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Lung Cancer |

Metastatic Non-small Cell Lung Cancer of Donor Origin Post Bilateral Lung Transplant

Fang-Yu Chao*, MD; Seth Force, MD; Anthony Gal, MD; E. Clinton Lawrence, MD; David Neujahr, MD; Felix Fernandez, MD; Allan Pickens, MD; Anisha Patel, MS; Marianne Foster, MS; Shiyong Li, MD; Remzi Bag, MD
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Emory University, Atlanta, GA


Chest. 2012;142(4_MeetingAbstracts):572A. doi:10.1378/chest.1384941
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Abstract

SESSION TYPE: Cancer Case Report Posters II

PRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION: Since the first case of donor-acquired lung cancer following pulmonary transplantation was described in 2001, only 4 cases of lung cancer of donor origin have been reported. We present one more patient with non-small cell lung carcinoma of donor origin.

CASE PRESENTATION: A female patient with the alpha-1 antitrypsin deficiency and end-stage emphysema received a bilateral lung transplantation at the age 58. The donor was a 51 year-old man who died of head trauma, with a 20 pack-year smoking history, schizophrenia and childhood polio. Both the donor and the recipient were Cytomegalovirus and Epstein-Barr virus positive. Immunosuppressive therapy included basiliximab for induction, tacrolimus, azathioprine and prednisolone. Five months after transplantation, the patient had left lower lobe pneumonia from Nocardia with a decreased lung function. Computer tomography (CT) of the chest revealed an enlarged left hilar lymph node deemed to be reactive. The consolidation improved initially with antibiotics but worsened during a later hospitalization. A follow-up CT scan 24 months after transplantation (Fig. 1) revealed an 18X11 mm nodule in the superior segment of the left lower lobe, positive with positron emission tomography (PET). She had a transbronchial biopsy showing atypical cells and further underwent a left lower lobe wedge resection 25 months after transplantation. The pathology of the nodule and ipisilateral hilar lymph node showed large cell carcinoma. Fluorescence in-situ hybridization was performed at the tumor cells, using DNA probes for the X and Y chromosomes to determine the origin. It showed 81% XY and confirmed the donor origin of the carcinoma. Restaging PET-CT 29 months after transplantation (Fig.2) showed interval increase in size and activity of the left lung mass abutting the hilum as well as multiple new lesions in the liver and bones. The patient declined chemotherapy, opted for home hospice and ultimately died.

DISCUSSION: In most cases, cancer in organ transplant recipients arises from cells of recipient origin (most commonly skin cancer or lymphoma). The rapid progression of the carcinoma in this patient might suggest immunosuppression leads to accelerated development of lung cancer which might have metastasized when the primary lesion could not be detected.

CONCLUSIONS: Immunosuppression in lung transplantation is required to protect the graft from rejection, but concomitantly compromises immunological control mechanisms against infection and cancer. More study is needed for adjusted immunosuppression protocol in patients developing cancer.

1) De Soyza AG, Dark JH, Parums DV, Curtis A, Corris PA. Donor-acquired small cell lung cancer following pulmonary transplantation. Chest 2001;120:1030-1.

2) Beyer EA, DeCamp MM, Smedira NG, Farver C, Mehta A, Warshawsky I. Primary adenocarcinoma in a donor lung: evaluation and surgical management. J Heart Lung Transplant 2003;22:1174-7.

DISCLOSURE: The following authors have nothing to disclose: Fang-Yu Chao, Seth Force, Anthony Gal, E. Clinton Lawrence, David Neujahr, Felix Fernandez, Allan Pickens, Anisha Patel, Marianne Foster, Shiyong Li, Remzi Bag

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Emory University, Atlanta, GA

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