Pancoast tumor

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]

Synonyms and keywords:: superior sulcus tumor, Pancoast’s apex syndrome, Pancoast’s disease, Pancoast’s pain syndrome, malignant neoplasm.

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]

Overview

A Pancoast tumor, also known as superior sulcus tumor, defined primarily by its location at the pulmonary apex. The tumor can cause compression of a brachiocephalic vein, subclavian artery, phrenic nerve, recurrent laryngeal nerve, or, compression of a sympathetic ganglion.

Historical Perspective

Pancoast tumor was first described by Hare in 1838. In 1924, Henry K. Pancoast discovered the association between apical chest tumors, characteristic pain distribution, and Horner’s syndrome. In 1954, external beam radiation was used for the treatment of associated pain by Haas and colleagues. In 1990’s a combination of chemotherapy and radiotherapy was found to be associated with better prognosis and treatment outcome.

Classification

The staging of the pancoast tumor is based on the TNM system. Pancoast tumors staging starts at T3 always, as there is an invasion of the chest wall. Invasion of the vertebral body or the subclavian vessels is regarded as T4.

Pathophysiology

Pancoast tumor is the type of lung cancer that is associated with invasion of the apical chest wall. The location of Pancoast tumor in the superior sulcus results in an invasion of adjacent structures and in its characteristic clinical presentation. The progression of Pancoast tumor usually involves spread across the pleural apex to invade the following structures by direct extension into lymphatic vessels in the endothoracic fascia, intercoastal nerves, lower roots of brachial plexus, stellate ganglion, sympathetic chain, adjacent ribs, adjacent vertebra bodies, extension to the spinal cord can result in cord compression, subclavian artery or subclavian vein. The development of Pancoast syndrome is the result of tumors in the superior pulmonary sulcus is characterized by pain along ulnar nerve distribution and Horner’s syndrome.

Causes

Most common cause of Pancoast tumor is non–small cell lung carcinoma (NSCLC). Common types of non-small cell lung carcinoma (NSCLC) presenting as Pancoast tumor are squamous cell cancer, adenocarcinoma and large cell carcinoma. Less common causes of Pancoast tumor includes small cell cancer as it rarely presents as a peripheral tumor. Pancoast syndrome is classically associated with Pancoast tumor. Rare causes of Pancoast syndrome include desmoid tumor, metastasis, hematologic neoplasms, and infections that may present as a tumor localized to the lung apex.

Differential Diagnosis

Pancoast tumor must be differentiated from other causes of mass located in the apical region of the chest which may present with pain in the shoulder region. Differential diagnosis includes most common other conditions that cause hemoptysis, cough, dyspnea, wheeze, chest pain, shoulder pain, unexplained weight loss, unexplained loss of appetite, and fatigue such as superior vena cava syndrome, thoracic outlet syndrome, cervical disk disease, pneumonia/bronchitis, carcinoid tumor, infectious granuloma and thyroid mass.

Epidemiology and Demographics

Pancoast tumors are a rare type of non-small cell lung cancers (NSCLC), account for fewer than 5% of all lung cancers. In the United States, the age-adjusted prevalence of pancoast tumor is estimated to be 5 per 100,000. The prevalence of lung cancer significantly increases among smokers and individuals with chronic exposure to risk factors for lung cancer. In 2014 the incidence of Pancoast tumor was approximately 3 cases per 100,000. Lung cancer is more common in older adults. It is rare in people under age 45. Males are thought to be more predisposed to the development of lung cancer. This gender discrepancy is often attributed to the historically increased rate of smoking among males compared to females. The male to female ratio for the incidence of lung cancer is approximately 1.4 to 1. There is no racial predilection for Pancoast tumor. The incidence of lung cancer is lower in developing countries than in developed countries. It is unknown whether this decreased incidence is due to decreased cancer rates or decreased detection rates. Western Europe and the U.S. have the highest incidence of lung cancer.

Risk Factors

Common risk factors in the development of Pancoast tumor include asbestos exposure for prolonged period of time, exposure to gold, nickel, smoking, secondary smoke exposure.

Screening

There is insufficient evidence to recommend routine screening for Pancoast tumor.

Natural History, Complications and Prognosis

The patient experiences non-specific symptoms such as cough, hemoptysis, dyspnea, chest pain, dysphonia, dysphagia, lack of appetite, weight loss, and fatigue from 3 weeks to 3 months before seeking medical attention. Without treatment, the patient will develop initial symptoms of cough and chest pain, which may eventually lead to Pancoast syndrome. The symptoms of Pancoast syndrome start as referred pain to the shoulder. Without treatment, the tumor may invade surrounding tissues to cause pain along the ulnar nerve distribution, atrophy of hand muscles and spinal cord compression. The complications associated with Pancoast tumor are breathing difficulties, pneumonia, hemoptysis, pain, pleural effusion, metastasis, Horner’s syndrome, superior vena cava syndrome, Compression of the spinal cord and paraplegia (paralysis of the lower half of the body with involvement of both legs) develop when the tumor extends into the intervertebral foramina (opening between two vertebrae). The prognosis of Pancoast tumor depends on the stage of the tumor at diagnosis. The presence of the following is associated with a poor prognosis among patients with Pancoast tumor includes Horner syndrome, spread to the mediastinal lymph nodes, incomplete resection of tumor, involvement of supraclavicular lymph node, vertebral body invasion, metastasis to the brain.

Diagnosis

Diagnostic study of choice

CT scan is the gold standard test for the diagnosis of Pancoast tumor. MRI imaging should be performed for evaluation of chest wall invasion, examination of vascular structures and brachial plexus involvement, evaluation of resectability of the tumor.

History and Symptoms

The hallmark of Pancoast tumor is lung cancer located in the apex of the lung. A positive history of shoulder pain and atrophy of hand musculature, Horner’s syndrome and forearm edema is suggestive of Pancoast Syndrome. The most common symptoms of Pancoast tumor include cough, hemoptysis, dyspnea, chest pain, lack of appetite, weight loss, fatigue, symptoms of Pancoast Syndrome resulting from Pancoast tumor include shoulder pain along the vertebral border of the scapula, Horner’s syndrome and weakness of hand muscles. Less common symptoms of Pancoast syndrome include paraplegia.

Physical Examination

Common physical examination findings of Pancoast tumor include decreased/absent breath sounds, pallor, low-grade fever, and tachypnea. On physical examination, Pancoast tumor may present with features of lethargy, emaciation, confusion, low-grade fever, decreased SPO2, tachypnea, tachycardia, low BP, decreased/absent breath sounds, bone pain, fractures (usually in the vertebrae, femur, pelvic bones, and the ribs), pallor, decreased sweating on ipsilateral side of the face, ptosis, miosis, anhydrosis, supraclavicular lymphadenopathy, cranial nerve palsies, tingling and pain along the distribution of ulnar nerve, clubbing of fingers, weakness of arms and hands, hemiplegia, paraplegia, shoulder pain, edematous swelling of the ipsilateral arm.

Laboratory Tests

Pancoast tumor is a subtype of lung cancer located at the lung apex. There are no characteristic diagnostic lab findings associated with Pancoast tumor. The laboratory findings associated with lung cancer are the following neutropenia, hyponatremia, hypokalemia, hypercalcemia, respiratory acidosis, hypercarbia, hypoxia, and tumor cells in sputum and pleural effusion cytology. There are no ECG findings associated with Pancoast tumor.

Electrocardiogram

There are no ECG findings associated with Pancoast tumor.

Chest X-ray

An x-ray may be helpful in the diagnosis of Pancoast tumor. Lordotic view on x-ray is helpful in visualizing Pancoast tumor because of its characteristic location in the apical portion of the lung. Findings on an x-ray suggestive of Pancoast tumor include opacity at the apex of the lung or in the superior sulcus area, the spread of the tumor can result in rib invasion that is observed as a bone destruction of posterior ribs, vertebral body infiltration, enlargement of the mediastinum.

CT scan

CT scan is diagnostic of Pancoast tumor. CT scan has a limited ability to determine the extent of invasion of the primary tumor into adjoining structures when compared to MRI scan. Findings on CT scan of the chest suggestive of Pancoast tumor include invasion of brachial plexus, invasion of the chest wall and/or mediastinum, the extension of the tumor into vena cava, trachea and esophagus, subclavian-vessel involvement is assessed by contrast CT scanning.

MRI

MRI is helpful in the diagnosis of Pancoast tumor. MRI offers greater detail in the evaluation of chest wall invasion, examination of vascular structures and brachial plexus involvement and resectability of the tumor.

Ultrasound

On endobronchial and endoscopic ultrasound, characteristic findings of lung cancer may include: enlarged lymph nodes and local invasion to adjacent bronchial structures and mediastinum. Endobronchial ultrasound is a first-line diagnostic modality for mediastinal staging.

Other Imaging Findings

A bone scan may demonstrate bone metastases. FDG(18 F fluoro deoxyglucose) PET scans along with contrast enhanced CT may be helpful in the diagnosis of extent of Pancoast tumor.

Other Diagnostic Studies

A bone scan may demonstrate bone metastases. FDG(18 F fluorodeoxyglucose) PET scans along with contrast enhanced CT may be helpful in the diagnosis of the extent of Pancoast tumor. Other diagnostic studies for evaluating the spread of Pancoast tumor include bone scintigraphy, PET scan, molecular tests, and biopsy.

Treatment

The optimal management approach of Pancoast tumor depends on a series of characteristics, that include pre-treatment evaluation, location, and adequate staging. Common treatment options for management include radiation therapy alone, radiation therapy and surgery, concurrent chemotherapy with radiation therapy and surgery, surgery alone (for selected patients).

Medical Therapy

Chemotherapeutic regimens are based on platinum agents such as cisplatin, carboplatin, oxaliplatin, and satraplatin. Alternative regimens include paclitaxel, gemcitabine, or etoposide. Chemotherapeutic regimens are adjusted based on individual characteristics and body surface. The regimen adjustment according to tumor evolution has demonstrated longer survival rates, optimal symptom control, and higher quality of life.

Surgery

Surgery is the mainstay of therapy for early-stage Pancoast tumor. Surgical procedure selection will depend on the histology, margins, and size of the tumor. Common surgical procedures for the treatment of Pancoast tumor, include lung resection with lobectomy, lung resection with pneumonectomy with or without lymph node dissection, thoracotomy with the removal of the entire lung or lobe (lobectomy) along with regional lymph nodes (peribronchial and perihilar lymph node dissection) and pathological evaluation. If evidence of lymph node extension of the disease is present adjuvant chemotherapy should be administered. Surgical resection is not recommended for patients with advanced or metastatic lung carcinoma. Surgical staging of the mediastinum is considered standard if accurate evaluation of the nodal status is needed to determine therapy. Surgical treatment consists of a thoracotomy with removal of the entire lung or lobe along with regional lymph nodes and contiguous structures. Pneumonectomy is used if the tumor involves the main bronchus, extends across a fissure or is located such that wide excision is required. Survival following ‘curative’ resection is approximately 30% at 5 years and 15% at 10 years. The best results are found in squamous cell carcinoma followed by large-cell carcinoma and the adenocarcinoma. If the tumor is inoperable, stereotactic ablative radiation therapy should be administered.

Primary Prevention

Pancoast tumor is a subtype of lung cancer localized to the lung apex. Effective measures for the primary prevention of lung cancer include smoking cessation and avoidance of second-hand smoking. Lifestyle changes, such as a healthy diet rich with fruits and vegetables and regular exercise, might decrease the risk of developing cancer in general.

Secondary Prevention

Secondary prevention for lung cancer consists of smoking cessation and screening. Secondary chemoprevention focuses on blocking the development of lung cancer in individuals in whom a precancerous lesion has been detected.

References

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Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]

Overview

In 1838, Hare was the first to describe Pancoast tumor. In 1924, Henry K. Pancoast discovered the association between apical chest tumors, characteristic pain distribution, and Horner’s syndrome. In 1954, external beam radiation was used for the treatment of associated pain by Haas and colleagues. In 1990’s, a combination of chemotherapy and radiotherapy was found to be associated with better prognosis and treatment outcome.

Historical Perspective

In 1838, Hare was the first to describe Pancoast tumor.^[1]^[2]^[3]^[4]
In 1924, Henry K. Pancoast discovered the association between apical chest tumors, characteristic pain distribution, and Horner’s syndrome.
In 1954, external beam radiation was used for the treatment of associated pain by Haas and colleagues.
Combination of lobectomy and external beam radiation was developed by Chardack and MacCallum to achieve long-term survival.
In 1990’s, a combination of chemotherapy and radiotherapy was found to be associated with better prognosis and treatment outcome.

References

↑ Panagopoulos N, Leivaditis V, Koletsis E, Prokakis C, Alexopoulos P, Baltayiannis N, Hatzimichalis A, Tsakiridis K, Zarogoulidis P, Zarogoulidis K, Katsikogiannis N, Kougioumtzi I, Machairiotis N, Tsiouda T, Kesisis G, Siminelakis S, Madesis A, Dougenis D (2014). “Pancoast tumors: characteristics and preoperative assessment”. J Thorac Dis. 6 Suppl 1: S108–15. doi:10.3978/j.issn.2072-1439.2013.12.29. PMC 3966151. PMID 24672686.
↑ HERBUT PA, WATSON JS (1946). “Tumor of the thoracic inlet producing the Pancoast syndrome; a report of 17 cases and a review of the literature”. Arch Pathol (Chic). 42: 88–103. PMID 20995639.
↑ HAAS LL, HARVEY RA, LANGER SS (1954). “Radiation management of otherwise hopeless thoracic neoplasms”. J Am Med Assoc. 154 (4): 323–6. PMID 13108717.
↑ Shaw RR, Paulson DL, Kee JL (1961). “Treatment of Superior Sulcus Tumor by Irradiation Followed by Resection”. Ann. Surg. 154 (1): 29–40. PMC 1465837. PMID 17859668.

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Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

The staging of the pancoast tumor is based on the TNM system. Pancoast tumors staging starts at T3 always, as there is an invasion of the chest wall. Invasion of the vertebral body or the subclavian vessels is regarded as T4.

Classification

The staging of pancoast tumor is based on the TNM system.^[1]^[2]^[3]
Pancoast tumors staging starts at T3 always, as there is invasion of chest wall. Invasion of vertebral body or the subclavian vessels is regarded as T4.

Stage	T	N	M
IIB	T3	N0	M0
IIIA	T3	N1-2	M0
IIIB	T4	Any N	M0
IIIB	Any T	N3	M0
IV	Any T	Any N	M1

TNM-8th Edition
T	T1	Tumor size ≤3cm in greatest dimension
	T2	Tumor size >3cm to ≤5cm Tumor of any size that invades the visceral pleura involves main bronchus, irrespective of distance to the carina shows an atelectasis or obstructive pneumonitis that extends to the hilum
	T3	Tumor size >5cm to 7cm Pancoast tumor that involves thoracic nerve roots T1 and T2 only. Tumor of any size that invades the chest wall invades the pericardium invades the phrenic nerve involves main bronchus, irrespective of distance to the carina shows one or more satellite nodules in the same lung lobe
	T4	Tumor size >7cm Involvement of C8 or higher nerve roots, brachial plexus, subclavian vessels or spine Tumor of any size that invades mediastinal fat or mediastinal structures invades the diaphragm involves the carina shows one or more satellite nodules in another lobe on the ipsilateral side
N	N0	No regional lymph node metastasis
	N1	Nodes are ipsilateral nodes within the lung up to hilar nodes.
	N2	Nodes represent ipsilateral mediastinal or subcarinal lymphadenopathy.
	N3	Nodes represent contralateral mediastinal or contralateral hilar lymphadenopathy or any scalene or supraclavicular nodes.
M	M0	No distant metastasis
M	M1	Distant metastasis

References

↑ Naruke T (1993). “Significance of lymph node metastases in lung cancer”. Semin. Thorac. Cardiovasc. Surg. 5 (3): 210–8. PMID 8353149.
↑ Kraut MJ, Vallières E, Thomas CR (2003). “Pancoast (superior sulcus) neoplasms”. Curr Probl Cancer. 27 (2): 81–104. PMID 12717414.
↑ Mountain CF (1986). “A new international staging system for lung cancer”. Chest. 89 (4 Suppl): 225S–233S. PMID 3514171.

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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]

Overveiw

Pancoast tumor is the type of lung cancer that is associated with invasion of the apical chest wall. The location of Pancoast tumor in the superior sulcus results in an invasion of adjacent structures and in its characteristic clinical presentation. The progression of Pancoast tumor usually involves spread across the pleural apex to invade the following structures by direct extension into lymphatic vessels in the endothoracic fascia, intercostal nerves, lower roots of brachial plexus, stellate ganglion, sympathetic chain, adjacent ribs, adjacent vertebra bodies, extension to the spinal cord can result in cord compression, subclavian artery or subclavian vein. The development of Pancoast syndrome is the result of tumors in the superior pulmonary sulcus is characterized by pain along ulnar nerve distribution and Horner’s syndrome.

Pathophysiology

Pancoast tumor is the type of lung cancer that is associated with invasion of the apical chest wall. The location of Pancoast tumor in the superior sulcus results in an invasion of adjacent structures and in its characteristic clinical presentation.^[1]^[2]^[3]^[4]
The progression of Pancoast tumor usually involves spread across the pleural apex to invade the following structures by direct extension:
- Lymphatic vessels in the endothoracic fascia
- Intercostal nerves
- Lower roots of brachial plexus
- Stellate ganglion
- Sympathetic chain
- The first, second, or third rib
- First or second thoracic vertebra bodies or intervertebral foramina
- Extension to the spinal cord can result in cord compression
- Subclavian artery
- Subclavian vein
The development of Pancoast syndrome is the result of tumors in the superior pulmonary sulcus is characterized by pain along ulnar nerve distribution and Horner’s syndrome.

Gross Pathology

On gross pathology, findings will depend on the histological subtype of Pancoast tumor.
Lung adenocarcinoma gross pathology findings, include:^[5]

Spherical tumor with well-defined borders
Homogeneous gray-white cut surface
Involvement of the thoracic wall
Usually found in the peripheral lung

Large cell lung cancer gross pathology findings, include:^[5]

Well-defined borders
Resemblance to gross findings in adenocarcinoma
No signs of anthracosis
Involvement of the thoracic wall

Squamous cell lung cancer gross pathology findings, include:^[5]

Lung mass
Usually centrally located
Associated with a large airway
Usually have a central cavitation

Microscopic Pathology

On microscopic pathology, findings will depend on the histological type of Pancoast tumor.^[5]

Lung adenocarcinoma microscopic pathology findings, include:

Nuclear atypia
Eccentrically placed nuclei
Abundant cytoplasm with mucin vacuoles
Often conspicuous nucleoli
Lack of intercellular bridges.
Different patterns, include: acinar, lepidic, micropapillary, papillary, and solid.

Large cell lung cancer microscopic pathology findings, include:

Large polygonal cells and anaplastic cells
No squamous or glandular differentiation
Moderately abundant cytoplasm
Vesicular nuclei, prominent nucleoli

Squamous cell lung cancer microscopic pathology findings include:

Central nucleus
Dense appearing cytoplasm, usually eosinophilic
Small nucleolus
Intracellular bridges (classic feature)

On immunohistochemistry, the findings depend on the histological type of Pancoast tumor.^[6]^[5]

Common immunohistochemistry markers used for Pancoast tumor subtyping, include:

TTF-1 for adenocarcinoma
p63 and high-molecular-weight keratins for squamous cell carcinoma
Lack of staining with neuroendocrine markers (chromogranin A, synaptophysin, and CD56)

References

↑ Paulson DL (1975). “Carcinomas in the superior pulmonary sulcus”. J. Thorac. Cardiovasc. Surg. 70 (6): 1095–104. PMID 1186286.
↑ Pitz CC, de la Rivière AB, van Swieten HA, Duurkens VA, Lammers JW, van den Bosch JM (2004). “Surgical treatment of Pancoast tumours”. Eur J Cardiothorac Surg. 26 (1): 202–8. doi:10.1016/j.ejcts.2004.02.016. PMID 15201002.
↑ Glassman LR, Hyman K (2013). “Pancoast tumor: a modern perspective on an old problem”. Curr Opin Pulm Med. 19 (4): 340–3. doi:10.1097/MCP.0b013e3283621b31. PMID 23702478.
↑ Panagopoulos N, Leivaditis V, Koletsis E, Prokakis C, Alexopoulos P, Baltayiannis N, Hatzimichalis A, Tsakiridis K, Zarogoulidis P, Zarogoulidis K, Katsikogiannis N, Kougioumtzi I, Machairiotis N, Tsiouda T, Kesisis G, Siminelakis S, Madesis A, Dougenis D (2014). “Pancoast tumors: characteristics and preoperative assessment”. J Thorac Dis. 6 Suppl 1: S108–15. doi:10.3978/j.issn.2072-1439.2013.12.29. PMC 3966151. PMID 24672686.
↑ ^5.0 ^5.1 ^5.2 ^5.3 ^5.4 Non small cell lung cancer. Libre Pathology. http://librepathology.org/wiki/Non-small_cell_lung_carcinoma Accessed on February 22, 2016
↑ Capelozzi VL (2009). “Role of immunohistochemistry in the diagnosis of lung cancer”. J Bras Pneumol. 35 (4): 375–82. PMID 19466276.

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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]

Overview

Most common cause of Pancoast tumor is non–small cell lung carcinoma (NSCLC). Common types of non-small cell lung carcinoma (NSCLC) presenting as Pancoast tumor are squamous cell cancer, adenocarcinoma and large cell carcinoma. Less common causes of Pancoast tumor includes small cell cancer as it rarely presents as a peripheral tumor. Pancoast’s syndrome is classically associated with Pancoast tumor. Rare causes of Pancoast’s syndrome include desmoid tumor, metastasis, hematologic neoplasms, and infections that may present as a tumor localized to the lung apex.

Causes

Most common cause of Pancoast tumor is non–small cell lung carcinoma (NSCLC).^[1]^[2]^[3]^[4]^[5]
Common types of non-small cell lung carcinoma (NSCLC) presenting as Pancoast tumor are squamous cell cancer, adenocarcinoma and large cell carcinoma.
Less common causes of Pancoast tumor includes small cell cancer as it rarely presents as a peripheral tumor.
Pancoast’s syndrome is classically associated with Pancoast tumor.
Rare causes of Pancoast’s syndrome include:^[6]^[7]^[8]^[9]^[10]
- Desmoid tumor–intrathoracic fibromatosis
- Metastatic spread from:
- Hematologic neoplasms:
- Infections such as:
  - Bacterial
  - Fungal
    - Aspergillosis
    - Allescheriasis
    - Cryptococcosis
- Hemangiopericytoma
- Adenoid cystic carcinoma
- Lymphoma
- Vascular aneurysms
- Cervical rib syndrome
- Mycotic subclavian artery aneurysm
- Hydatid cyst presenting as carotid pseudoaneurysm

References

↑ Panagopoulos N, Leivaditis V, Koletsis E, Prokakis C, Alexopoulos P, Baltayiannis N, Hatzimichalis A, Tsakiridis K, Zarogoulidis P, Zarogoulidis K, Katsikogiannis N, Kougioumtzi I, Machairiotis N, Tsiouda T, Kesisis G, Siminelakis S, Madesis A, Dougenis D (2014). “Pancoast tumors: characteristics and preoperative assessment”. J Thorac Dis. 6 Suppl 1: S108–15. doi:10.3978/j.issn.2072-1439.2013.12.29. PMC 3966151. PMID 24672686.
↑ Jocelyn PC (1978). “The reduction of diamide by rat liver mitochondria and the role of glutathione”. Biochem. J. 176 (3): 649–64. PMC 1186286. PMID 747642.
↑ Glassman LR, Hyman K (2013). “Pancoast tumor: a modern perspective on an old problem”. Curr Opin Pulm Med. 19 (4): 340–3. doi:10.1097/MCP.0b013e3283621b31. PMID 23702478.
↑ Amin R (1986). “Bilateral Pancoast’s syndrome in a patient with carcinoma of the cervix”. Gynecol. Oncol. 24 (1): 126–8. PMID 3754528.
↑ Mills PR, Han LY, Dick R, Clarke SW (1994). “Pancoast syndrome caused by a high grade B cell lymphoma”. Thorax. 49 (1): 92–3. PMC 474122. PMID 8153951.
↑ “Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 18-2000. A 45-year-old woman with a thoracic mass and Pancoast’s syndrome”. N. Engl. J. Med. 342 (24): 1814–21. 2000. doi:10.1056/NEJM200006153422408. PMID 10853005.
↑ Chong KM, Hennox SC, Sheppard MN (1993). “Primary hemangiopericytoma presenting as a Pancoast tumor”. Ann. Thorac. Surg. 55 (2): 9. PMID 8431033.
↑ Hatton MQ, Allen MB, Cooke NJ (1993). “Pancoast syndrome: an unusual presentation of adenoid cystic carcinoma”. Eur. Respir. J. 6 (2): 271–2. PMID 8383065.
↑ Vandenplas O, Mercenier C, Trigaux JP, Delaunois L (1991). “Pancoast’s syndrome due to Pseudomonas aeruginosa infection of the lung apex”. Thorax. 46 (9): 683–4. PMC 463373. PMID 1948800.
↑ Gallagher KJ, Jeffrey RR, Kerr KM, Steven MM (1992). “Pancoast syndrome: an unusual complication of pulmonary infection by Staphylococcus aureus”. Ann. Thorac. Surg. 53 (5): 903–4. PMID 1570995.

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Differentiating Pancoast Tumor from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]

Overview

Pancoast tumor must be differentiated from other causes of mass located in the apical region of the chest which may present with pain in the shoulder region. Differential diagnosis includes most common other conditions that cause hemoptysis, cough, dyspnea, wheeze, chest pain, shoulder pain, unexplained weight loss, unexplained loss of appetite, and fatigue such as superior vena cava syndrome, thoracic outlet syndrome, cervical disk disease, pneumonia/bronchitis, carcinoid tumor, infectious granuloma and thyroid mass.

Differential Diagnosis

Pancoast tumor must be differentiated from other causes of mass located in the apical region of the chest which may present with pain in the shoulder region.The table below summarizes the findings that differentiate apical mass in the chest from the most common other conditions that cause hemoptysis, cough, dyspnea, wheeze, chest pain, shoulder pain, unexplained weight loss, unexplained loss of appetite, and fatigue

The following table summarizes the differentiation of various lung tumors based on histological and topographical features:^[1]^[2]^[3]^[4]^[5]^[6]^[7]^[8]^[9]^[10]^[11]^[12]^[13]

Abrevations: HPV: human papillomavirus; CEA: Carcino embryogenic antigen; TTF1: Thyroid transcription factor-1; EMA: Epithelial membrane antigen; CK: Cyto keratin; CD: Cluster differentiation; NCAM: Neural Cell Differentiation Molecule; MMP’s: Mettaloprotineases matrix ; GFAP: Glial fibrocilliary acid protein
			Risk/Epidemiology	Pleuripotent cells	Topography	Gross	Histology	Immunohistochemistry	Imaging	Metastasis
Pancoast Tumor	Squamous cell carcinoma (SCC)		Cigarette smokers Arsenic	Epithelial cells	Central	White or grey lesions Focal carbon pigment deposits Cavitations Intraluminal polypoid masses Infiltration	Exophytic Intra-epithelial Without invasion Cells with clear cytoplasm Peripheral palisading of nuclei. Poor differentiation	Keratin Cytokeratins CEA Thyroid transcription factor-1 (TTF-1)	Chest x-ray: Lordotic view on chest x-ray is helpful in visualizing Pancoast tumor because of its characteristic location in the apical portion of the lung. opacity at the apex of the lung or in the superior sulcus area, the spread of the tumor can result in rib invasion that is observed as a bone destruction of posterior ribs, vertebral body infiltration. Enlargement of the mediastinum. CT scan is diagnostic of Pancoast tumor. CT scan has a limited ability to determine the extent of invasion of the primary tumor into adjoining structures when compared to MRI scan. Subclavian-vessel involvement is assessed by contrast CT scanning. MRI is helpful in the diagnosis of Pancoast tumor. MRI offers greater detail in the evaluation of chest wall invasion, examination of vascular structures and brachial plexus involvement and resectability of the tumor. Other diagnostic studies for evaluating the spread of Pancoast tumor include bone scintigraphy, PET scan, molecular tests and biopsy.	Liver Breast Bone
	Small cell carcinoma		Smoking Radon exposure	Bronchial precursor cell	Peripheral	White-tan, soft, friable perihilar masses Extensive necrosis 5% peripheral coin lesions	Sheet-like growth Nesting Trabeculae Peripheral palisading Rosette formation High mitotic rate	CD56 Chromogranin Synaptophysin TTF-1		Bone marrow Liver
	Adenocarcinoma		Smoking	Columnar cells of bronchioles	Peripheral	Single or multiple lesions Different in size Peripheral distribution Gray-white central fibrosis Pleural puckering Anthracotic pigmentation Necrosis Cavitation Hemorrhage Lobulated or ill defined edges	Nuclear atypia Eccentrically placed nuclei Abundant cytoplasm with mucin vacuoles Often conspicuous nucleoli Lack of intercellular bridges. Different patterns, include: acinar, lepidic, micropapillary, papillary, and solid.	Epithelial markers CEA CK7 TTF-1		Aerogenous spread is characteristic Brain Bone Adrenal glands Liver Kidney Gastrointestinal Tract
Benign Lung Tumors^[14]
Papilloma^[15]	Squamous cell papilloma		HPV 6 and 11 Men Median age of diagnosis is 54 years	Epithelial cells	Endobronchial	Cauliflower-like lesions Tan-white soft to semifirm protrutions	Loose fibrovascular core Stratified squamous epithelium Acanthosis Binucleate forms and perinuclear halos Koilocytosis	N/A	Well circumscribed Homogenous Non-calcified Solitary mass	N/A
Papilloma^[15]	Glandular papilloma		Rare Mean age of diagnosis is 68 years	Goblet cells of respiratory epithelium	Endobronchial	White to tan endobronchial polyps that measure from 0.7-1.5 cm	Thick arborizing stromal stalks Thin-walled blood vessels Non-ciliated or ciliated epithelium	N/A	Well circumscribed Homogenous Non-calcified Solitary mass	N/A
Adenoma^[16]	Alveolar adenoma		Mean age of diagnosis is 53 years Female predominance	Alveolar pneumocytes Septal mesenchyme	All lung lobes Lower lobes Hilar	0.7-6.0 cm Well demarcated smooth Lobulated, multicystic Soft to firm Pale yellow to tan cut surfaces	Non-encapsulated Multicystic masses Cuboidal cell linning Squamous metaplasia Myxoid and collagenous interstitium	Keratin CEA Surfactant protein TTF-1 Actin	Well circumscribed Homogenous Non-calcified Solitary mass	N/A
	Papillary adenoma^[17]		Mean age of diagnosis is 32 years Male predominance	Bronchioloalveolar cell	No lobar predilection Involves alveolar parenchyma	Well defined Encapsulated Soft, spongy to firm mass Granular gray white/ brown 1.0- 4.0 cm	Infiltration Papillary growth pattern Fibrovascular cores Cuboidal to columnar epithelial linning Cilitated and oxyphilic cells Occasional eosinophilic intranuclear inclusions	Cytokeratin Clara cell protein TTF-1 Surfactant apoprotein CEA	Incidental finding	N/A
	Mucinous cystadenoma		No sex predilection Mean age of diagnosis is 52 years	Mucus glands of the bronchus	Central	White-pink to tan Smooth and shiny tumors Gelatinous mucoid solid core 0.7-7.5 cm	Numerous mucin-filled cystic spaces Non-dilated microacini, glands, tubules and papillae	EMA Cytokeratins CEA	Coin lesion Air-meniscus sign	N/A
Malignant Lung Tumors^[18]
Variants of lung carcinoma			Risk Factors/Epidemiology	Pleuripotent cell	Topography	Gross	Histology	Immunohistochemistry	Imaging	Metastasis
Squamous cell carcinoma (SCC)^[19]	Papillary		Cigarette smokers Arsenic	Epithelial cells	Central	White or grey lesions Focal carbon pigment deposits Cavitations Intraluminal polypoid masses Infiltration	Exophytic Intra-epithelial Without invasion	Keratin Cytokeratins CEA Thyroid transcription factor-1 (TTF-1)	Lobar or entire lung collapse Shift of the mediastinum to the ipsilateral side Hilar, perihilar or mediastinal masses	Liver Breast Bone
	Clear cell						Cells with clear cytoplasm
	Basaloid						Peripheral palisading of nuclei. Poor differentiation
Small cell carcinoma^[20]			Smoking Radon exposure	Bronchial precursor cell	Peripheral	White-tan, soft, friable perihilar masses Extensive necrosis 5% peripheral coin lesions	Sheet-like growth Nesting Trabeculae Peripheral palisading Rosette formation High mitotic rate	CD56 Chromogranin Synaptophysin TTF-1	Hilar or perihilar masses Mediastinal lymphadenopathy Lobar collapse	Bone marrow Liver
Adenocarcinoma^[21]^[22]^[23]	Acinar adenocarcinoma		Smoking	Columnar cells of bronchioles	Peripheral	Single or multiple lesions Different in size Peripheral distribution Gray-white central fibrosis Pleural puckering Anthracotic pigmentation Necrosis Cavitation Hemorrhage Lobulated or ill defined edges	Irregular-shaped glands Malignant cells: Hyperchromatic nuclei Fibroblastic stroma	Epithelial markers CEA CK7 TTF-1	Peripheral nodules under 4.0 cm in size Central location as a hilar or perihilar mass Rarely show cavitations. Hilar adenopathy Adenocarcinomas account for the majority of small peripheral cancers identified radiologically.	Aerogenous spread is characteristic Brain Bone Adrenal glands Liver Kidney Gastrointestinal Tract
	Papillary adenocarcinoma						Papillae Necrosis Surrounding invasion Cuboidal to columnar epithelial linning Mucinous or non-mucinous
	Bronchio-alveolar carcinoma	Non-mucinous					Clara cells Type II cells
		Mucinous					Low grade differentiation Composed of: Tall columnar cells Basal nuclei Pale cytoplasm resembling goblet cells Varying amounts of cytoplasmic mucin Cytologic atypia
		Mixed non-mucinous and mucinous or indeterminate					Mixed type of cells Low to high grade differentiated cells.
	Solid adenocarcinoma with mucin production	Fetal adenocarcinoma					Consists glandular elements: Tubules of glycogen-rich Non-ciliated cells Subnuclear and supranuclear glycogen vacuoles Rounded morules of polygonal cells with abundant eosinophilic and finely granular cytoplasm
		Mucinous (“colloid”) carcinoma					Dissecting pools of mucin containing neoplastic cells
		Mucinous cystadenocarcinoma					Partial fibrous tissue capsule Central cystic change with mucin pooling Neoplastic mucinous epithelium grows along alveolar walls
		Signet ring adenocarcinoma					Focal Cells with nuclei displaced to sides Components of other cells are present.
		Clear cell adenocarcinoma					Clear cells with no nuclei
Variants of lung carcinoma			Risk Factors/Epidemiology	Pleuripotent cell	Topography	Gross	Histology	Immunohistochemistry	Imaging	Metastasis
Large cell carcinoma^[24]	Basaloid large cell carcinoma of the lung		Approximately 10% of lung cancers Smoking	Neuro endocrine cells Suprabasal bronchial cells	Peripheral masses Bronchi	Soft, pink-tan tumor Necrosis and occasional hemorrhage Cavitations Exophytic bronchial growth	Invasive growth pattern Peripheral palisading Small, monomorphic, cuboidal fusiform	Chromogranin Synaptophysin CD56 Cytokeratin	Large, peripheral masses	Pleura Liver Bone Brain Abdominal lymph nodes Pericardium
	Clear cell carcinoma of the lung						Clear cells
	Lymphoepithelioma-like carcinoma of the lung						Syncytial growth pattern Eosinophilic nucleoli Lymphocytic infiltration Invasive Amyloid deposition
	Large-cell lung carcinoma with rhabdoid phenotype						Eosinophilic cytoplasmic globules Small foci of adenocarcinoma Eosinophilic inclusions
	Mixed type						Mixture of: Adenocarcinoma Squamous cell carcinoma Giant cell carcinoma Spindle cell carcinoma
Variants of lung carcinoma			Risk Factors/Epidemiology	Pleuripotent cell	Topography	Gross	Histology	Immunohistochemistry	Imaging	Metastasis
Sarcomatoid carcinoma^[25]	Carcinosarcoma		Accounts for only 0.3-1.3% of all lung malignancies Mean age at diagnosis is 60 years Tobacco smoking Asbestos exposure	Undifferentiated epithelial cells	Central or peripheral Upper lobes	> 5 cm Well circumscribed Grey, yellow or tan creamy, gritty, Mucoid and/or hemorrhagic with significant necrosis Sessile or pedunculated Infiltrative	Biphasic Mixture of carcinomatous and sarcomatous cells	Keratin S-100	No specific imaging features	Aggressive tumor Esophagus, jejunum, and rectum Kidney
	Spindle cell carcinoma						Only spindle shaped tumor cells Lymphoplasmacytic infiltrates	Keratin EMA Cytokeratin Vimentin CEA TTF-1
	Giant cell carcinoma						Multi- and/or mononucleated tumor giant cells
	Pleomorphic carcinoma						Poorly differentiated Mixture of spindle cells and/or giant cells Fibrous or myxoid stroma
	Pulmonary blastoma						Biphasic Mixture of epithelial and mesenchymal stroma	Keratin EMA CEA Chromogranin A
Variants of lung carcinoma			Risk Factors/Epidemiology	Pleuripotent cell	Topography	Gross	Histology	Immunohistochemistry	Imaging	Metastasis
Carcinoid tumor^[26]	Typical carcinoid Atypical carcinoid		Most common in males Mean age of diagnosis 45	Neuroendocrine cells of lung	Typical carcinoids are throughout the lungs Atypical carcinoid is more commonly peripheral	Firm, well demarcated, tan to yellow tumors	Uniform polygonal cells Nuclear atypia Pleomorphism The most common patterns are the organoid and trabecular Highly vascularized fibrovascular stroma Focal necrosis	Cytokeratin Chromogranin Synaptophysin CD57 CD56 S-100 protein	Well defined pulmonary nodules Calcifications is often seen. Intense contrast enhancement	Liver Bone
Salivary gland tumors^[27]	Mucoepidermoid carcinoma		Most patients presents in the third and fourth decade Constitutes of less than 1% tumor No association with cigarette smoking or other risk factors	Primitive cells of tracheobronchial origin	Bronchial glands	Ranging in size from 0.5-6 cm Soft, polypoid, and pink-tan in colour High-grade lesions are infiltrative	Exophytic endobronchial growth Surface epithelium lacking changes of in-situ carcinoma Absence of individual cell keratinization Transitional areas to low grade mucoepidermoid carcinoma	GFAP	Well-circumscribed oval or lobulated mass Calcifications Post-obstructive pneumonic infiltrates	Rare Liver Bones Adrenal gland Brain
	Adenoid cystic carcinoma		Constitutes less than 1% of all lung tumors Most commonly seen in fourth and fifth decades of life	Primitive cells of tracheobronchial origin	Trachea	Gray-white or tan polypoid lesions Size ranges from 1–4 cm Infiltrative margins	Invades other cell layers Heterogeneous cellularity Cribriform pattern Perineural invasion	Immunoperoxidase Cytokeratin Vimentin Actin Calponin S-100 protein p53 GFAP	Well circumscribed Nodule	Liver Brain Bone Spleen Kidney Adrenal glands
	Epithelial-myoepithelial carcinoma		Age ranges from 33 to 71 years No association with smoking	Myoepithelial cells	Endobronchial	Solid to gelatinous in texture White to gray in colour	Myoepithelial cells Dual layer of cells lining ducts Low mitotic activity	MNF116 EMA SMA and S-100	Reflects airway obstruction	Breast
Variants of lung carcinoma			Risk Factors/Epidemiology	Pleuripotent cell	Topography	Gross	Histology	Immunohistochemistry	Imaging	Metastasis
Preinvasive lesions^[28]	Squamous carcinoma in situ		Most commonly seen in fifth or sixth decades Mostly seen in women	Basal cells of squamous epithelium	Bronchi	Focal or multi-focal plaque-like greyish lesions Nonspecific erythema Even nodular or polypoid lesions	Goblet cell hyperplasia Basal cell hyperplasia Squamous dysplasia Angiogenic squamous dysplasia Micropapillomatosis	EGFR HER2/neu p53 MCM2 Ki-67 Cytokeratin 5/6 Bcl-2 VEGF Folate binding protein p16	Cauliflower like Mosaic pattern	Liver Brain Bone Spleen
	Atypical adenomatous hyperplasia			Surfactant apoprotein Clara cell specific 10kDd protein	Pleura Upper lobes	Multiple grey to yellow foci 1mm to 10mm in size	Intranuclear inclusions Clara cells and type II pneumocytes Thickened alveolar walls Discontinuous lining of cells Moderate atypia Pseudopapillae	CEA MMPs E-cadherin ß-catenin CD44v6 TTF-1 TP53	Typically not visualized on radiographs Small non-solid nodules Ground-glass opacity
	Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia			Pulmonary neuroendocrine cells	Endobronchial	Early lesions are: Small, gray-white nodules Resembling ‘miliary bodies’ Larger carcinoid tumors are: Firm Homogeneous Well-defined Grey or yellow-white masses	Nodular aggregates Fibrosis due to proliferation Invade locally Fibrous stroma aggregates to form ‘tumorlets’. Carcinoids are tumorlets >5cm.	Keratin CEA	Mosaic pattern of air trapping Sometimes with nodules Thickened bronchial and bronchiolar walls
Variants of lung carcinoma			Risk Factors/Epidemiology	Pleuripotent cell	Topography	Gross	Histology	Immunohistochemistry	Imaging	Metastasis
Mesenchymal tumors^[29]	Epithelioid haemangioendothelioma / Angiosarcoma		Caucasian 80% are women	Endothelial cells	Intravascular	0.3-2.0 cm circumscribed mass Gray-white or gray-tan firm tissue Yellow flecks Central calcifications Cut surface has a cartilaginous consistency	Round to oval-shaped nodules Central sclerosis Hypocellular zone Peripheral cellular zone Calcifications Intranuclear cytoplasmic inclusions	CD31 CD34 Factor VIII (von Willebrand factor) Cytokeratin	Multiple Bilateral Small nodules 1-2 cm in size Can mimic pulmonary Langerhans’ cell histiocytosis. Calcifications	Liver Bone Soft tissue
	Pleuropulmonary blastoma		Most common in children Median age of diagnosis is 2 years	Thoracic splanchnopleural mesenchyme	Pleura Lung	Purely cystic Thin-walled Rarely solid Firm to gelatinous Upto 15 cm	Type I Purely cystic Lined by respiratory type epithelium Underneath malignant cells Type II Partial or complete overgrowth of the septal stroma Type III Mixed cells	Vimentin S-100 protein	Unilateral Localized airfilled cysts Septal thickening or an intracystic mass	Brain Spinal cord Skeletal system Eyes Pancreas
	Chondroma		Young women	Chondrocytes Cartilaginous cells	Peripheral lesions in lung Primary lesion seen in Stomach Bone Paraganglia	Peripheral Solid lesions Calcified	Capsulated lobules Hypocellular Features of malignancy are absent	N/A	Multiple Well circumscribed lesions “Pop-corn” calcifications	Benign in nature
	Congenital peribronchial myofibroblastic tumor		Rare Sporadic Complicated by Polyhydramnios Non-immune hydrops fetalis	Spindle cells	Along the bronchi	5-10 cm Well-circumscribed Non-encapsulated Smooth or multinodular surface The cut surface has a tann-grey to yellow-tan fleshy appearance Hemorrhage Necrosis	Fascicles of spindle cells Bronchial invasion Peribronchial distribution Cystic foci of hemorrhage	Vimentin	Well circumscribed Opaque hemithorax Heterogeneous mass	Rare
	Diffuse pulmonary lymphangiomatosis		Children Young adults of both sexes	Smooth muscle cells of lymphatic vessels	Along the lymphatic distribution	Prominence of the bronchovascular bundles along Pleura Interlobular pulmonary septa Mediastinum	Anastomosing endothelial-lined cells along lymphatic routes Spindle cells Intra alveolar siderophages	Vimentin	Increased interstitial markings Thickening of the: Interlobular septa Fissures Central airways Pleura	Skin Bone
	Inflammatory myofibroblastic tumor		Previous viral infections HHV8 Children	Myofibroblastic cells	Localized to bronchi	Solitary Round rubbery masses Yellowish-gray discoloration Average size of 3.0 cm Non-encapculated Calcifications No local invasion	Mixture of spindle cells Fibroblastic Myofibroblastic Arranged in fascicles Cytologic atypia Touton type giant cells Plasma cells Lymphoid follicles	Vimentin Actin p80	Solitary mass Regular borders Spiculated appearance Accompanied by Post-obstructive pneumonia Atelectasis	Rare
	Pulmonary artery sarcoma		Mean age of diagnosis is 49.3 years Commonly misdiagnosed as pulmonary embolism	Mesenchymal cells of the intima Primitive cells of the bulbus cordi in the trunk of pulmonary artery	Pulmonary trunk most commonly involving: Right pulmonary artery Left pulmonary artery Pulmonary valve Right ventricular outflow tract	Mucoid or gelatinous clots filling vascular lumens The cut surface may show Firm fibrotic areas Bony/gritty or chondromyxoid foci Hemorrhage and necrosis are common in high-grade tumors	Spindle cells in A myxoid background Collagenized stroma Recanalized thrombi	Vimentin Osteopontin Factor VIII CD31 CD34	Findings overlap with those of chronic thromboembolic disease Decreased vascularity Heterogeneous soft tissue density Smooth vascular tapering	Lung parenchyma Mediastinum
	Pulmonary vein sarcoma		Most common in women Mean age of diagnosis is 49	Smooth muscle	Pulmonary vein	Fleshy-tan tumor Can occlude the lumen of the involved vessel 3.0- 20.0 cm Invasion of wall of the vein	Smooth muscle differentiation Moderate to highly cellular spindle cell neoplasms Epithelioid morphology	Vimentin Desmin Actin Keratin		N/A

References

↑ {{Small cell lung cancer [Internet]. BMJ Publishing Group Limited 2015 [updated 2014 Oct 29]. Available from: http://bestpractice.bmj.com/best-practice/monograph/1081/diagnosis/differential.html}}
↑ Bhatt M, Kant S, Bhaskar R (2012). “Pulmonary tuberculosis as differential diagnosis of non-small cell lung cancer”. South Asian J Cancer. 1 (1): 36–42. doi:10.4103/2278-330X.96507. PMC 3876596. PMID 24455507.
↑ Kamiya K, Yoshizu A, Misumi Y, Hida N, Okamoto H, Yoshida S (2011). “[Lung abscess which needed to be distinguished from lung cancer; report of a case]”. Kyobu Geka. 64 (13): 1204–7. PMID 22242302.
↑ Matsuoka T, Uematsu H, Iwakiri S, Itoi K (2013). “[Chronic eosinophilic pneumonia presenting as a solitary nodule, suspicious of lung cancer;report of a case]”. Kyobu Geka. 66 (10): 941–3. PMID 24008649.
↑ Beeson, Michael S. “Superior Vena Cava Syndrome”. Retrieved 2008-03-24.
↑ Radiation Oncology/Palliation/SVC Syndrome. WikiBooks https://en.wikibooks.org/wiki/Radiation_Oncology/Palliation/SVC_Syndrome Accessed on January 13, 2016
↑ Bruzzi JF, Komaki R, Walsh GL, Truong MT, Gladish GW, Munden RF, Erasmus JJ (2008). “Imaging of non-small cell lung cancer of the superior sulcus: part 1: anatomy, clinical manifestations, and management”. Radiographics. 28 (2): 551–60, quiz 620. doi:10.1148/rg.282075709. PMID 18349457.
↑ Foroulis CN, Zarogoulidis P, Darwiche K, Katsikogiannis N, Machairiotis N, Karapantzos I, Tsakiridis K, Huang H, Zarogoulidis K (September 2013). “Superior sulcus (Pancoast) tumors: current evidence on diagnosis and radical treatment”. J Thorac Dis. 5 Suppl 4: S342–58. doi:10.3978/j.issn.2072-1439.2013.04.08. PMC 3791502. PMID 24102007.
↑ Marulli G, Battistella L, Mammana M, Calabrese F, Rea F (June 2016). “Superior sulcus tumors (Pancoast tumors)”. Ann Transl Med. 4 (12): 239. doi:10.21037/atm.2016.06.16. PMC 4930518. PMID 27429965.
↑ Thoracic outlet syndrome Mount Sinai Hospital, New York
↑ Stepansky F, Hecht EM, Rivera R, Hirsh LE, Taouli B, Kaur M, Lee VS. Dynamic MR angiography of upper extremity vascular disease: pictorial review. Radiographics. 2008 Jan-Feb;28(1):e28. Epub 2007 Oct 29. PMID 17967936
↑ Superior Vena Cava Syndrome.Dr Amir Rezaee and Radswiki et al. Radiopedia http://radiopaedia.org/articles/superior-vena-cava-obstruction Accessed on January 13, 2016
↑ Erasmus JJ, Connolly JE, McAdams HP, Roggli VL (2000). “Solitary pulmonary nodules: Part I. Morphologic evaluation for differentiation of benign and malignant lesions”. Radiographics. 20 (1): 43–58. doi:10.1148/radiographics.20.1.g00ja0343. PMID 10682770.
↑ Gümüştaş S, Inan N, Akansel G, Ciftçi E, Demirci A, Ozkara SK (June 2012). “Differentiation of malignant and benign lung lesions with diffusion-weighted MR imaging”. Radiol Oncol. 46 (2): 106–13. doi:10.2478/v10019-012-0021-3. PMC 3472932. PMID 23077446.
↑ Maxwell RJ, Gibbons JR, O’Hara MD (January 1985). “Solitary squamous papilloma of the bronchus”. Thorax. 40 (1): 68–71. PMC 459982. PMID 3969658.
↑ Shiota Y, Matsumoto H, Sasaki N, Taniyama K, Hashimoto S, Sueishi K (1998). “Solitary bronchioloalveolar adenoma of the lung”. Respiration. 65 (6): 483–5. doi:10.1159/000029319. PMID 9817965.
↑ Kanchustambham V, Saladi S, Patolia S, Mahmoud Assaf S, Stoeckel D (March 2017). “A Rare Case of a Benign Primary Pleomorphic Adenoma of the Lung”. Cureus. 9 (3): e1069. doi:10.7759/cureus.1069. PMC 5375953. PMID 28409070.
↑ Kelley LC, Puette M, Langheinrich KA, King B (November 1994). “Bovine pulmonary blastomas: histomorphologic description and immunohistochemistry”. Vet. Pathol. 31 (6): 658–62. doi:10.1177/030098589403100605. PMID 7863581.
↑ Roth E, Smidt D (January 1970). “[Studies on early ejaculate collection using electroejaculation in German improved land-swines and Goettinger miniature pigs]”. Berl. Munch. Tierarztl. Wochenschr. (in German). 83 (1): 7–11. PMID 5528918.
↑ Jackman DM, Johnson BE (2005). “Small-cell lung cancer”. Lancet. 366 (9494): 1385–96. doi:10.1016/S0140-6736(05)67569-1. PMID 16226617.
↑ Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. “Chapter 13, box on morphology of adenocarcinoma”. Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN 1-4160-2973-7.
↑ Soda M, Choi YL, Enomoto M, Takada S, Yamashita Y, Ishikawa S; et al. (2007). “Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer”. Nature. 448 (7153): 561–6. doi:10.1038/nature05945. PMID 17625570.
↑ Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Adenocarcinoma_%283950819000%29.jpg
↑ Rossi G, Mengoli MC, Cavazza A, Nicoli D, Barbareschi M, Cantaloni C, Papotti M, Tironi A, Graziano P, Paci M, Stefani A, Migaldi M, Sartori G, Pelosi G (January 2014). “Large cell carcinoma of the lung: clinically oriented classification integrating immunohistochemistry and molecular biology”. Virchows Arch. 464 (1): 61–8. doi:10.1007/s00428-013-1501-6. PMID 24221342.
↑ Huang SY, Shen SJ, Li XY (October 2013). “Pulmonary sarcomatoid carcinoma: a clinicopathologic study and prognostic analysis of 51 cases”. World J Surg Oncol. 11: 252. doi:10.1186/1477-7819-11-252. PMC 3850921. PMID 24088577.
↑ Dahabreh J, Stathopoulos GP, Koutantos J, Rigatos S (March 2009). “Lung carcinoid tumor biology: treatment and survival”. Oncol. Rep. 21 (3): 757–60. PMID 19212636.
↑ Elnayal A, Moran CA, Fox PS, Mawlawi O, Swisher SG, Marom EM (July 2013). “Primary salivary gland-type lung cancer: imaging and clinical predictors of outcome”. AJR Am J Roentgenol. 201 (1): W57–63. doi:10.2214/AJR.12.9579. PMC 3767141. PMID 23789697.
↑ Greenberg AK, Yee H, Rom WN (2002). “Preneoplastic lesions of the lung”. Respir. Res. 3: 20. PMC 107849. PMID 11980589.
↑ Koenigkam-Santos M, Sommer G, Puderbach M, Safi S, Schnabel PA, Kauczor HU, Heussel CP (April 2014). “Primary intrathoracic malignant mesenchymal tumours: computed tomography features of a rare group of chest neoplasms”. Insights Imaging. 5 (2): 237–44. doi:10.1007/s13244-013-0306-0. PMC 3999366. PMID 24407922.

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Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]

Overveiw

Pancoast tumors are a rare type of non-small cell lung cancers (NSCLC), account for fewer than 5% of all lung cancers. In the United States, the age-adjusted prevalence of pancoast tumor is estimated to be 5 per 100,000. In 2014, the incidence of Pancoast tumor was approximately 3 per 100,000 individuals. It is rare in people under age 45. Males are thought to be more predisposed to the development of lung cancer. The male to female ratio for the incidence of lung cancer is approximately 1.4 to 1. There is no racial predilection for Pancoast tumor. The incidence of lung cancer is lower in developing countries than in developed countries. Western Europe and the U.S. have the highest incidence of lung cancer.

Epidemiology and Demographics

Pancoast tumors are a rare type of non-small cell lung cancers (NSCLC), account for fewer than 5% of all lung cancers.^[1]^[2]

Prevalence

In the United States, the age-adjusted prevalence of pancoast tumor is estimated to be 5 per 100,000 individuals.^[3]^[4]
The prevalence of lung cancer significantly increases among smokers and individuals with chronic exposure to risk factors for lung cancer.

Incidence

In 2014, the incidence of Pancoast tumor was approximately 3 per 100,000 individuals.^[3]^[4]
According to the American Cancer Society, an estimated 3,000 nonsmoking adults will die each year from lung cancer related to breathing secondhand smoke.
Each year more people die of lung cancer than breast, colon, and prostate cancers combined.
It is unclear whether the increased incidence of lung cancer is due to increased cancers or improved cancer detection (e.g. screening techniques).

Age

Lung cancer is more common in older people. It is rare in people under age 45.^[5]

Gender

Males are thought to be more predisposed to the development of lung cancer. This gender discrepancy is often attributed to the historically increased rate of smoking among males compared to females.^[4]
The male to female ratio for the incidence of lung cancer is approximately 1.4 to 1.

Race

There is no racial predilection for Pancoast tumor.^[4]

Developing Countries

The incidence of lung cancer is lower in developing countries than in developed countries. It is unknown whether this decreased incidence is due to decreased cancer rates or decreased detection rates.^[5]

Developed Countries

Western Europe and the U.S. have the highest incidence of lung cancer.^[3]

References

↑ Howlader N, Noone AM, Krapcho M, Garshell J, Miller D, Altekruse SF, Kosary CL, Yu M, Ruhl J, Tatalovich Z, Mariotto A, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2011, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2011/, based on November 2013 SEER data submission, posted to the SEER web site, April 2014.
↑ Siegel, Rebecca; Ma, Jiemin; Zou, Zhaohui; Jemal, Ahmedin (2014). “Cancer statistics, 2014”. CA: A Cancer Journal for Clinicians. 64 (1): 9–29. doi:10.3322/caac.21208. ISSN 0007-9235.
↑ ^3.0 ^3.1 ^3.2 Ginsberg RJ, Martini N, Zaman M, Armstrong JG, Bains MS, Burt ME, McCormack PM, Rusch VW, Harrison LB (June 1994). “Influence of surgical resection and brachytherapy in the management of superior sulcus tumor”. Ann. Thorac. Surg. 57 (6): 1440–5. PMID 8010786.
↑ ^4.0 ^4.1 ^4.2 ^4.3 “Gender in lung cancer and smoking research” (PDF). World Health Organization. 2004. Retrieved 2007-05-26.
↑ ^5.0 ^5.1 Johnson DE, Goldberg M (June 1997). “Management of carcinoma of the superior pulmonary sulcus”. Oncology (Williston Park, N.Y.). 11 (6): 781–5, discussion 785–6. PMID 9189936.

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Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]

Overview

Common risk factors in the development of Pancoast tumor include asbestos exposure for prolonged period of time, exposure to gold, nickel, smoking, secondary smoke exposure.

Risk Factors

Common risk factors in the development of Pancoast tumor include:^[1]^[2]
- Asbestos exposure for prolonged period of time
- Exposure to gold, nickel
- Smoking
- Secondary smoke exposure

References

↑ Kraut MJ, Vallières E, Thomas CR (2003). “Pancoast (superior sulcus) neoplasms”. Curr Probl Cancer. 27 (2): 81–104. PMID 12717414.
↑ Nikolaos P, Vasilios L, Efstratios K, Panagiotis A, Christos P, Nikolaos B, Antonios H, Tsakiridis K, Zarogoulidis P, Zarogoulidis K, Katsikogiannis N, Kougioumtzi I, Machairiotis N, Tsiouda T, Machairiotis N, Madesis A, Vretzakis G, Kolettas A, Dimitrios D (2014). “Therapeutic modalities for Pancoast tumors”. J Thorac Dis. 6 Suppl 1: S180–93. doi:10.3978/j.issn.2072-1439.2013.12.31. PMC 3966148. PMID 24672693.

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Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]

Overview

There is insufficient evidence to recommend routine screening for Pancoast tumor.

Screening

There is insufficient evidence to recommend routine screening for Pancoast tumor.
The current guidelines for screening of lung cancer that results in pancoast tumor is as follows:
- In 2013, a clinical practice guideline by the U.S. Preventive Services Task Force (USPSTF) recommended screening for lung cancer among smokers and former smokers who are between 55 to 80 years old and who have smoked 30 pack-years or more and either continue to smoke or have quit within the past 15 years (grade B recommendation).^[1]
- Clinical practice guidelines issued by the American College of Chest Physicians in 2013 recommend:^[2]^[3]^[4]
  - For smokers and former smokers who are age 55 to 74 and who have smoked for 30 pack-years or more and either continue to smoke or have quit within the past 15 years, it was suggest that annual screening with low dose computed tomography (LDCT) should be offered in settings that can deliver the comprehensive care provided to National Lung Screening Trial (NLST) participants.

References

↑ “http://www.uspreventiveservicestaskforce.org/uspstf13/lungcan/lungcanfinalrs.htm”. Retrieved 31 December 2013. External link in |title= (help)
↑ Detterbeck FC, Mazzone PJ, Naidich DP, Bach PB (2013). “Screening for Lung Cancer: Diagnosis and Management of Lung Cancer, 3rd ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines”. Chest. 143 (5 Suppl): e78S–92S. doi:10.1378/chest.12-2350. PMID 23649455. Summary in JournalWatch
↑ Midthun, David E. (2016). “Early detection of lung cancer”. F1000Research. 5: 739. doi:10.12688/f1000research.7313.1. ISSN 2046-1402.
↑ Midthun, David E. (2011). “Screening for Lung Cancer”. Clinics in Chest Medicine. 32 (4): 659–668. doi:10.1016/j.ccm.2011.08.014. ISSN 0272-5231.

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Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mazia Fatima, MBBS [2]

Overview

The patient experiences non-specific symptoms such as cough, hemoptysis, dyspnea, chest pain, dysphonia, dysphagia, lack of appetite, weight loss, and fatigue from 3 weeks to 3 months before seeking medical attention. Without treatment, the patient will develop initial symptoms of cough and chest pain, which may eventually lead to Pancoast’s syndrome. The symptoms of Pancoast’s syndrome start as referred pain to the shoulder. Without treatment, the tumor may invade surrounding tissues to cause pain along the ulnar nerve distribution, atrophy of hand muscles and spinal cord compression. The complications associated with Pancoast tumor are breathing difficulties, pneumonia, hemoptysis, pain, pleural effusion,metastasis, Horner’s syndrome, superior vena cava syndrome, compression of the spinal cord, and paraplegia (paralysis of the lower half of the body with involvement of both legs) develop when the tumor extends into the intervertebral foramina (opening between two vertebrae). The prognosis of Pancoast tumor depends on the stage of the tumor at diagnosis. The factors associated with a poor prognosis among patients with Pancoast tumor include Horner’s syndrome, spread to the mediastinal lymph nodes, incomplete resection of tumor, involvement of supraclavicular lymph node, vertebral body invasion, metastasis to the brain.

Natural History

The patient experiences non-specific symptoms such as cough, hemoptysis, dyspnea, chest pain, dysphonia, dysphagia, lack of appetite, weight loss, and fatigue from 3 weeks to 3 months before seeking medical attention.^[1]^[2]^[3]
Without treatment, the patient will develop initial symptoms of cough and chest pain, which may eventually lead to Pancoast’s syndrome.
The symptoms of Pancoast’s syndrome start as referred pain to the shoulder. Without treatment, the tumor may invade surrounding tissues to cause pain along the ulnar nerve distribution, atrophy of hand muscles, and spinal cord compression.

Complications

Pancoast tumor is a subtype of lung cancer that is located at the apex of the lung.The complications associated with Pancoast tumor are:^[1]^[2]^[3]^[4]^[5]

Breathing difficulties

Lung cancer patients can experience trouble breathing especially when tumors grow and block the airways. Also, it is possible for fluid to build up in the lungs of the patients which makes it difficult for the lungs to fully expand when inhaling.

Pneumonia

If cancer grows in the airway, it may obstruct airflow, causing breathing difficulties. This can lead to accumulation of secretions behind the blockage, predisposing the patient to pneumonia.

Hemoptysis (coughing up blood)

Occasionally lung cancer can cause bleeding in the airways which results in the patient coughing up blood.

Pain

It is possible that Pancoast tumor will cause shoulder pain as well, especially if it spreads to the surrounding tissue resulting in Pancoast’s syndrome.

Pleural effusion

Lung cancer can cause fluid to build up in the lungs which can cause breathing difficulties.

Metastasis

In many cases, lung cancer will spread out to other parts of the body. Some of the more common places lung cancer metastasizes to are the bones, liver, brain, and adrenal glands.

Horner’s syndrome

Tumors in the apex of the lung, known as Pancoast tumors, may invade the local part of the sympathetic nervous system, leading to changed sweating patterns and eye muscle problems (a combination known as Horner’s syndrome).

Superior vena cava syndrome
- SVCS is a group of symptoms caused by obstruction of the superior vena cava. More than 60% of cases of superior vena cava obstruction are caused by malignant causes, typically a tumor outside the vessel compressing the vessel wall.
Compression of the spinal cord
- Spinal cord compression and paraplegia (paralysis of the lower half of the body with involvement of both legs) develop when the tumor extends into the intervertebral foramina (opening between two vertebrae).

Surgical Complications

Bronchopleural fistula

It is when air leaks from a pneumonectomy bronchial stump.
Experienced in approximately 2% of patients that undergo a pneumonectomy.
It commonly occurs approximately 7 to 10 days after surgery.

Hemothorax

In majority of cases, it occurs from bronchial vessels or lung parenchyma.
It may have the symptoms of hypovolemia.
Usually, it can be treated by transfusion.

Atelectasis
Sputum retention
Wound infection
Wound dehiscence
Air embolism
Respiratory failure associated with or without ARDS

Vascular complications

Neurological complications

Klumpke-Déjérine syndrome
Horner’s syndrome (miosis, ptosis, and enophthalmos)

Chemo-radiotherapy complications

Prognosis

The prognosis of Pancoast tumor depends on the stage of the tumor at diagnosis.^[6]^[7]^[8]
The presence of the following is associated with a poor prognosis among patients with Pancoast tumor:
- Horner’s syndrome
- Spread to the mediastinal lymph nodes
- Incomplete resection of tumor
- Involvement of supraclavicular lymph node
- Vertebral body invasion
- Metastasis to the brain
Pancoast tumor is associated with a 5 year survival rate as follows depending on the stage of disease:

Stage Of Pancoast Tumor	5 year survival rate
IIB	47%
IIIA	14%
IIIB	16%

References

↑ ^1.0 ^1.1 Glassman LR, Hyman K (July 2013). “Pancoast tumor: a modern perspective on an old problem”. Curr Opin Pulm Med. 19 (4): 340–3. doi:10.1097/MCP.0b013e3283621b31. PMID 23702478.
↑ ^2.0 ^2.1 Panagopoulos N, Leivaditis V, Koletsis E, Prokakis C, Alexopoulos P, Baltayiannis N, Hatzimichalis A, Tsakiridis K, Zarogoulidis P, Zarogoulidis K, Katsikogiannis N, Kougioumtzi I, Machairiotis N, Tsiouda T, Kesisis G, Siminelakis S, Madesis A, Dougenis D (March 2014). “Pancoast tumors: characteristics and preoperative assessment”. J Thorac Dis. 6 Suppl 1: S108–15. doi:10.3978/j.issn.2072-1439.2013.12.29. PMC 3966151. PMID 24672686.
↑ ^3.0 ^3.1 Jones DR, Detterbeck FC (July 1998). “Pancoast tumors of the lung”. Curr Opin Pulm Med. 4 (4): 191–7. PMID 10813231.
↑ Jones, DR (Jul 1998). “Pancoast tumors of the lung”. Current Opinion in Pulmonary Medicine. 4 (4): 191–197. PMID 10813231. Unknown parameter |coauthors= ignored (help)
↑ Eren S, Karaman A, Okur A (2006). “The superior vena cava syndrome caused by malignant disease. Imaging with multi-detector row CT”. Eur J Radiol. 59 (1): 93–103. doi:10.1016/j.ejrad.2006.01.003. PMID 16476534.
↑ Komaki R, Roth JA, Walsh GL, Putnam JB, Vaporciyan A, Lee JS, Fossella FV, Chasen M, Delclos ME, Cox JD (September 2000). “Outcome predictors for 143 patients with superior sulcus tumors treated by multidisciplinary approach at the University of Texas M. D. Anderson Cancer Center”. Int. J. Radiat. Oncol. Biol. Phys. 48 (2): 347–54. PMID 10974447.
↑ Ginsberg RJ, Martini N, Zaman M, Armstrong JG, Bains MS, Burt ME, McCormack PM, Rusch VW, Harrison LB (June 1994). “Influence of surgical resection and brachytherapy in the management of superior sulcus tumor”. Ann. Thorac. Surg. 57 (6): 1440–5. PMID 8010786.
↑ Johnson DE, Goldberg M (June 1997). “Management of carcinoma of the superior pulmonary sulcus”. Oncology (Williston Park, N.Y.). 11 (6): 781–5, discussion 785–6. PMID 9189936.

Template:WH Template:WS

Diagnosis

Treatment

Case Studies

Case #1

References

Template:WH Template:WS

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[pmid23702478-1] 1.0 ^1.1 Glassman LR, Hyman K (July 2013). “Pancoast tumor: a modern perspective on an old problem”. Curr Opin Pulm Med. 19 (4): 340–3. doi:10.1097/MCP.0b013e3283621b31. PMID 23702478.

[pmid24672686-2] 2.0 ^2.1 Panagopoulos N, Leivaditis V, Koletsis E, Prokakis C, Alexopoulos P, Baltayiannis N, Hatzimichalis A, Tsakiridis K, Zarogoulidis P, Zarogoulidis K, Katsikogiannis N, Kougioumtzi I, Machairiotis N, Tsiouda T, Kesisis G, Siminelakis S, Madesis A, Dougenis D (March 2014). “Pancoast tumors: characteristics and preoperative assessment”. J Thorac Dis. 6 Suppl 1: S108–15. doi:10.3978/j.issn.2072-1439.2013.12.29. PMC 3966151. PMID 24672686.

[pmid10813231-3] 3.0 ^3.1 Jones DR, Detterbeck FC (July 1998). “Pancoast tumors of the lung”. Curr Opin Pulm Med. 4 (4): 191–7. PMID 10813231.

[Jones-4] Jones, DR (Jul 1998). “Pancoast tumors of the lung”. Current Opinion in Pulmonary Medicine. 4 (4): 191–197. PMID 10813231. Unknown parameter |coauthors= ignored (help)

[pmid16476534-5] Eren S, Karaman A, Okur A (2006). “The superior vena cava syndrome caused by malignant disease. Imaging with multi-detector row CT”. Eur J Radiol. 59 (1): 93–103. doi:10.1016/j.ejrad.2006.01.003. PMID 16476534.

[pmid10974447-6] Komaki R, Roth JA, Walsh GL, Putnam JB, Vaporciyan A, Lee JS, Fossella FV, Chasen M, Delclos ME, Cox JD (September 2000). “Outcome predictors for 143 patients with superior sulcus tumors treated by multidisciplinary approach at the University of Texas M. D. Anderson Cancer Center”. Int. J. Radiat. Oncol. Biol. Phys. 48 (2): 347–54. PMID 10974447.

[pmid8010786-7] Ginsberg RJ, Martini N, Zaman M, Armstrong JG, Bains MS, Burt ME, McCormack PM, Rusch VW, Harrison LB (June 1994). “Influence of surgical resection and brachytherapy in the management of superior sulcus tumor”. Ann. Thorac. Surg. 57 (6): 1440–5. PMID 8010786.

[pmid9189936-8] Johnson DE, Goldberg M (June 1997). “Management of carcinoma of the superior pulmonary sulcus”. Oncology (Williston Park, N.Y.). 11 (6): 781–5, discussion 785–6. PMID 9189936.

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[24]

[25]

[26]

[27]

[28]

[29]

[1]

[2]

[3]

[4]

[5]

[1]

[2]

[1]

[2]

[3]

[4]

[1]

[2]

[3]

[4]

[5]

[6]

[7]

[8]

Pancoast tumor

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differential Diagnosis

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic study of choice

History and Symptoms

Physical Examination

Laboratory Tests

Electrocardiogram

Chest X-ray

CT scan

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

References

Overview

Historical Perspective

References

Overview

Classification

References

Overveiw

Pathophysiology

Gross Pathology

Microscopic Pathology

References

Overview

Causes

References

Overview

Differential Diagnosis

The following table summarizes the differentiation of various lung tumors based on histological and topographical features:[1][2][3][4][5][6][7][8][9][10][11][12][13]

References

Overveiw

Epidemiology and Demographics

Prevalence

Incidence

Age

Gender

Race

Developing Countries

Developed Countries

References

Overview

Risk Factors

References

Overview

Screening

References

Overview

Natural History

Complications

Prognosis

References

Diagnosis

Treatment

Case Studies

References

Looking for the patient version?

The following table summarizes the differentiation of various lung tumors based on histological and topographical features:^[1]^[2]^[3]^[4]^[5]^[6]^[7]^[8]^[9]^[10]^[11]^[12]^[13]