Is elevation of the serum β-d-glucan level a paradoxical sign for Trichosporon fungemia in patients with hematologic disorders?

SummaryThe detection of serum 1,3-β-d-glucan (BDG) has been reported to be useful for the diagnosis and therapeutic monitoring of various invasive fungal infections. Although Trichosporon fungemia is increasingly recognized as a fatal mycosis in immunocompromised patients, the utility of this assay for Trichosporon fungemia is still unknown. In our experience (28 cases), the level of BDG rose in about half of the patients with hematologic disorders who developed Trichosporon fungemia. Among them, early death from this infection was more frequently seen in BDG-negative patients than in BDG-positive patients. In addition, overall survival was also significantly worse in BDG-negative patients than in BDG-positive patients. There were no significant differences between these two patient groups in terms of clinical background. Unlike for other invasive fungal infections, elevation of BDG level may indicate a paradoxical sign for Trichosporon fungemia in patients with hematologic disorders

Effect of Retinoic Acid on the Growth and the Expression of the Human Papillomavirus 16 E6 and E7 Genes of the Cervical Carcinoma Cell Lines

Human papillomavirus type 16 (HPV16) is involved in the development of cervical carcinoma and its viral gene products E6 and E7 are believed to be essential for the carcinogenic process. We analyzed the effect of retinoic acid (RA) on the growth and/or HPV16 E6 and E7 gene expression in the HPV16-containing cervical carcinoma cell lines SiHa, CaSki and QG-U and the HPV-free cell lines C33A and EBC-1. RA (10-6 M) suppressed the growth of SiHa cells by more than 90% and of QG-U cells by about 40% ; however, the growth of CaSki, C33A and EBC-1 cells was not affected by RA. Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was applied for investigation of the relationship between RA and the level of HPV16 E6/E7 mRNA. As a result, the E6/E7 mRNA level in SiHa and QG-U was reduced by RA by about 60% and 75%, respectively, while RA had no obvious effect on the E6 and E7 gene expression in CaSki cells. The chloramphenicol acetyltransfer-ase (CAT) assay showed that transcription driven by HPV16 non-coding region (NCR) was suppressed by RA by about 75%. These results suggest that at least a part of the growth suppression of SiHa and QG-U by RA is mediated by sup-pression of E6 and E7 expression

A Case of Mucosal Cancer of the Stomach Treated by Endoscopic Submucosal Dissection after Which Nodal Metastasis Became Evident

An 82-year-old male was referred to our institution for evaluation and treatment of a protruding lesion in the stomach. Esophagogastroduodenoscopy (EGD) showed a small protruding lesion and a large superficial elevated lesion on the lesser curvature of the stomach (macroscopic type: 0-I and 0-IIa, resp.). CT and endoscopic ultrasonography (EUS) visualized a small round lymph node (LN) 11 mm in size near the lesser curvature, although submucosal invasion was not evident. These two lesions were resected en bloc by endoscopic submucosal dissection (ESD). Pathological examination of the resected specimen showed moderately differentiated tubular adenocarcinoma (tub2) and well-differentiated tubular adenocarcinoma (tub1), respectively, which were limited to the mucosal layer. Because lymphatic-vascular involvement was not detected by hematoxylin and eosin (HE) staining, additional gastrectomy was not performed. Two months after ESD, follow-up EUS and CT showed an enlarged LN. EUS-guided fine needle aspiration (EUS-FNA) for the LN revealed metastasis. Therefore, total gastrectomy with LN dissection was performed. His postoperative course was uneventful. After discharge, he has been followed up at the outpatient department without any sign of recurrence for 5 years. Histological reexamination of the ESD specimen using immunohistochemistry showed lymphatic invasion of cancer cells in the lamina propria of the 0-I lesion 13 mm in size

Analysis of Cellular Oncogene Amplification in Human Lung Cancers

Twenty-six lung cancer tissues from operation or autopsy and eight lung cancer cell lines were examined for an amplification of the ten different cellular oncogenes, c-myc, N-myc, L-myc, c-erbB-1, c-erbB-2, c-fos, v-sis, c-H-ras, v-K-ras, and N-ras, by the Southern blot hybridization. In small cell lung cancer(SCLC), one SCLC tissue(13-1) out of four SCLC tissues and one SCLC cell line contained three fold amplifications of the L-myc oncogene. In non-SCLC, one adenocarcinoma cell line(SLO51) and one large cell carcinoma cell line(SLC-30) showed an amplification of the c-myc oncogene at four fold normal amount and twenty fold amplifications of the c-erbB-1 oncogene respectively, out of twenty-two non-SCLC tissues and seven non-SCLC cell lines. Other lung cancer tissues and cell lines did not show any detectable amplifications or rearrangements of oncogenes. These results suggest that an amplification of the studied oncogenes may not always be associated with carcinogenesis even in lung cancer cell lines. Compared with lung cancer cell lines, the frequency of an amplification of oncogenes in lung cancer tissues was low, especially in non-SCLC tissues