No abstract

Reported herein is an extremely rare case of primary pulmonary myxoid sarcoma (PPMS). A 31-year-old man presented with a 2.7 cm-sized pulmonary tumor surrounded by capsule-like fibrosis. The patient has been free of disease for 5.8 years after surgery. This tumor focally showed endobronchial features, and consisted of reticular cords of oval, short spindle, or polygonal cells with swollen vesicular nuclei accompanied by an abundant myxoid stroma, closely resembling extraskeletal myxoid chondrosarcoma. Tumor cells were diffusely positive for vimentin and focally positive for epithelial membrane antigen, but were negative for cytokeratin, TTF-1, Napsin A, S-100 protein, CD34, desmin, smooth-muscle actin, CD10, p63, calponin, h-caldesmon, c-kit, HMB-45, synaptophysin, or glial fibrillary acid protein. Our reverse transcription-polymerase chain reaction using the formalin-fixed, paraffin-embedded tumor tissues detected EWSR1-CREB1 fusion transcript, but could not demonstrate EWSR1-ATF1 fusion or EWSR1/TAF15/TFG-NR4A3 fusion. These findings indicate that the current tumor is an additional case of PPMS with EESR1-CREB1 fusion, recently reported by Thway et al. Some cases of PPMS can behave in an indolent manner.

We report a case of a 67-year-old woman with an invasive ciliated muconodular papillary tumor (CMPT) that developed in her right middle lobe. The current tumor was incidentally detected during a follow-up imaging examination for a large cell carcinoma that was resected 10 years previously. Partial removal of the middle lobe showed a 2 cm-sized, solid and myxoid tumor located in the peripheral region. Histologically, this tumor primarily consisted of ciliated columnar cells, mucous cells, and basal cells, all of which had relatively swollen nuclei and were proliferating in a lepidic or papillary/micropapillary manner. These features were consistent with those of previously reported CMPT. In addition, atypical spindle tumor cells with more swollen nuclei, which were partly continuous to less atypical basal tumor cells, were focally found and invaded fibrous stroma in a reticular fashion. Immunohistochemically, both basal cells and atypical spindle tumor cells were positive for pancytokeratin, cytokeratin 5/6, and p40. Increased p53 positivity was found in these invading spindle cells compared with basal tumor cells. Neither BRAF V600E nor V600K mutation was detected. We concluded that this tumor was an extremely rare invasive case of CMPT, possibly representing malignant transformation of basal tumor cell components of CMPT.

CK7 + CHs occur relatively frequently in non-neoplastic liver disease, associated with centrilobular scarring and the presence of CK7-positive periportal hepatocytes, and appear to be a non-specific phenomenon with respect aetiology of underlying disease. CK7 + CHs may represent age-dependent activation of hepatic progenitor cells or a regenerative phenomenon of hepatocytes themselves, both of which might contribute to liver regeneration.

This study examined 47 cases of lung cancer concomitant with other tumors and found eight cases (17 %) with nine foci of tumor-to-tumor metastasis, defined as metastasis of lung cancer into another tumor. Donor lung cancers were four adenocarcinomas, two squamous cell carcinomas, and two small cell carcinomas. Tumor-to-tumor metastasis was found in five of six renal cell carcinomas (83 %), one of eight thyroid papillary carcinomas (13 %), one of three adrenocortical adenomas (33 %), one of three pancreatic endocrine microadenomas (33 %), and another lung cancer (one of six cases of multiple lung cancers, 17 %). The higher recipient incidence in renal cell carcinoma was statistically significant compared with prostatic carcinoma (0/16, P < 0.001), colorectal carcinoma (0/7, P = 0.005), and gastric carcinoma (0/5, P = 0.015). Generalized metastases were found in 88 % of the tumor-to-tumor metastasis cases. The total clinical course of patients with tumor-to-tumor metastasis was shorter than that of the patients without tumor-to-tumor metastasis (mean, 5.4 versus 18.8 months; P = 0.046). Tumor-to-tumor metastasis sometimes mimicked undifferentiated recipient tumor cells. Immunostains for thyroid transcription factor 1 (TTF-1), Napsin A, cytokeratin 7 (CK7), and CK5/6 were useful to confirm tumor-to-tumor metastasis. However, TTF-1-, Napsin A-, and/or CK7-negative lung adenocarcinoma components metastasized to renal cell carcinoma in three cases, and recipient renal cell carcinomas were focally Napsin A+ (two cases) or CK7+ (two cases). Tumor-to-tumor metastasis can occur as a result of metastasis from lung cancer with more aggressive behavior. Tumor-to-tumor metastasis should be carefully distinguished from undifferentiated recipient tumor cells.