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Ann Thorac Surg 2005;80:340-342
© 2005 The Society of Thoracic Surgeons


Case report

Primary Pulmonary Collision Cancer Consisting of Large Cell Carcinoma and Adenocarcinoma

Shoji Nakata, MDa, Yoshika Nagata, MDa, Masakazu Sugaya, MDa, Manabu Yasuda, MDa, Toshihiro Yamashita, MDa, Mitsuhiro Takenoyama, MDa, Takeshi Hanagiri, MDa, Masaru Morita, MDa, Tetsuo Hamada, MDb, Kenji Sugio, MDa,*, Kosei Yasumoto, MDa

a Second Department of Surgery, University of Occupational and Environmental Health, Kitakyushu, Japan
b Department of Pathology, University of Occupational and Environmental Health, Kitakyushu, Japan

Accepted for publication December 29, 2003.

* Address reprint requests to Dr Sugio, Second Department of Surgery, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan (Email: kensugio{at}med.uoeh-u.ac.jp).


    Abstract
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 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
A case of pulmonary collision tumor is herein reported. An abnormal shadow was discovered in the right lung of a 53-year-old man. A right upper lobectomy with a mediastinal lymph node dissection was performed. Based on the findings of a postoperative pathologic examination, this tumor was considered to be a collision tumor of large cell carcinoma and adenocarcinoma, as the distribution of each tumor was clearly separated. This case is the first report of a primary pulmonary collision tumor consisting of large cell carcinoma and adenocarcinoma.


    Introduction
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 Abstract
 Introduction
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 Acknowledgments
 References
 
A collision tumor, which is a special entity of multiple primary lung cancers, is defined as two independent neoplasms invading each other, and they have been reported in various organs. In previous studies the frequency of multiple primary lung cancers was reported to range from 1.4% to 5.1% [1, 2]. We herein report a rare case of a primary pulmonary collision tumor consisting of large cell carcinoma and adenocarcinoma.

A 53-year-old Japanese man was admitted to our hospital for an evaluation of a lung tumor that had been detected by a chest roentgenogram during a follow-up examination for a cerebral infarction. He had smoked 20 cigarettes a day for 33 years and had been a construction worker for 28 years. His chest roentgenogram on admission showed a mass measuring 4.2 x 4.0 cm in size in his right upper lung field, which had pleural indentation and spiculation. Chest computed tomography showed a mass in his right upper lobe. Neither hilar nor mediastinal lymphadenopathy was demonstrated (Fig 1). The serum concentration of squamous cell carcinoma-related antigen was 2.4 ng/mL (normal range, 0 to 1.5 ng/mL) and carcino embroyonic antigen was 2.8 ng/mL (normal range, 0 to 2.5 ng/mL). A transbronchial lung biopsy revealed histologic, poorly differentiated carcinoma. Routine brain computed tomography, abdominal computed tomography, and bone scintigraphy revealed no metastatic lesion. The clinical stage of the tumor was T2N0M0 (stage IB).



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Fig 1. Computed tomography of the chest shows a dumbbell-shaped mass in the right upper lobe. However, we saw no lymphadenopathy or pleural effusion.

 
Based on the findings previously mentioned, a right upper lobectomy and lymph node dissection was performed on April 18th, 2002. No pleural effusion, dissemination, or pulmonary metastasis was observed. The cut surface of the right upper lobe showed both a distinct grayish-white portion and a black portion (Fig 2).



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Fig 2. Macroscopic findings of the resected right upper lobe. The cut surface of the right upper lobe shows a distinct grayish-white portion and a black portion of the tumor (top). Topographic presentation shows two different components (bottom). (Ad. = adenocarcinoma.)

 
A histopathologic examination showed the carcinoma to be composed of two histologic, distinct subtypes, which consisted of a well differentiated papillary adenocarcinoma and a large cell carcinoma having large, clear cells with either irregularly shaped or giant nuclei. There was no transitional zone of adenocarcinoma to large cell carcinoma (Fig 3). Based on these findings, we diagnosed a primary collision tumor of lung. No metastatic lesion could be observed in the resected regional lymph nodes (T2N0M0, stage IB). The postoperative course was uneventful. No evidence of recurrence has been observed at 16 months postoperatively.



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Fig 3. Pathologic findings of the tumor shows two histologic, distinct subtypes separated by an interlobular fibrovascular stroma. (a) There is no transitional zone. (b) The large cell carcinoma has a clear cell and a clumped nucleus. (c) Adenocarcinoma is shown as a well-differentiated and papillary type.

 

    Comment
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 Abstract
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 Acknowledgments
 References
 
Collision tumors have been reported in various organs including the cervix, anorectal junction, oral cavity, liver, urinary bladder, and gastroesophageal junction. Collision tumors are defined as follows: (1) Two distinct topographically separate sites of origin for the two components must be present; (2) there must be at least some separation of the two components so that despite intimate mixing at the points of juxtaposition, a dual origin can still be recognized; and (3) at the areas of collision, in addition to the intimate mixing of the two components, some transitional patterns may be seen. Collision tumors are a special entity of synchronous multiple primary lung cancer and the incidence of synchronous multiple primary lung cancer in the reported series ranges from 0.3% to 3.0% [3, 4].

Several genetic changes are related to multistage carcinogenesis involving progression from pre-neoplastic lesions to malignant tumor development [5], and these are also consistent with the "field cancerization" process, whereby the whole tissue region is repeatedly exposed to environmental carcinogenic damage including tobacco smoke, which may result in the occurrence of multiple independent foci of cancer. The relative risk of lung cancer in smokers of 20 or more cigarettes a day is 20 to 30 times higher than in nonsmokers [6]. Regarding the influence of air pollution, the excess risk is reported to increase for large cell carcinoma (relative risk 2.6) and small cell carcinoma (relative risk 2.0) [7] in the center of the city. In previous reports, all patients with primary pulmonary collision cancer had a long history of smoking, including our present case.

It is difficult to diagnose pulmonary collision tumors before performing a surgical resection, because there are no characteristic clinical features. In our case, a chest computed tomography showed a dumbbell-shaped mass. In the resected specimen, each component of large cell carcinoma and adenocarcinoma was clearly separated both macroscopically and microscopically. At the point of collision, there were no histologic, transitional features. We believe there has not been no reports in the literature of a collision tumor consisting of large cell carcinoma and adenocarcinoma.

The prognosis of collision cancer is dependent on the biological behavior of each original cancer or on the progress of the disease. In NSCLC the most reliable prognostic factor is the TNM stage. The 5-year survival rate of pathologic stage IB was reported to be 60.1% in an analysis of lung cancer registry for 7,408 cases of resections in 1994 [8]. Therefore, a careful follow-up is necessary for our patient who was diagnosed with stage IB, even though no evidence of recurrence has been observed for 15 months postoperatively.


    Acknowledgments
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
We thank Dr Brian Quinn for his critical comments and for his help preparing this article.


    References
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 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 

  1. James W, John F, John R, Charles D, et al. Surgery second lung cancers Chest 2000;118:1621-1625.[Abstract/Free Full Text]
  2. Samuel A, Dennis M, Christopher A. The results of modern surgical therapy for multiple primary lung cancers Chest 1997;112:693-701.[Abstract/Free Full Text]
  3. Martini N, Melamed MR. Multiple primary lung cancers J Thorac Cardiovasc Surg 1975;70:606-612.[Abstract]
  4. Marcel T, Pieter Z, Aart B, et al. Survival in synchronous vs single lung cancer Chest 2000;118:952-958.[Abstract/Free Full Text]
  5. Sugio K, Kishimoto Y, Virmani AK, Hung JY, Gadzer AF. K-ras mutations are a relatively late event in the pathogenesis of lung carcinomas Cancer Res 1994;54:5811-5815.[Abstract/Free Full Text]
  6. Saracci R. Asbestos and lung canceran analysis of the epidemiological evidence on the asbestos-smoking interaction. Int J Cancer 1977;15:323-331.
  7. Fabio B, Massimo B, Furio C, et al. Air pollution and lung cancer in Trieste, Italy Am J Epidem 1995;141:1161-1169.[Abstract/Free Full Text]
  8. Shirakusa T, Kobayashi K. Lung cancer in Japananalysis of lung cancer registry for resected cases in 1994. Jpn J Lung Canc 2002;42:555-566(in Japanese).




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