral
body, or carina; or separate tumor nodules in a different
ipsilateral lobe

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