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Postgraduate Education Corner: Chest Imaging and Pathology for Clinicians |

An 82-Year-Old Woman With Left Upper Lobe AtelectasisLeft Upper Lobe Atelectasis FREE TO VIEW

Vandana Seeram, MBBS; Adil Shujaat, MBBS; Lisa Jones, MD; Abubakr Bajwa, MBBS, FCCP
Author and Funding Information

From the Department of Pulmonary/Critical Care (Drs Seeram, Shujaat, Jones, and Bajwa), and the Department of Sleep Medicine (Dr Bajwa), University of Florida, Jacksonville, FL.

Correspondence to: Vandana Seeram, MBBS, Department of Pulmonary/Critical Care, University of Florida, 655W 8th S, Jacksonville, FL 32209: e-mail: Vandana.seeram@jax.ufl.edu


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2012;142(6):1669-1674. doi:10.1378/chest.11-2925
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Published online

An 82-year-old woman was seen in the pulmonary clinic for complaints of shortness of breath and intermittent wheeze associated with cough productive of scanty white phlegm. This persisted despite treatment with an inhaled bronchodilator and two courses of antibiotics and prednisone that were prescribed by her primary care physician prior to evaluation in the pulmonary clinic. She was a lifelong nonsmoker with a medical history significant only for a partial colectomy, secondary to two reportedly malignant polyps in her colon, 5 years previously. She did not require any additional treatment after the colectomy and was told that she did not require any follow-up.

Physical examination was unremarkable at the time of initial evaluation in the pulmonary clinic. CBC count with differential, basic metabolic panel and hepatic panel was unremarkable. A chest radiograph showed atelectasis of the left upper lobe (Figs 1A, 1B), which was confirmed on CT scan (Figs 1C, 1D). Flexible bron­choscopy performed the subsequent week revealed an endobronchial lesion in the left main-stem bronchus partially occluding the left upper lobe bronchus (Fig. 2). Endobronchial biopsy specimens using forceps were sent for pathology, and bronchial brushings and washings were sent for cytology.

Figure Jump LinkFigure 1. A, Chest radiograph posteroanterior view demonstrating a Luftsichel sign, which is seen in left upper lobe collapse. This is a paraaortic crescent of air caused by expansion of the superior segment of the left lower lobe due to left upper lobe collapse. It usually extends anywhere from the left apex to the left superior pulmonary vein. B, Chest radiograph lateral view demonstrating an anteriorly displaced major fissure running parallel to the anterior chest wall that is seen as the left upper lobe collapses up against the anterior chest wall. C, CT chest scan revealing left upper lobe atelectasis with diffuse increased density throughout the left upper lobe accompanied by marked anterior displacement of the left major fissure and hyperinflation of the left lower lobe marked by attenuation of the lower lobe vasculature. D, CT chest scan section at the level of the carina suggesting an endobronchial lesion involving the anterior wall of the proximal left main bronchus with complete obstruction of the distal left main-stem/proximal left upper lobe bronchus, with only minimal residual air within the collapsed left upper lobe. Note that the left main fissure is again markedly shifted. Findings are suggestive of endobronchial neoplasia.Grahic Jump LocationGrahic Jump Location
Figure Jump LinkFigure 2. Bronchoscopic view of the left main-stem bronchus, with endobronchial lesion in the anterolateral aspect obstructing the left upper lobe bronchus takeoff. The opening to the left lower lobe segments remains patent.Grahic Jump Location

The initial pathology revealed infiltrative atypical lymphoid tissue that was highly suspicious for lymphoma, but more tissue was requested for a definitive diagnosis. The neoplastic cells stained positive for LCA and CD20 and negative for CD3, cytokeratins (AE 1:3, MAK-6), S-100 protein, and thyroid transcription factor-1. The bronchial brushings also revealed atypical cells that were suspicious for malignancy (Fig 3).

Figure Jump LinkFigure 3. A, Clusters of large B cells (hematoxylin and eosin stain; original magnification × 20). B, Tumor cells showing CD20 positivity.Grahic Jump Location

In the interim, the patient’s lactate dehydroge­nase level and a flow cytometric analysis of her peripheral blood revealed no evidence of an overt B-cell lymphop­roliferative disorder or an acute myeloproliferative disorder. A PET-CT scan showed increased fluorodeoxyglucose (FDG) uptake in the area of the left main-stem bronchus, with increased soft tissue density tracking along this structure. Maximal standardized uptake value (SUV) was 17.1. There was also left hilar lymphadenopathy with hypermetabolic activ­ity and SUV measuring 22.89, as well as bilateral subcentimeter pulmonary nodules that did not demonstrate increased FDG activity (Fig 4).

Figure Jump LinkFigure 4. Fused PET-CT scan revealing increased fluorodeoxyglucose uptake involving the left main-stem bronchus with increased soft tissue density tracking along it. Maximal standardized uptake value (SUV) is 17.1. There is additional hypermetabolic activity in the left hilar region, with an SUV of 22.89. A, Axial view. B, Coronal view.Grahic Jump Location

Flexible bronchoscopy was repeated to obtain more tissue, as well as to perform endobronchial ultrasound-guided transbronchial needle aspiration of the left hilar lymph node. Specimens were sent for flow cytometric analysis and pathology. Enough tissue was obtained for the pathologist to make a definitive diag­nosis on this occasion, and additional fresh tissue was sent for flow cytometric analysis.

What is the diagnosis?
Diagnosis: Diffuse large B-cell lymphoma
Clinical Discussion

Diffuse large B-cell lymphoma (DLBCL) is the most common primary pulmonary lymphoma (PPL) after mucosa-associated lymphoid tissue (MALT)-type lymphoma. PPL is very rare. Although extranodal forms of lymphoma account for 24% to 50% of cases of non-Hodgkin’s lymphoma (NHL), PPL accounts for only 2% to 4% of extranodal NHL, <1% of NHL, and only 0.5% to 1% of primary pulmonary malignancies.1

A review of the literature indicated a relative paucity of data on diffuse large B-cell PPL, with even fewer data on the clinical and roentgenographic signs at the time of diagnosis. The optimal treatment and prognostic factors of this disease are poorly defined.2,3

DLBCL is often associated with immunosuppression, as seen in solid organ (heart/lung) allograft recipients on OKT3 or cyclosporin A, or in HIV infection.1 DLBCL is rarely seen in immunocompetent patients. It presents in the sixth to seventh decade in such individuals.

We describe an 82-year-old white woman with a fairly acute cough and lobar collapse on chest CT scan. Most reported cases present with respiratory symptoms, of which cough is the most frequent. Dyspnea, chest pain, and hemoptysis have also been described. Constitutional and B symptoms, including fever, fatigue, diaphoresis, and weight loss, although less common, occurred in 16% to 37% of cases in differ­ent series.2,4,5

In the primary care setting, the patient had bronchospasm described and was treated with corticosteroids and antibiotics that reportedly intermittently helped her symptoms, likely because of intermittent mucus plugging and lobar atelectasis in the affected region. Initial bronchoscopic evaluation revealed a large amount of thin and easily suctioned mucus at the level of the left upper lobe bronchus, and repeated imaging of her chest showed resolution of her lobar atelectasis.

Radiologic Discussion

Radiologic findings are various in pulmonary DLBCL and include solitary or multiple pulmonary nodules, masses, consolidation, hilar/mediastinal adenopathy, pleural effusion, and, rarely, direct chest wall invasion. It is rare for an endobronchial lesion to be the primary presentation of lymphoma. Only a few cases describing a similar scenario are reported in the literature, more often in Hodgkin’s disease than in NHL.6-8 Chest radiographs and CT scans revealed endobronchial lesions with varying degrees of lobar collapse in approximately one-half of the cases with endobronchial involvement.6-8

The patient presented with left upper lobe collapse and on bronchoscopic evaluation was found to have almost-complete occlusion of her left upper lobe bronchus by an endobronchial lesion. Although bronchoscopic examination was performed in previous case series, diagnosis via direct bronchoscopic biopsy was achieved in only 10% to 16% of patients reported previously.2,4,9

Her chest radiograph posteroanterior view showed low left lung volume and haziness of the left lung with obliteration of the left heart border. A Luftsichel sign was also noted, with a paraaortic crescent of air caused by expansion of the superior segment of the left lower lobe due to left upper lobe collapse.

The fused PET-CT images of the patient, which were obtained by combining the nuclear medicine PET image molecular function with the anatomical detail on CT images, showed a highly metabolically active tumor with increased FDG uptake involving the left main-stem bronchus with a maximal SUV of 17.1 and in the left hilar region with an SUV of 22.89. The intensity of the accumulation of radio-labeled glucose on PET scanning may be determined by calculating the SUV. In patients with NHL, the highest mean and median values of SUV were observed in patients with DLBCL.10

Pathologic Discussion

The Ann Arbor staging system with Cotswold mod­ification, which was originally developed for staging of Hodgkin’s lymphoma, has been adapted for staging of NHL.11 Non-MALT types of PPL include all NHLs without the features listed previously, as classified histologically by the working formulation.12 The stag­ing classification used for these extranodal lymphomas is as follows:

  • Stage I E: involvement of lung only (can be bilateral)

  • Stage II 1E: involvement of lung and hilar lymph nodes

  • Stage II 2E: involvement of lung and mediastinal lymph nodes

  • Stage II 2EW: involvement of lung and adjacent chest wall or diaphragm

  • Stage III: involvement of lung and lymph nodes below diaphragm

  • Stage IV: diffuse involvement of one or more extralymphatic organs or tissues

More recently, in 2008, the International Agency for Research on Cancer published the fourth edition of the World Health Organization Classification of Tumors of Hematopoietic and Lymphoid Tissues,13 which provides a greater appreciation of the stratification and subclassification of DLBCL as follows:

  • Extranodal marginal zone B-cell MALT-type lymphoma

  • Diffuse large B-cell lymphoma, not otherwise specified

  • T-cell/histiocyte-rich large B-cell lymphoma

  • DLBCL associated with chronic inflammation

  • Epstein-Barr virus (EBV) + DLBCL of the elderly

  • Primary mediastinal (thymic) large B-cell lymphoma

  • Intravascular large B-cell lymphoma

  • Primary cutaneous DLBCL, leg type

The differentiation between MALT-type lymphoma and extranodal DLBCL is based primarily on morphologic features. Large clusters or sheets of large B cells are sufficient to warrant the diagnosis of DLBCL. The term “high-grade MALT-type lymphoma” should not be used for DLBCL because this may lead to inappropriate undertreatment of DLBCL which is generally associated with a worse prognosis.11,14,15

The differential diagnosis of an endobronchial lesion is extensive and includes benign as well as malignant causes. Primary malignancies most commonly include bronchogenic carcinoma and carcinoid tumors but can also include lymphomas, as in our case; tumors of salivary origin such as adenoid cystic carcinoma and mucoepidermoid carcinoma; Kaposi sarcoma; malignant melanomas; and metastatic spread from renal, breast, and primary colon carcinomas. Numerous benign tumors may also present as endobronchial lesions and, even though they are rare (1.9% of all lung tumors),16 these include hamartoma, leiomyoma, lipoma, neurogenic tumor, inflammatory polyps (fibroepithelial polyp), amyloidoma, papilloma, and pleomorphic adenoma (benign mixed tumor)

Lymphomatoid granulomatosis is an EBV-associated lymphoproliferative disorder primarily involving the lung and can be classified as a form of large B-cell lymphoma in most cases. There are varying numbers of CD20-positive large lymphoid cells within a background of CD3-positive reactive small lymphocytes and these may mimic PPLs in clinical presentation and in the finding of monomorphic foci of atypical lymphoid cells secondarily involving the lung.17 Anaplastic lymphoma kinase and anaplastic T-cell lymphoma may also cause tracheal and endobronchial lesions that may mimic pulmonary DLBCL.18,19 As mentioned in the new World Health Organization classification of DLBCL in 2008, EBV and DLBCL of the elderly is a distinct clinicopathologic entity that may also present as extranodal disease and should be considered in the differential diagnosis.20

Multiple studies have demonstrated that the prognosis in NHL depends far more on the histopathology and is secondarily influenced by clinical parameters. Because the stage usually depends only on tumor location and the number of disease sites, it is not a true measure of tumor burden, which is an important prognostic determinant. Elevated serum lactate dehydrogenase level and hilar/mediastinal lymphadenopathy at diagnosis have been independently associated with a poor overall survival. From a prognostic viewpoint, it is important to determine the T- or B-immunophenotype of the tumor cells for diagnosis21 because primarily pulmonary B-cell lymphoma is a low-grade malignancy and complete resection may be curative. The patient was not considered a surgical candidate because of the proximity of the endobronchial lesion to her left main-stem bronchus. Even if she were, she would have opted for a more conservative approach with chemotherapy alone, secondary to her age and family obligations.

Treatment options for nonbulky limited NHL include a combined modality of abbreviated chemotherapy plus involved-field radiation vs longer regimens of chemotherapy alone. There was no difference in failure-free or overall survival between the two treatment arms and no evidence of a plateau in the survival curve at 10 year follow-up.22 The preferred chemotherapy regimen is cyclophosphamide, doxorubicin, vincristine, and prednisone with the addition of rituximab (R-CHOP) for improving the overall survival.

A bone marrow biopsy was performed. It revealed normocellular marrow with trilinear hematopoiesis with maturation, and no tumor (especially no evidence of diffuse large B-cell lymphoma) or granulomas were seen. Flow cytometric analysis of the bone marrow aspirate revealed no overt evidence of a B-cell lymphoproliferative disorder.

The patient was started on R-CHOP chemotherapy for her stage II E diffuse large B-cell lymphoma and has received five cycles so far with dramatic resolution of her respiratory symptoms. A repeat PET-CT scan after three cycles showed no metabolic activity in the region of the left hilum (Figs 5, 6)

Figure Jump LinkFigure 5. Posttreatment CT chest scan at the level of the carina with resolved left upper lobe atelectasis and no endobronchial lesion visible in the left main-stem bronchus.Grahic Jump Location
Figure Jump LinkFigure 6. Posttreatment fused PET-CT scan without a metabolically active tumor of the left main-stem bronchus or left hilar region compared with pretreatment imaging.Grahic Jump Location

Diffuse large B-cell PPL is an extremely rare entity with nonspecific signs and symptoms. When diagnosed early and treated appropriately, these tumors are associated with a good prognosis and excellent long-term survival. Despite the patient having an elevated lactate dehydrogenase and left hilar lymphadenopathy, which have been associated with worse outcomes, she has done remarkably well and is asymptomatic after conventional therapy with single-modality R-CHOP chemotherapy.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Other contributions: This work was performed at the University of Florida, Jacksonville, Florida.

Cadranel J, Wislez M, Antoine M. Primary pulmonary lymphoma. Eur Respir J. 2002;20(3):750-762. [CrossRef] [PubMed]
 
Ferraro P, Trastek VF, Adlakha H, Deschamps C, Allen MS, Pairolero PC. Primary non-Hodgkin’s lymphoma of the lung. Ann Thorac Surg. 2000;69(4):993-997. [CrossRef] [PubMed]
 
Habermann TM, Ryu JH, Inwards DJ, Kurtin PJ. Primary pulmonary lymphoma. Semin Oncol. 1999;26(3):307-315. [PubMed]
 
Kim JH, Lee SH, Park J, et al. Primary pulmonary non-Hodgkin’s lymphoma. Jpn J Clin Oncol. 2004;34(9):510-514. [CrossRef] [PubMed]
 
Huang J, Lin T, Li ZM, Xu R, Huang H, Jiang W. Primary pulmonary non-Hodgkin’s lymphoma: a retrospective analysis of 29 cases in a Chinese population. Am J Hematol. 2010;85(7):523-525. [CrossRef] [PubMed]
 
Trédaniel J, Peillon I, Fermé C, Brice P, Gisselbrecht C, Hirsch A. Endobronchial presentation of Hodgkin’s disease: a report of nine cases and review of the literature. Eur Respir J. 1994;7(10):1852-1855. [CrossRef] [PubMed]
 
Berkman N, Lafair J, Okon E, Polliack A. Obstructive solitary bronchial non-Hodgkin’s lymphoma—a rare presentation of primary extranodal disease. Leuk Lymphoma. 1992;8(4-5):405-407. [CrossRef] [PubMed]
 
McRae WM, Wong CS, Jeffery GM. Endobronchial non-Hodgkin’s lymphoma. Respir Med. 1998;92(7):975-977. [CrossRef] [PubMed]
 
Fiche M, Caprons F, Berger F, et al. Primary pulmonary non-Hodgkin’s lymphomas. Histopathology. 1995;26(6):529-537. [CrossRef] [PubMed]
 
Papajík T, Mysliveček M, Sedová Z, et al. Standardised uptake value of18F-FDG on staging PET/CT in newly diagnosed patients with different subtypes of non-Hodgkin’s lymphoma. Eur J Haematol. 2011;86(1):32-37. [CrossRef] [PubMed]
 
Rosenberg SA. Validity of the Ann Arbor staging classification for the non-Hodgkin’s lymphomas. Cancer Treat Rep. 1977;61(6):1023-1027. [PubMed]
 
Harris NL, Jaffe ES, Diebold J, et al. World Health Organization classification of neoplastic diseases of the hematopoietic and lymphoid tissues: report of the Clinical Advisory Committee meeting-Airlie House, Virginia, November 1997. J Clin Oncol. 1999;17(12):3835-3849. [PubMed]
 
Swerdlow SH, Campo E, Harris NL, et al. WHO Classification of Tumors of Haematopoietic and Lymphoid Tissues. 20084th ed. Lyon, France: IARC Press;
 
Radaszkiewicz T, Dragosics B, Bauer P. Gastrointestinal malignant lymphomas of the mucosa-associated lymphoid tissue: factors relevant to prognosis. Gastroenterology. 1992;102(5):1628-1638. [PubMed]
 
Neri N, Jesús Nambo M, Avilés A. Diffuse large B-cell lymphoma primary of lung. Hematology. 2011;16(2):110-112. [CrossRef] [PubMed]
 
Ko JM, Jung JI, Park SH, et al. Benign tumors of the tracheobronchial tree: CT-pathologic correlation. AJR Am J Roentgenol. 2006;186(5):1304-1313. [CrossRef] [PubMed]
 
Katzenstein AL, Doxtader E, Narendra S. Lymphomatoid granulomatosis: insights gained over 4 decades. Am J Surg Pathol. 2010;34(12):e35-e48. [CrossRef] [PubMed]
 
Tan DS, Eng PC, Lim ST, Tao M. Primary tracheal lymphoma causing respiratory failure [published corrction appears inJ Thorac Oncol. 2008;3(10)1193]. J Thorac Oncol. 2008;3(8):929-930. [CrossRef] [PubMed]
 
Fernandez FG, Denlinger CE, Crabtree TD. Primary non-Hodgkin’s lymphoma of the trachea. J Thorac Oncol. 2010;5(3):403-404. [CrossRef] [PubMed]
 
Xu FP, Liu YH, Zhuang HG, et al. Clinicopathological features of Epstein-Barr virus-positive diffuse large B-cell lymphoma in elderly [in Chinese]. Zhonghua Bing Li Xue Za Zhi. 2011;40(9):616-621. [PubMed]
 
Tamura A, Komatsu H, Yanai N, et al The Japan National Chest Hospital Study Group for Lung Cancer Primary pulmonary lymphoma: relationship between clinical features and pathologic findings in 24 cases. Jpn J Clin Oncol. 1995;25(4):140-152. [PubMed]
 
Miller TP, LeBlanc M, Spier C, et al. CHOP alone compared to CHOP plus radiotherapy for early stage aggressive non-Hodgkin’s lymphomas: update of the Soutwest Oncology Group (SWOG) randomized trial. Blood. 2001;98(3):724. [CrossRef]
 

Figures

Figure Jump LinkFigure 1. A, Chest radiograph posteroanterior view demonstrating a Luftsichel sign, which is seen in left upper lobe collapse. This is a paraaortic crescent of air caused by expansion of the superior segment of the left lower lobe due to left upper lobe collapse. It usually extends anywhere from the left apex to the left superior pulmonary vein. B, Chest radiograph lateral view demonstrating an anteriorly displaced major fissure running parallel to the anterior chest wall that is seen as the left upper lobe collapses up against the anterior chest wall. C, CT chest scan revealing left upper lobe atelectasis with diffuse increased density throughout the left upper lobe accompanied by marked anterior displacement of the left major fissure and hyperinflation of the left lower lobe marked by attenuation of the lower lobe vasculature. D, CT chest scan section at the level of the carina suggesting an endobronchial lesion involving the anterior wall of the proximal left main bronchus with complete obstruction of the distal left main-stem/proximal left upper lobe bronchus, with only minimal residual air within the collapsed left upper lobe. Note that the left main fissure is again markedly shifted. Findings are suggestive of endobronchial neoplasia.Grahic Jump LocationGrahic Jump Location
Figure Jump LinkFigure 2. Bronchoscopic view of the left main-stem bronchus, with endobronchial lesion in the anterolateral aspect obstructing the left upper lobe bronchus takeoff. The opening to the left lower lobe segments remains patent.Grahic Jump Location
Figure Jump LinkFigure 3. A, Clusters of large B cells (hematoxylin and eosin stain; original magnification × 20). B, Tumor cells showing CD20 positivity.Grahic Jump Location
Figure Jump LinkFigure 4. Fused PET-CT scan revealing increased fluorodeoxyglucose uptake involving the left main-stem bronchus with increased soft tissue density tracking along it. Maximal standardized uptake value (SUV) is 17.1. There is additional hypermetabolic activity in the left hilar region, with an SUV of 22.89. A, Axial view. B, Coronal view.Grahic Jump Location
Figure Jump LinkFigure 5. Posttreatment CT chest scan at the level of the carina with resolved left upper lobe atelectasis and no endobronchial lesion visible in the left main-stem bronchus.Grahic Jump Location
Figure Jump LinkFigure 6. Posttreatment fused PET-CT scan without a metabolically active tumor of the left main-stem bronchus or left hilar region compared with pretreatment imaging.Grahic Jump Location

Tables

References

Cadranel J, Wislez M, Antoine M. Primary pulmonary lymphoma. Eur Respir J. 2002;20(3):750-762. [CrossRef] [PubMed]
 
Ferraro P, Trastek VF, Adlakha H, Deschamps C, Allen MS, Pairolero PC. Primary non-Hodgkin’s lymphoma of the lung. Ann Thorac Surg. 2000;69(4):993-997. [CrossRef] [PubMed]
 
Habermann TM, Ryu JH, Inwards DJ, Kurtin PJ. Primary pulmonary lymphoma. Semin Oncol. 1999;26(3):307-315. [PubMed]
 
Kim JH, Lee SH, Park J, et al. Primary pulmonary non-Hodgkin’s lymphoma. Jpn J Clin Oncol. 2004;34(9):510-514. [CrossRef] [PubMed]
 
Huang J, Lin T, Li ZM, Xu R, Huang H, Jiang W. Primary pulmonary non-Hodgkin’s lymphoma: a retrospective analysis of 29 cases in a Chinese population. Am J Hematol. 2010;85(7):523-525. [CrossRef] [PubMed]
 
Trédaniel J, Peillon I, Fermé C, Brice P, Gisselbrecht C, Hirsch A. Endobronchial presentation of Hodgkin’s disease: a report of nine cases and review of the literature. Eur Respir J. 1994;7(10):1852-1855. [CrossRef] [PubMed]
 
Berkman N, Lafair J, Okon E, Polliack A. Obstructive solitary bronchial non-Hodgkin’s lymphoma—a rare presentation of primary extranodal disease. Leuk Lymphoma. 1992;8(4-5):405-407. [CrossRef] [PubMed]
 
McRae WM, Wong CS, Jeffery GM. Endobronchial non-Hodgkin’s lymphoma. Respir Med. 1998;92(7):975-977. [CrossRef] [PubMed]
 
Fiche M, Caprons F, Berger F, et al. Primary pulmonary non-Hodgkin’s lymphomas. Histopathology. 1995;26(6):529-537. [CrossRef] [PubMed]
 
Papajík T, Mysliveček M, Sedová Z, et al. Standardised uptake value of18F-FDG on staging PET/CT in newly diagnosed patients with different subtypes of non-Hodgkin’s lymphoma. Eur J Haematol. 2011;86(1):32-37. [CrossRef] [PubMed]
 
Rosenberg SA. Validity of the Ann Arbor staging classification for the non-Hodgkin’s lymphomas. Cancer Treat Rep. 1977;61(6):1023-1027. [PubMed]
 
Harris NL, Jaffe ES, Diebold J, et al. World Health Organization classification of neoplastic diseases of the hematopoietic and lymphoid tissues: report of the Clinical Advisory Committee meeting-Airlie House, Virginia, November 1997. J Clin Oncol. 1999;17(12):3835-3849. [PubMed]
 
Swerdlow SH, Campo E, Harris NL, et al. WHO Classification of Tumors of Haematopoietic and Lymphoid Tissues. 20084th ed. Lyon, France: IARC Press;
 
Radaszkiewicz T, Dragosics B, Bauer P. Gastrointestinal malignant lymphomas of the mucosa-associated lymphoid tissue: factors relevant to prognosis. Gastroenterology. 1992;102(5):1628-1638. [PubMed]
 
Neri N, Jesús Nambo M, Avilés A. Diffuse large B-cell lymphoma primary of lung. Hematology. 2011;16(2):110-112. [CrossRef] [PubMed]
 
Ko JM, Jung JI, Park SH, et al. Benign tumors of the tracheobronchial tree: CT-pathologic correlation. AJR Am J Roentgenol. 2006;186(5):1304-1313. [CrossRef] [PubMed]
 
Katzenstein AL, Doxtader E, Narendra S. Lymphomatoid granulomatosis: insights gained over 4 decades. Am J Surg Pathol. 2010;34(12):e35-e48. [CrossRef] [PubMed]
 
Tan DS, Eng PC, Lim ST, Tao M. Primary tracheal lymphoma causing respiratory failure [published corrction appears inJ Thorac Oncol. 2008;3(10)1193]. J Thorac Oncol. 2008;3(8):929-930. [CrossRef] [PubMed]
 
Fernandez FG, Denlinger CE, Crabtree TD. Primary non-Hodgkin’s lymphoma of the trachea. J Thorac Oncol. 2010;5(3):403-404. [CrossRef] [PubMed]
 
Xu FP, Liu YH, Zhuang HG, et al. Clinicopathological features of Epstein-Barr virus-positive diffuse large B-cell lymphoma in elderly [in Chinese]. Zhonghua Bing Li Xue Za Zhi. 2011;40(9):616-621. [PubMed]
 
Tamura A, Komatsu H, Yanai N, et al The Japan National Chest Hospital Study Group for Lung Cancer Primary pulmonary lymphoma: relationship between clinical features and pathologic findings in 24 cases. Jpn J Clin Oncol. 1995;25(4):140-152. [PubMed]
 
Miller TP, LeBlanc M, Spier C, et al. CHOP alone compared to CHOP plus radiotherapy for early stage aggressive non-Hodgkin’s lymphomas: update of the Soutwest Oncology Group (SWOG) randomized trial. Blood. 2001;98(3):724. [CrossRef]
 
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