AD, BAC, and AAH in the case patient might have
occurred as a result of second-hit mutations L861Q and
L858R in the setting of a germline V843I mutation.
However, the effects of the EGFR V843I mutation on
EGFR signaling and the molecular importance of the dou-
ble mutation on EGFR exon 21 are unknown. The patient’s
father and a brother had died of lung cancer. However,
another brother and a sister, each of whom had germline
EGFR V843I mutation, have not developed lung cancer
despite being almost 70 years old. The role of germline
EGFR V843I mutation in multifocal lung carcinogenesis and
the familial occurrence of lung cancer in the case patient are
still unclear. In vitro experiments are needed to clarify the
effects of EGFR V843I mutation on EGFR signaling, as is
accumulation of clinical cases to determine the role of
germline EGFR mutation in lung carcinogenesis.
References
1. Zwirewich CV, Miller RR, Muller NL. Multicentric adenocar-
cinoma of the lung: CT-pathologic correlation. Radiology
1990;176:185–90.
2. Bell DW, Gore I, Okimoto RA, et al. Inherited susceptibility to
lung cancer may be associated with the T790M drug resis-
tance mutation in EGFR. Nat Genet 2005;37:1315– 6.
3. Blons H, Côté JF, Le Corre D, et al. Epidermal growth factor
receptor mutation in lung cancer is linked to bronchioloal-
veolar differentiation. Am J Surg Pathol 2006;30:1309–15.
4. Tang X, Shigematsu H, Bekele N, et al. EGFR tyrosine kinase
domain mutations are detected in histologically normal re-
spiratory epithelium in lung cancer patients. Cancer Res
2005;65:7568 –72.
5. Ji H, Li D, Chen L, et al. The impact of human EGFR kinase
domain mutations on lung tumorigenesis and in vivo sensi-
tivity to EGFR-targeted therapies. Cancer Cells 2006;9:485–95.
6. Shih J-Y, Gow C-H, Yu C-J, et al. Epidermal growth factor
receptor mutation in needle biopsy/aspiration samples pre-
dicts response to gefitinib therapy and survival of patients
with advanced non–small cell lung cancer. Int J Cancer
2006;118:963–9.
7. Leone F, Cavalloni G, Pignochino Y, et al. Somatic mutation of
epidermal growth factor recepter in bile duct and gallbladder
carcinoma. Clin Cancer Res 2006;12:1680 –5.
8. Knudson AG Jr. Overview: genes that predispose to cancer.
Mutat Res 1991;247:185–90.
Pseudocavitating
Bronchioloalveolar Carcinoma
Followed Over a Decade
Jason P. Shaw, MD, Pablo A. Bejarano, MD,
and Richard J. Thurer, MD
Department of Surgery, Division of Cardiothoracic Surgery,
and Department of Pathology, University of Miami Miller
School of Medicine, Miami, Florida
A 38-year-old woman with bronchioloalveolar carcinoma
(BAC) had a slow-growing cavitary nodule for nearly a
decade. When she was hospitalized because of pneumo-
nia 9 years earlier, a chest computed tomography scan
showed a 1.5-cm cavitary right upper lobe nodule. At 1, 3,
and 9 years computed tomography scans showed slow
growth of the nodule to 2.4 cm, corresponding to a
volume doubling time of 1494 days. Thoracoscopic bi-
opsy and lobectomy were performed. Pathologic analysis
revealed a well-differentiated mucinous BAC (T1N0M0).
Pseudocavitation in solitary BAC is rare. A longer period
of surveillance may be required to rule out malignancy in
this setting. Surgical resection remains the mainstay of
therapy.
(Ann Thorac Surg 2008;85:1432– 4)
© 2008 by The Society of Thoracic Surgeons
W
ith more widespread use of computed tomography
(CT) of the lung, small bronchioloalveolar carci-
nomas (BACs) are being diagnosed with increasing fre-
quency. Bronchioloalveolar carcinomas are generally
thought to have a more indolent course than other
subtypes of adenocarcinoma of the lung. While CT ap-
pearance varies, the presence of BAC as a solitary cavi-
tary nodule is rare. We report the case of a slow-growing
BAC in a young woman that highlights the importance of
prolonged surveillance or resection when BAC is in-
cluded in the differential diagnosis.
A 38-year-old woman with nonpleuritic chest pain and a
long-standing right upper lobe cavitary lesion, with a 3
pack-year smoking history, was referred for thoracic
surgical evaluation. Nine years previously the patient
had been hospitalized because of pneumonia involving
the posterior segment of the right upper lobe. Results of
tuberculin skin testing were negative. When a chest
radiograph at 6-month follow-up showed a persistent
mass, a CT scan of the chest was obtained, which re-
vealed a 1.5-cm rounded lesion with central lucency (Fig
1A). Bronchoscopy performed 1 year after initial presen-
tation was nondiagnostic. A chest CT scan obtained 9
years after initial presentation demonstrated the lesion in
the right upper lobe measuring 2.4 cm. A fluorodeoxy-
glucose positron emission tomography scan demon-
strated no uptake. Thoracoscopic biopsy followed by
lobectomy with lymph node dissection was performed.
Pathologic analysis revealed a 2.5-cm well-differentiated
mucinous BAC (T1N0M0) (Figs 2, 3). The patient had an
uneventful hospital course and was discharged on post-
operative day 4.
During nearly a decade, CT scans had been obtained at
various institutions, at 6 months and at 1, 3, and 9 years
after initial presentation (Figs 1A-D). Review of the scans
revealed a largest tumor diameter of 1.5 cm, 1.5 cm, 1.6 cm,
and 2.4 cm, respectively, suggesting tumor stability at
1 year. However, calculation of tumor volume from each CT
scan (V =/6 ab
2
, where a is the largest diameter and b
is the largest diameter perpendicular to a) showed an
increase in tumor volume at each interval, with volumes of
1.3 cm
3
, 1.4 cm
3
, 1.8 cm
3
, and 5.6 cm
3
, respectively. Tumor
Accepted for publication Oct 1, 2007.
Address correspondence to Dr Shaw, Department of Surgery, Division of
Cardiothoracic Surgery, University of Miami Miller School of Medicine, PO
Box 016960 (R-114), Miami, FL 33010; e-mail: jason.shaw@mssm.edu.
1432 CASE REPORT SHAW ET AL Ann Thorac Surg
PSEUDOCAVITATING BRONCHIOLOALVEOLAR CARCINOMA 2008;85:1432– 4
© 2008 by The Society of Thoracic Surgeons 0003-4975/08/$34.00
Published by Elsevier Inc doi:10.1016/j.athoracsur.2007.10.031
FEATURE ARTICLES