Monthly monitoring of HBV DNA is useful for preventing HBV reactivation-related hepatitis among B-NHL patients with resolved HBV infection following R-steroid-chemo (UMIN000001299).

Previously, we proposed a rare autosomal recessive inherited enteropathy characterized by persistent blood and protein loss from the small intestine as chronic nonspecific multiple ulcers of the small intestine (CNSU). By whole-exome sequencing in five Japanese patients with CNSU and one unaffected individual, we found four candidate mutations in the SLCO2A1 gene, encoding a prostaglandin transporter. The pathogenicity of the mutations was supported by segregation analysis and genotyping data in controls. By Sanger sequencing of the coding regions, 11 of 12 other CNSU patients and 2 of 603 patients with a diagnosis of Crohn’s disease were found to have homozygous or compound heterozygous SLCO2A1 mutations. In total, we identified recessive SLCO2A1 mutations located at seven sites. Using RT-PCR, we demonstrated that the identified splice-site mutations altered the RNA splicing, and introduced a premature stop codon. Tracer prostaglandin E2 uptake analysis showed that the mutant SLCO2A1 protein for each mutation exhibited impaired prostaglandin transport. Immunohistochemistry and immunofluorescence analyses revealed that SLCO2A1 protein was expressed on the cellular membrane of vascular endothelial cells in the small intestinal mucosa in control subjects, but was not detected in affected individuals. These findings indicate that loss-of-function mutations in the SLCO2A1 gene encoding a prostaglandin transporter cause the hereditary enteropathy CNSU. We suggest a more appropriate nomenclature of “chronic enteropathy associated with SLCO2A1 gene” (CEAS).

Oligodendrogliomas typically show loss of heterozygosity (LOH) on chromosomes 1p and 19q, which correlates with their response to chemotherapy, whereas low-grade astrocytomas are characterized by frequent TP53 mutations and lack of sensitivity to alkylating therapeutic agents. Unequivocal histological distinction of low-grade diffuse astrocytomas from oligodendrogliomas and oligoastrocytomas is often difficult. To elucidate the relationships between morphological phenotype and genetic profile, we screened 19 oligodendrogliomas (WHO grade II) and 23 low-grade diffuse astrocytomas (WHO grade II) for TP53 mutations and LOH on 1p and 19q. In oligodendrogliomas, LOH on chromosomes 1p and/or 19q was found in 15 cases (79%) and TP53 mutation was detected in 4 cases (21%). The presence of a typical perinuclear halo in >50% of tumour cells and a chicken-wire vascular pattern were significantly associated with LOH on 1p or 19q (93% of cases). This suggests that oligodendrogliomas with classical histologic features are likely to have a better prognosis. In low-grade diffuse astrocytomas, LOH on chromosomes 1p and/or 19q was found in three cases (13%) and TP53 mutation was detected in ten cases (43%). Histologically, five low-grade astrocytomas (22%) contained small areas with oligodendroglial differentiation, but this did not correlate with the presence of TP53 mutations or LOH on 1p and 19q. In both oligodendrogliomas and astrocytomas, LOH on chromosomes 1p or 19q and TP53 mutation were mutually exclusive. Methylation of the promoter of the gene for O (6)-methylguanine-DNA methyltransferase (MGMT), a DNA repair protein, which confers resistance to chemotherapy with alkylating agents, was detected in 47% of oligodendrogliomas and 48% of low-grade diffuse astrocytomas. There was no correlation with LOH on chromosomes 1p/19q, suggesting that MGMT may not be a prognostic marker for oligodendrogliomas.

In selected patients with ocular adnexal MALT lymphoma, no initial therapy might be an acceptable approach, because 70% of patients remained untreated at a median of 8.6 years, and their survival was comparable to that of reports on immediate therapy.

We investigated the location, size, and shape of cervical lymph nodes in head and neck cancer, using a 7.5-MHz ultrasound scanner. First, the different criteria for normal size were obtained for cervical lymph nodes in each region; lymph nodes greater than 9 mm in thickness in the internal jugular chain or greater than 7 mm in thickness in the submandibular and submental chains should be suspected of harboring metastatic foci. Second, meta· static nodes showed a more rounded configuration than A precise evaluation of the presence of meta· stasis to the cervical lymph nodes is mandatory in the management of head and neck malignancies. X-ray computed tomography (CT), 1 magnetic resonance imaging (MRI), and ultrasound 2 -4 have been used to evaluate lymphadenopathy in the neck. Recent reports on ultrasonography in the neck suggest its high efficiency in detecting small, nonpalpable lymphadenopathy. Although size has been used to diagnose me~ tastasis in lymph nodes, few studies have dealt with their internal structure.To determine the size and shape criteria for normal lymph nodes in each region in the neck, as well as to clarify any abnormal patterns of internal structure in metastatic lymph nodes, we conducted a correlative Received July 20, 1987, from the Departments of "Radiology, fOral Surgery. *Otolaryngology. and §Laboratory Medicine, School of Medi· cine, Shinshu University. Asahi, Matsumoto, Japan. Revised manuscript accepted for publication October 29, 1987. Address correspondence and reprint requests to Dr. F. Sakai: De· partment of Radiology, School of Medicine, Shinshu University, Asahi, Matsumoto, 390, Japan. nonmetastatic ones. Third, a comparative study of metastatic lymph nodes between the in vivo and in vitro ultrasonograms and the corresponding histopathological findings disclosed that an echogenic region in an ultrasonogram of a metastatic node was caused by coagulation necrosis, and a cystic area of liquefaction necrosis. KEY WORDS; ultrasonography, lymphadenopathy, echogenicity, size of lymph node. (/ Ultrasound Med 7: 305, 1988)