lung cancer

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LUNG CANCER

Rommel D. Bayot, MD, FPCP, FPCCPPhilippine Heart Center

FEU-NRMF Medical Center

(UPDATED 2009)

LUNG CANCER• Affects 94,000 males and 78,000 females

(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

• 5- year survival rate

- local disease: 50%

- with regional disease: 20%

- overall: 14%

LUNG CANCER

• WHO classification :1. Squamous or epidermoid carcinoma2. Small cell (or oat cell) carcinoma3. Adenocarcinoma (including bronchioalveolar)4. Large cell (or large cell anaplastic) carcinoma5. Others: Undifferentiated Carcinoma, Carcinoid, Bronchial Gland Tumors (Adenoid Cystic Carcinoma. Mucoepidermoid Tumors)

LUNG CANCER• 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/ endobronchialgrowth

- managed by chemotherapy with or w/o radiotherapy2. Non-small cell varieties (Squamous, adenocarcinoma, large cell, bronchioalveolar, and mixed versions)

Non-small cell CA

• 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 Cancer

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)

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

Hallmarks of Human Cancer Cells

• Chromosomal alterations

• Chromosomal instability

• Tumor suppressors

• Alterations in DNA methylation

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

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Chromosomal Losses

• Non Small Cell Lung Ca–3p, 8p, 9p, 13q, 17p

• Small Cell Lung Ca–3p, 4q, 5q, 8p, 10q 13q, 17p

Chromosomal Gains

• Non Small Cell Lung Ca–1q, 3q, 5p, 8q

• Small Cell lung Ca–3q, 5p, 8q

Tumor Suppression

• 2 events– Deletion of a large chromosomal DNA segment of

one allele

– Smaller mutation or epigenetic inactivation of the other allele

• Tumor Suppressor Gene– Genes whose reduced function can lead to

neoplastic change

Knudson Hypothesis

• An individual with an inherited predisposition to cancer inherits one normal and one mutant tumor suppressor gene

• A non-predisposed individual must acquire somatic mutations in both the maternal and paternal suppressor gene alleles to initiate tumor formation

Alterations in DNA Methylation

• 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/ MDM2/ p14ARF Pathway

• 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 treatment of lung cancers, especially in stage I cancers.

• MDM2– Ubiquitin E3 ligase; oncogene– Interacts with p53 and targets the p53 protein for

degradation– Paradoxically in association with a favorable

prognosis

• p14ARF– Exerts growth inhibition by inhibiting the

ubiquitin E3 ligase activity of MDM2

– Deletion may promote tumor-promoting activity of oncogenes

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 Cancer

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 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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• 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


• The present pandemic of lung cancer followed the introduction of cigarettes

• Role of carcinogens in disease causation

• First identified occupational respiratory carcinogen: Radon


• 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

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

• 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


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

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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

– Dose-response relationship (number of cigarettes smoked) steepest for Small Cell Undifferentiated Carcinoma

– Chloromethyl ethers, Radon exposure exhibit specificity for Small Cell Lung Cancer

– 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

Occurrence by Histologic TypeEpidemiology 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

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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• 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

Environmental and Occupational Agents 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

• 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

– 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)

• 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

• 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

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• Diet– Specific micronutrients may have anti

carcinogenic activity– Tomatoes, cruciferous vegetables

• Reduces risk–β - carotene

• Increased risk– Vitamin C

• Protective association– Vitamin A

• Studies yield null findings

– Alcohol drinking• Highest consumption categories associated

with increased risk

– Lower BMI• Increased lung cancer risk relative to heavier

persons

– Concomitant effects of smoking (?)

• Environmental exposures– Occupational exposures

– Asbestos

– Radiation

– Air pollution• Atmospheric air pollution

• Indoor air pollution

Occupational Carcinogens for Lung CA

Proven SuspectedArsenic Acrylonitrile

Asbestos Beryllium

Bis(chloromdethyl)ether Vinyl chloride

Chromium Silica

Mustard gas Iron ore

Nickel Wood dust

Polycyclic aromatic hydrocarbon

Ionizing radiation

Asbestos

• Fibrous, naturally occuring silicate material

• Peak incidence occur 30 -35 years after initial exposure

• In combination with smoking, act synergistically to increase lung cancer risk– Mechanism:

• Alter deposition pattern in the lung

• Enhance retention of asbestos fibers

Radiation

• Types of Radiation– Low Linear Energy Transfer (LET)

• X-rays

• γ-rays• Associated with higher risk when exposure occur at

higher dose rate

– High Linear Energy Transfer (LET)• Neutrons

• Radon

• Nonthreshold dose-response relationship

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Air Pollution

• Atmospheric Air Pollution• Polycyclic aromatic hydrocarbons, arsenic,

nickel, chromium

• Indoor Air Pollution– Most important indoor air pollutants in

never smokers:• Passive smoking• Radon• Others: asbestos, unprocessed solid fuels

Host Factors

• Genetic susceptibility– History of lung cancer predicts increased risk;

mendelian codominant autosomal gene

– Genetic factors may be more important at younger ages; association stronger in ages 40 – 59 years than older persons

Scheme linking nicotine addiction and lung cancer via tobacco smoke carcinogens and their induction of

multiple mutations in critical genes

nicotineaddiction

PAH, NNK andOther carcinogens

DNAadducts

Mutations and otherChanges: RAS, MYC,p53, p16, RB, FHIT,

And other critical genes

LungCancer

Cigarettesmoking

Metabolicactivation

Persistencemiscoding

Metabolic detoxification

Excretion Normal DNA

Repair

Apoptosis

• HIV and Lung Cancer– Greater than 2 fold increased risk

– Predominance of non small cell lung ca• Adenocarcinoma

• Squamous cell

– Most are males

– Median age of 45 years or less

• HIV and Lung Cancer– Potential reasons for the increased risk:

• HIV acting as viral carcinogen

• Defective immune surveillance

• Recurrent opportunistic infections and parenchymal lung inflammations leading to inflammatory foci and scar carcinomas

• Acquired Lung Diseases and Lung Ca– Diseases that obstruct airflow

• COPD

– Diseases that restrict lung capacity• Pneumoconioses

• Presence of silicosis is associated with an increased risk

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Bronchogenic Carcinoma

• Screening for Lung cancer

– There is no role for screening for lung cancer, even in high risk individuals

American Cancer Society

US Preventive Services Task Force

– Sputum cytology, chest radiograph

– LD - CT• The thinner the slice, the more noncalcified

nodules are detected

• Consistently detected NSCLC as stage IA in 60 –90% of cases; major improvement in 5-year survival

Presenting Symptoms of BronchogenicCarcinoma

Symptoms Percentage of Patients

Cough 45 – 75%

Weight loss 8 – 68%

Dyspnea 37 – 58%

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. cough3. dyspnea4. symptoms of lung abscess resulting from tumor cavitation

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Clinical manifestations

• Central or endobronchial growth of primary tumor may cause:1. Cough2. Hemoptysis3. Wheeze and stridor4. Dyspnea5. Post-obstructive pneumonitis (fever and productive cough)

Pancoast’s (Superior Sulcus Tumor) Syndrome

• Results from local extension of a tumor (usually Squamouscell CA) growing in the apex of the lung

• Involve the 8th cervical, 1st and 2nd thoracic nerves• Present with shoulder pain that cha. radiates in the ulnar

distribution of the arm• Often with radiologic destruction of the 1st and 2nd ribs• Other problems of regional spread:

- Superior vena cava syndrome from vascular obstruction- Precordial and cardiac extension w/ tamponade- Arrhythmia or cardiac failure- Lymphatic obstruction with pleural effusion- Lymphangitic spread through the lungs with hypoxemia and dyspnea

Paraneoplastic Syndromes In Lung CA

Syndrome Histologic Type

Endocrine and Metabolic Cushing syndrome

SIADH

HypercalcemiaGynecomastia

Small cell CA

Small cell CA

Squamous cell CALarge cell CA

Connective tissue Clubbing & hypertrophicpulmonary osteoarthropathy

Squamous cell, adenoCA, large cell

Neuromuscular Peripheral neuropathy

Subacute cerebellerdegeneration, Myasthenia (Eaton-Lambert), Dermatomyositis

Small cell CA

Small cell CA

Small cell CA

All

Paraneoplastic Syndromes In Lung CA

Cardiovascular ThrombophlebitisNon-bacterial verrucous endocarditis

Adenocarcinoma

Hematologic AnemiaDICEosinophiliaThrombocytosis

All

Cutaneous AcanthosisnigricansErythema gyratum

All

Staging of Primary Tumor

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Primary Tumor TNM Staging for NSCLCTx 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

T1a

T1b

Tumor = 3cm surrounded by lung or visceral pleura, not more proximal to the lobar bronchus

Tumor = 2 cm

Tumor > 2cm but = 3cm

T2

T2a

T2b

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

Tumor > 3 cm but = 5 cm


Primary Tumor TNM Staging

T3 Tumor >7 cm; or directly invading chest wall, diaphragm, phrenic nerve, mediastinal pleura, orParietal pericardiumOr 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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Staging of MediastinalLymph 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• LYMPH NODE DIAMETER OF 1.0 CM IS USED TO

DISTINGUISH NORMAL FROM ABNORMAL

• SHORT AXIS DIAMETER OF NODE IS USED

• SHORT AXIS MEDIASTINAL NODE CORRELATES MOST CLOSELY WITH THE ACTUAL NODE DIAMETER

• UPPER LIMIT OF 1.5 CMS IS USUALLY USED FOR NODES IN THE SUBCARINAL REGION

Normal Size (Diameter) of Thoracic LNS

• Anterior Mediastinum < 6 mm

• Aortopuimonary Window < 15 mm• Hilar < 10 mm• 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 CASTAGE TNM subset

IAIB

T1a,b, N0 M0T2a N0 M0

IIA

IIB

T1a,b N1 M0T2a N1 M0T2b N0 M0

T2b N1 M0T3 N0 M0

IIIA

T3 N1 M0T1-3 N2 M0T4 N0,1 M0

IIIBT4 N2 M0

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 mediastinalcontralateral hilar, and ipsilateralsupraclavicular nodes

- Advanced stage- with involvement of contralateralhemithorax

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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

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 neoadjuvantCRx 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 modalitiesStage 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 intraoperativebrachytherapy

• Proximal airway involvement (<2 cm from carina) without mediastinal nodes: sleeve resection if possible preserving distal normal lung or pneumonectomy

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


Stage IIIB disease with carinal invasion (T4) but without N2 involvement:

• Consider pneumonectomy with tracheal sleeve resection with direct reanastomosis to contralateral mainstem bronchus

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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


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

• Early stage Lung Cancer– Stage I and II

• surgical disease

• Locally Advanced Lung Cancer– Stage IIIA and B

• Chemotherapy + radiotherapy

• Metastatic Disease– Stage IV

• chemotherapy

Staging for Small Cell Lung Ca

• Limited Disease (LD)– Limited to one hemithorax

• Supraclavicular and mediastinallymphadenopathy

– Chemotherapy + radiotherapy

• Extensive Disease (ED)– Any disease outside of the hemithorax

– Chemotherapy

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 smoking2. age =35 yrs, relatively large lesion3. lack of calcification4. chest symptoms- asso. atelectasis, pneumonitis, or adenopathy5. growth of the lesion revealed by comparison with old CXR

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• Radiographic criteria which reliably predict a benign nature of solitary pulmonary nodule:1. lack of growth over a period of > 2 yrs2. characteristic patterns of calcification:

a. dense nidusb. multiple punctate focic. “bull’s-eye” calcification- (granuloma)d. “popcorn ball” calcification-(hamartoma)

TNM Staging of Non-small Cell CASTAGE TNM subset

IAIB

T1a,b, N0 M0T2a N0 M0

IIA

IIB

T1a,b N1 M0T2a N1 M0T2b N0 M0

T2b N1 M0T3 N0 M0

IIIA

T3 N1 M0T1-3 N2 M0T4 N0,1 M0

IIIBT4 N2 M0

T1-4 N3 M0

IV Any T, any N, M1a,b

The EndGod Bless!

KDE, 2009

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Primary Tumor TNM Staging for NSCLCTx 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

T1a

T1b

Tumor = 3cm surrounded by lung or visceral pleura, not more proximal to the lobar bronchus

Tumor = 2 cm

Tumor > 2cm but = 3cm

T2

T2a

T2b

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



Primary Tumor TNM Staging

T3 Tumor >7 cm; or directly invading chest wall, diaphragm, phrenic nerve, mediastinal pleura, orParietal pericardiumOr 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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