Expression of a murine homolog of apoptosis-inducing human IL-24/MDA-7 in murine tumors fails to induce apoptosis or produce anti-tumor effects.

Expression of human interleukin (IL)-24 in tumors achieved anti-tumor effects through apoptosis. IL-24 also induced secretion of proinflammatory cytokines, suggesting the role in immunity. We showed that murine IL-24 transcripts started from the second initiation codon and that expressed mIL-24 in tumors failed to induce apoptosis. Proliferation of murine cells expressing mIL-24 was the same as that of the parent cells and inoculation of the mIL-24-expressing tumors into syngeneic mice did not produce anti-tumor effects. Secretory mIL-24 did not induce the expression of the IL-6, TNF-α or IFN-γ gene in spleen cells. Expression of mIL-24 receptor subunits, IL-22R and IL-20R1, was undetectable in spleen cells even though they were stimulated by anti-CD3, anti-CD40 antibody or concanavalin A. Transduction of murine tumors with adenoviruses expressing the human IL-24 gene however suppressed the viability and decreased the tumor growth. These data suggest that mIL-24 is functionally irrelevant to the human counterpart.

[Case of shakuyakukanzoto-induced CD4 dominant pneumonitis diagnosed on day eight of the challenge test].

We report a case of drug-induced pneumonia associated with the herbal medine Syakuyakukanzo-to. A 82-year-old man was admitted to our hospital complaining of cough, fever, and dyspnea after administration of shakuyakukanzoto for two weeks. Drug-induced lymphocyte stimulation tests were negative, but bronchoalveolar lavage showed an increase in lymphocytes with an increased CD4/CD8 ratio. Cessation of the drug improved the patient's clinical and X-ray findings and then he was able to be discharged. He was admitted again for a challenge test. His clinical symptoms and X-ray findings became worse 8 days after re-administration, therefore we diagnosed drug-induced pneumonia caused by Shakuyakukanzoto. He has had no recurrence after discontinuance of the drug. To the best of our knowledge, there has been no previous case of drug-induced pneumonia due to Shakuyakukanzo-to reported in the world.

[A case of fatal MALT lymphoma of pulmonary origin with systemic metastasis and manifesting macroglobulinemia].

The patient was a 61-year-old man whose chest radiography showed infiltration in both lung fields. MALT lymphoma was diagnosed from transbronchial lung biopsy (TBLB) specimens. The serum monoclonal IgM level then increased, and plasma cells and lymphoplasmacytoid cells were found in a bone marrow examination, indicating macroglobulinemia as a complication. Despite chemotherapy, systemic metastasis led to the patient's death. Our report is accompanied with a review of literature, because no report of MALT lymphoma of pulmonary origin complicated with macroglobulinemia exists, and it is considered that the macroglobulinemia in this case was related to the MALT lymphoma.

[An autopsy case of tension pneumothorax due to the rupture of intrapulmonary cavity by mucormycosis during treatment with a ventilator].

 A 50-year-old man with chronic renal failure (hemodialysis treatment) and interstitial pneumonia (IP) was referred to our hospital for exacerbation of IP. We immediately administered a mechanical ventilation, broad spectrum antibiotics, steroid pulse therapy, and endoxan pulse therapy in the intensive care unit, but alveolar opacities became worse. Subsequently, an intrapulmonary cavity appeared in the left middle lung field on the chest X-ray and we also administered amphotericin B. However he died of tension pneumothorax on the tenth day of hospitalization. In an autopsy the rupture of the intrapulmonary cavity of the left S3 region was detected and we diagnosed as invasive pulmonary mucormycosis by Grocott stain of the cavitary lesion. We report a rare case that complicated by fatal tension pneumothorax during treatment with a ventilator in invasive pulmonary mucormycosis and review the literature.

Basaloid squamous-cell carcinoma of the lung in a young woman.

We report a rare case of basaloid squamous cell carcinoma of the lung in a young Japanese woman. An 18-year-old woman presented with productive cough. Chest radiogram and computed tomography (CT) revealed a tumor in the left hilum accompanied by partial atelectasis of the left upper lobe and pleural effusion. Transbronchial fine-needle aspiration cytology supported a tentative diagnosis of primary squamous-cell carcinoma of the lung. The clinical stage was T4N2M1, with multiple bone metastases. Despite a transient response to chemotherapy consisting of carboplatin and paclitaxel, the patient died because of tumor progression 2 months after the start of the chemotherapy. Necropsy established the diagnosis of basaloid squamous-cell carcinoma of the lung. Immunohistochemical studies of the necropsy specimen indicated that the tumor was positive for keratin, vimentin, and S100, and negative for chromogranin A, cytokeratin CAM5.2, and bcl-2. Besides the rarity of the disease itself, the present case seemed to have additional uniqueness in that the patient was 18 years old and female. This is the youngest patient with a case of basaloid squamous cell carcinoma of the lung ever reported.

The secreted form of the p40 subunit of interleukin (IL)-12 inhibits IL-23 functions and abrogates IL-23-mediated antitumour effects.

Interleukin (IL)-23 is a heterodimeric cytokine consisting of a novel p19 molecule and the p40 subunit of IL-12. Since secreted p40 can act as an antagonist for IL-12, we investigated whether p40 also inhibited IL-23-mediated immunological functions. p40 did not induce interferon (IFN)-gamma or IL-17 production from splenocytes but impaired IL-23-induced cytokine production by competitive binding to the IL-23 receptors. Furthermore, a mixed population of murine colon carcinoma Colon 26 cells transduced with the p40 gene and those transduced with the IL-23 gene developed tumours in syngenic mice, whereas the IL-23-expressing Colon 26 cells were completely rejected. p40 also suppressed IFN-gamma production of antigen-stimulated splenocytes and IL-23-mediated cytotoxic T-lymphocyte activities in the mice that rejected Colon 26 cells expressing IL-23. p40 can thereby antagonize IL-23 and is a possible therapeutic agent for suppression of IL-23 functions.