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We report a rare case of lung adenocarcinoma in which micropapillary components were considered to cause stump recurrence. A woman in her fifties was diagnosed with lung cancer in the right middle lobe with invasion to the upper lobe, which was treated by a right middle lobectomy together with upper lobe partial resection. The cancer was pathologically diagnosed as adenocarcinoma and had a free surgical margin. There was no recurrence during the following 5 years and 8 months, and thus periodical surveillance, including computed tomography, was stopped. However, 2 years and 7 months after this, she was discovered to have an abnormal shadow on chest radiography, and a thorough examination revealed a 3-cm-sized tumor involving the previous surgical margin. Therefore, she underwent right upper lobectomy. We pathologically re-evaluated the first tumor and found that it was an adenocarcinoma with a micropapillary component in the periphery, 6mm away from the surgical margin. In addition, a few tiny clusters of tumor cells were found to be floating within the alveolar spaces near the margin. The first and second tumors showed almost the same histological mixture of components of adenocarcinoma and the same EGFR mutation. From these results, we concluded the second tumor was a stump recurrence originating from the first tumor resection. This case illustrates the importance of careful pathological investigation when an autosuture instrument is used for a partial resection in a case of lung adenocarcinoma with micropapillary components. In such cases, it is particularly important to clarify if micropapillary components are floating near a stump., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

We report a case of well-differentiated fetal adenocarcinoma (WDFA) of the lung, with emphasis on dynamic CT (computed tomography) findings. The patient was a 38-year-old woman who was found to have a mass in the left upper lung field in chest radiograph screening. Chest radiograph showed a 5.5 cm well-defined mass in the left upper lung field. CT revealed a well-circumscribed mass measuring 5.5 × 5.5 × 5.0 cm with a lobulated margin in the left upper lobe. Intratumoral enhancing vasculature was noted in the early phase of dynamic CT. In the delayed phase, persistent and plateau enhancement was seen. The tumor also had consistently unenhanced areas, suggesting the presence of necrosis. Left upper lobectomy with mediastinal lymph node dissection was performed. The pathology specimen contained tubular glands consisting of non-ciliated columnar cells with areas of solid nests of epithelial cells with weakly eosinophilic cytoplasm (morule) mimicking fetal lung tissue. The tumor was moderately vascularized with areas of comedo necrosis; the stroma was relatively scanty. Final pathological diagnosis was WDFA with left hilar lymph node metastasis (stage T2bN1M0). This is the first report of dynamic CT findings of WDFA, a rare lung tumor. Although these findings are non-specific, they well reflected the pathological characteristics of this tumor.

Background: Focal ground-glass opacity (GGO) on thin-section computed tomography (CT) may be seen in atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ that has recently been renamed from bronchioloalveolar carcinoma (BAC) and various benign conditions., Case Presentation: We report a case of pulmonary focal fibrosis associated with microscopic arterio-venous fistula (AVF), which showed a focal area of GGO on thin-section CT. The patient was a 58-year-old woman with a GGO on thin-section CT which had increased in size over the period of 2 years. Slightly dilated vessels and thickened interlobular septa were also noted around the GGO. It was diagnosed preoperatively as adenocarcinoma in situ and a partial lung resection by video-assisted thoracic surgery (VATS) was performed. Pathological examination yielded a diagnosis of focal fibrosis associated with microscopic AVF., Conclusion: We speculate that the focal fibrosis was produced by a prolonged congestion due to the AVF and that the dilated vessels and thickening of interlobular septa on thin-section CT related to the AVF. Microscopic AVF may be one of the etiologies of focal fibrosis showing focal GGO on thins-section CT. Dilated vessels and thickened interlobular septa around the GGO might offer a clue to the diagnosis of this disease entity. In addition, it should be noted that focal fibrosis may increase in size.

Context: Podoplanin is a mucin-type glycoprotein and a lymphatic endothelial marker. Immunohistochemical staining for podoplanin is currently used as a routine pathologic diagnosis tool in Japan to identify lymphatic invasion of cancer cells. Recent reports suggest that podoplanin and other proangiogenic molecules are expressed in stromal fibroblasts and myofibroblasts., Objective: To analyze the distribution of podoplanin expression in tumor stroma and its clinical and biologic significance., Design: We performed immunohistochemistry for podoplanin on tissue microarrays from 1350 cases of 14 common cancer types., Results: Two hundred eighty-seven of 662 cases (43%) showed podoplanin expression in the stromal cells within cancer nests. Stromal podoplanin expression in 14 common cancer types was significantly associated with tumor stage (P < .001), lymph node metastases (P < .001), lymphatic invasion (P  =  .02), and venous invasion (P < .001). The stromal cells positive for podoplanin were also positive for α-smooth muscle actin but negative for desmin, confirming a myofibroblasts phenotype. In contrast, myofibroblasts in inflammatory fibrotic lung diseases were podoplanin negative. Lymphatic vessel density was greater in the stromas with podoplanin expression than in the stroma lacking podoplanin-expressing stromal cells (P  =  .01). Survival data were available for non-small cell lung cancer. Stromal podoplanin expression was associated with poorer prognosis in adenocarcinoma (P < .001) and remains statistically significant after adjustment for sex, age, and stage (P  =  .01)., Conclusion: Our data indicate that podoplanin expression in stromal myofibroblasts may function as a proangiogenic biomarker and may serve as a predictive marker of lymphatic/vascular spread of cancer cells and a prognostic marker of patient survival.

Computed tomography findings of pathologically proven pulmonary infarction associated with bronchogenic carcinoma are reported for two patients. In one case, the infarction was demonstrated as a well-defined pleura-based large nodule in the peripheral portion of the same lobe of the tumor. The nodule had a smooth, convex border and a linear strand from the apex of the lesion toward the hilum. The obstruction of the subsegmental pulmonary artery due to tumor invasion was considered the cause of pulmonary infarction. In the second case, the infarction was demonstrated as a rapidly appeared, pleura-based consolidation in the same lobe of the tumor with a blurred border. Obstruction of the pulmonary vein by a tumor might have played an important role in the development of the pulmonary infarction in association with a large pulmonary artery obstruction. We conclude that pulmonary infarction should be considered as a differential diagnosis when peripheral pulmonary nodules or masses are located in the same lobe as the primary cancer.

90K/Mac-2 Binding Protein (M2BP) plays a role in regulation of immune responses and cell adhesive ability in patients with cancer and infectious diseases. We previously reported that M2BP was highly expressed in lung cancer and that immune responses to M2BP were increased in many patients with lung cancer. To determine the involvement of M2BP in metastatic processes of cancer progression, we examined the ability of M2BP DNA-transduced lung carcinoma cell lines to adhere to extracellular matrices. Although expressions of cell-surface integrins were not modulated in the M2BP transfectants, they showed increased adhesiveness to fibronectin and collagen IV. We next analyzed the serum levels of M2BP in patients with lung cancer and normal donors and the relationships between M2BP expression and clinicopathological factors in the patients. The M2BP level was markedly elevated in the patients and was strongly correlated with nodal involvement and clinical staging. To determine whether expression of M2BP by cancer cells is modulated in the environment of tumor-bearing hosts, M2BP expression in M2BP-positive QG56 cells following exposure of the cells to pro-inflammatory cytokines was examined. The M2BP expression in QG56 cells was up-regulated by many of the cytokines that activate host protective immunity. The findings in this study suggest that M2BP plays a role in cancer metastasis by increased adhesiveness of cancer cells and that M2BP is increasingly produced even in a state of exposure to the host immune system. This molecule may be useful as a predictive factor of disease progression in lung cancer.