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author:("yamane, Koji")
1.  Unicystic ameloblastoma metastasizing to multiple cervical lymph nodes 
Journal of Surgical Case Reports  2013;2013(5):rjt033.
Ameloblastoma is the most common odontogenic tumor, but the incidence of its metastasis is extremely low. We report a case of unicystic ameloblastoma metastasizing to the cervical lymph nodes. This patient pointed out a radiolucent cystic lesion with impacted wisdom tooth in the left mandibular region, and recieved enucleation of the cystic lesion and removal of the wisdom tooth. Histopathogical diagnosis was unicystic ameloblastoma. Three years later, this patient complained of a swelling in the left submandibular region. A CT scan showed a bilobed cystic mass measuring 30 mm in diameter compressing the submandibular gland, and we performed extirpation of the mass with the submandibular gland and associated lymph nodes. Histologically, the lesion was cystic and lymph follicles were seen in the cyst-like wall. The laminated epithelium of cyst wall was ameloblastomatous epithelium, and two lymph nodes associated with cystic lesion also included ameloblastomatous epithelium. This is the first report of metastasizing unicystic ameloblastoma.
doi:10.1093/jscr/rjt033
PMCID: PMC3813790  PMID: 24964442
2.  CELLPEDIA: a repository for human cell information for cell studies and differentiation analyses 
CELLPEDIA is a repository database for current knowledge about human cells. It contains various types of information, such as cell morphologies, gene expression and literature references. The major role of CELLPEDIA is to provide a digital dictionary of human cells for the biomedical field, including support for the characterization of artificially generated cells in regenerative medicine. CELLPEDIA features (i) its own cell classification scheme, in which whole human cells are classified by their physical locations in addition to conventional taxonomy; and (ii) cell differentiation pathways compiled from biomedical textbooks and journal papers. Currently, human differentiated cells and stem cells are classified into 2260 and 66 cell taxonomy keys, respectively, from which 934 parent–child relationships reported in cell differentiation or transdifferentiation pathways are retrievable. As far as we know, this is the first attempt to develop a digital cell bank to function as a public resource for the accumulation of current knowledge about human cells. The CELLPEDIA homepage is freely accessible except for the data submission pages that require authentication (please send a password request to cell-info@cbrc.jp).
Database URL: http://cellpedia.cbrc.jp/
doi:10.1093/database/bar046
PMCID: PMC3204613  PMID: 22039163
3.  Expression of hepatocyte markers in mass-forming peripheral and periductal-infiltrating hilar intrahepatic cholangiocarcinomas 
Oncology Letters  2011;2(6):1041-1046.
In this study, the expression of hepatocyte markers, including α-fetoprotein (AFP), HepPar-1 antigen and arginase-1, was examined immunohistochemically in 14 mass-forming peripheral intrahepatic cholangiocarcinomas (ICCs) that arose from the peripheral portion of the biliary tree, and in 14 periductal-infiltrating hilar ICCs that arose from intrahepatic large bile ducts. Only 2 (14.3%) of the 14 hilar ICCs and 2 (14.3%) of the 14 peripheral ICCs expressed AFP or HepPar-1 antigen. Conversely, arginase-1 was expressed in 8 (57.1%) and 11 (78.6%) of the hilar and peripheral ICCs, respectively, and 4 (28.6%) hilar ICCs and 7 (50%) peripheral ICCs expressed arginase-1 in more than 10% of the cancer cells. The expression of arginase-1 did not differ between peripheral ICCs showing major histology of poorly differentiated adenocarcinoma and those showing other major histologies, including well-or moderately differentiated tubular adenocarcinoma or papillary adenocarcinoma. Results of the present study showed that common hepatocyte markers, including AFP and HepPar-1 antigen, are rarely but definitely expressed in hilar and peripheral ICCs, and that a third hepatocyte marker, arginase-1, is expressed at a high rate in both hilar and peripheral ICCs, irrespective of their histology. These results indicate that care should be taken when using arginase-1 as a hepatocyte marker for distinguishing between a poorly differentiated hepatocellular carcinoma and a mass-forming peripheral ICC showing the histology of poorly differentiated adenocarcinoma.
doi:10.3892/ol.2011.405
PMCID: PMC3406572  PMID: 22848265
α-fetoprotein; HepPar-1; arginase-1; cholangiocarcinoma; immunohistochemistry
4.  XPC branch-point sequence mutations disrupt U2 snRNP binding resulting in abnormal pre-mRNA splicing in xeroderma pigmentosum patients 
Human mutation  2010;31(2):167-175.
Mutations in two branch-point sequences (BPS) in intron 3 of the XPC DNA repair gene affect pre-mRNA splicing in association with xeroderma pigmentosum (XP) with many skin cancers (XP101TMA) or no skin cancer (XP72TMA), respectively. To investigate the mechanism of these abnormalities we now report that transfection of minigenes with these mutations revealed abnormal XPC pre-mRNA splicing that mimicked pre-mRNA splicing in the patients’ cells. DNA oligonucleotide-directed RNase H digestion demonstrated that mutations in these BPS disrupt U2 snRNP – BPS interaction. XP101TMA cells had no detectable XPC protein but XP72TMA had 29% of normal levels. A small amount of XPC protein was detected at sites of localized UV-damaged DNA in XP72TMA cells which then recruited other nucleotide excision repair (NER) proteins. In contrast, XP101TMA cells had no detectable recruitment of XPC or other NER proteins. Post-UV survival and photoproduct assays revealed greater reduction in DNA repair in XP101TMA cells than in XP72TMA. Thus mutations in XPC BPS resulted in disruption of U2 snRNP-BPS interaction leading to abnormal pre-mRNA splicing and reduced XPC protein. At the cellular level these changes were associated with features of reduced DNA repair including diminished NER protein recruitment, reduced post-UV survival and impaired photoproduct removal.
doi:10.1002/humu.21166
PMCID: PMC2815018  PMID: 19953607
XPC; DNA repair; pre-mRNA splicing; xeroderma pigmentosum; skin cancer; U2 snRNP
5.  Kaposi's Sarcoma-Associated Herpesvirus ORF57 Functions as a Viral Splicing Factor and Promotes Expression of Intron-Containing Viral Lytic Genes in Spliceosome-Mediated RNA Splicing▿  
Journal of Virology  2008;82(6):2792-2801.
Kaposi's sarcoma-associated herpesvirus (KSHV) ORF57 facilitates the expression of both intronless viral ORF59 genes and intron-containing viral K8 and K8.1 genes (V. Majerciak, N. Pripuzova, J. P. McCoy, S. J. Gao, and Z. M. Zheng, J. Virol. 81:1062-1071, 2007). In this study, we showed that disruption of ORF57 in a KSHV genome led to increased accumulation of ORF50 and K8 pre-mRNAs and reduced expression of ORF50 and K-bZIP proteins but had no effect on latency-associated nuclear antigen (LANA). Cotransfection of ORF57 and K8β cDNA, which retains a suboptimal intron of K8 pre-mRNA due to alternative splicing, promoted RNA splicing of K8β and production of K8α (K-bZIP). Although Epstein-Barr virus EB2, a closely related homolog of ORF57, had a similar activity in the cotransfection assays, herpes simplex virus type 1 ICP27 was inactive. This enhancement of RNA splicing by ORF57 correlates with the intact N-terminal nuclear localization signal motifs of ORF57 and takes place in the absence of other viral proteins. In activated KSHV-infected B cells, KSHV ORF57 partially colocalizes with splicing factors in nuclear speckles and assembles into spliceosomal complexes in association with low-abundance viral ORF50 and K8 pre-mRNAs and essential splicing components. The association of ORF57 with snRNAs occurs by ORF57-Sm protein interaction. We also found that ORF57 binds K8β pre-mRNAs in vitro in the presence of nuclear extracts. Collectively our data indicate that KSHV ORF57 functions as a novel splicing factor in the spliceosome-mediated splicing of viral RNA transcripts.
doi:10.1128/JVI.01856-07
PMCID: PMC2258979  PMID: 18184716
6.  Colorectal papillomavirus infection in colorectal cancer patients 
Purpose: Infection with human papillomaviruses (HPVs) is associated with the development of cervical cancer, but whether HPVs have a role in colorectal cancer remains controversial.
Experimental Design: To determine the relationship between HPV and colorectal cancer, we performed a retrospective, controlled study using tumor and tumor-adjacent colorectal tissues dissected from patients with colorectal cancer, as well as colorectal tissues from control individuals with no cancer. The samples were processed in a blinded fashion for nested PCR and in situ PCR detection of HPV DNAs. The PCR products were gel purified and sequenced for HPV genotyping.
Results: We found that colorectal tissues from 28 (51%) of 55 patients with colorectal cancer were positive for HPV DNA. Colorectal tissues from all 10 control individuals were negative for HPV DNA (P=0.0034). Of the 107 usable (GAPDH+) samples collected as paired colorectal tissues (tumor and tumor-adjacent tissues) from the patients, 38 (36%) had HPV16 (n=31), HPV18 (n=5), or HPV45 (n=2), with HPV DNA in both tumor and tumor-adjacent tissues of 10 paired samples, 13 in only the tumor, and 5 in only tumor-adjacent tissues. In situ PCR detection of the tumor tissues confirmed the presence of HPV DNA in tumor cells.
Conclusion: Our results suggest that colorectal HPV infection is common in patients with colorectal cancer, albeit at a low DNA copy number, with HPV16 being the most prevalent type. HPV infection may play a role in colorectal carcinogenesis.
doi:10.1158/1078-0432.CCR-04-1680
PMCID: PMC1479314  PMID: 15837733
Human papillomavirus type 16; Viral oncogenesis; Tumor virus infection; PCR
7.  Gene Structure and Expression of Kaposi's Sarcoma-Associated Herpesvirus ORF56, ORF57, ORF58, and ORF59▿  
Journal of Virology  2006;80(24):11968-11981.
Though similar to those of herpesvirus saimiri and Epstein-Barr virus (EBV), the Kaposi's sarcoma-associated herpesvirus (KSHV) genome features more splice genes and encodes many genes with bicistronic or polycistronic transcripts. In the present study, the gene structure and expression of KSHV ORF56 (primase), ORF57 (MTA), ORF58 (EBV BMRF2 homologue), and ORF59 (DNA polymerase processivity factor) were analyzed in butyrate-activated KSHV+ JSC-1 cells. ORF56 was expressed at low abundance as a bicistronic ORF56/57 transcript that utilized the same intron, with two alternative branch points, as ORF57 for its RNA splicing. ORF56 was transcribed from two transcription start sites, nucleotides (nt) 78994 (minor) and 79075 (major), but selected the same poly(A) signal as ORF57 for RNA polyadenylation. The majority of ORF56 and ORF57 transcripts were cleaved at nt 83628, although other nearby cleavage sites were selectable. On the opposite strand of the viral genome, colinear ORF58 and ORF59 were transcribed from different transcription start sites, nt 95821 (major) or 95824 (minor) for ORF58 and nt 96790 (minor) or 96794 (major) for ORF59, but shared overlapping poly(A) signals at nt 94492 and 94488. Two cleavage sites, at nt 94477 and nt 94469, could be equally selected for ORF59 polyadenylation, but only the cleavage site at nt 94469 could be selected for ORF58 polyadenylation without disrupting the ORF58 stop codon immediately upstream. ORF58 was expressed in low abundance as a monocistronic transcript, with a long 5′ untranslated region (UTR) but a short 3′ UTR, whereas ORF59 was expressed in high abundance as a bicistronic transcript, with a short 5′ UTR and a long 3′ UTR similar to those of polycistronic ORF60 and ORF62. Both ORF56 and ORF59 are targets of ORF57 and were up-regulated significantly in the presence of ORF57, a posttranscriptional regulator.
doi:10.1128/JVI.01394-06
PMCID: PMC1676266  PMID: 17020939
8.  Kaposi's Sarcoma-Associated Herpesvirus K8β Is Derived from a Spliced Intermediate of K8 Pre-mRNA and Antagonizes K8α (K-bZIP) To Induce p21 and p53 and Blocks K8α-CDK2 Interaction 
Journal of Virology  2005;79(22):14207-14221.
Kaposi's sarcoma-associated herpesvirus (KSHV) is a lymphotropic DNA tumor virus that induces Kaposi's sarcoma and AIDS-related primary effusion lymphoma. KSHV open reading frame 50 and K8 genes in early viral lytic infection express, respectively, a tricistronic and a bicistronic pre-mRNA, which undergo alternative splicing to create two major spliced mRNA isoforms, α and β, by inclusion (β) or exclusion (α) of an intron at nucleotides 75563 to 75645. This intron contains some suboptimal features, which cause the intron 5′ splice site (ss) to interact weakly with U1 snRNA and the 3′ ss to bind a U2 auxiliary factor, U2AF, with low affinity. Optimization of this intron in K8 (K8 intron 2) promoted the interaction of the 5′ ss with U1 and the 3′ ss with U2AF, resulting in a substantial increase in intron splicing. Splicing of K8 intron 2 has also been shown to be stimulated by the splicing of a downstream intron. This was confirmed by the insertion of a human β-globin intron into the K8β exon 3-exon 4 splice junction, which promoted splicing of K8β intron 2 and conversion of the K8β mRNA to the K8α mRNA that encodes a K-bZIP protein. Intron 2 contains a premature termination codon, yet the K8β mRNA is insensitive to nonsense-mediated mRNA decay, suggesting that the truncated K8β protein may have a biological function. Indeed, although the truncated K8β protein is missing only a C-terminal leucine zipper domain from the K-bZIP, its expression antagonizes the ability of the K-bZIP to induce p53 and p21 and blocks K-bZIP-CDK2 interaction through interfering K8α mRNA production.
doi:10.1128/JVI.79.22.14207-14221.2005
PMCID: PMC1280184  PMID: 16254356
9.  Requirement of a 12-Base-Pair TATT-Containing Sequence and Viral Lytic DNA Replication in Activation of the Kaposi's Sarcoma-Associated Herpesvirus K8.1 Late Promoter 
Journal of Virology  2004;78(5):2609-2614.
Kaposi's sarcoma-associated herpesvirus (KSHV) K8.1 late promoter consists of a minimal 24-bp sequence, with a TATA-like, 12-bp promoter core, AATATTAAAGGG, and is active on a reporter only in butyrate-induced KSHV-infected cells. The activity of the K8.1 promoter can be enhanced (>15-fold) by the KSHV left-end lytic origin of DNA replication (oriLyt-L) sequence while providing inefficient replication of plasmid DNA and is inhibited by viral DNA replication inhibitors, suggesting that activation of the K8.1 promoter on the reporter is involved in KSHV lytic DNA replication largely by trans.
doi:10.1128/JVI.78.5.2609-2614.2004
PMCID: PMC369211  PMID: 14963167

Results 1-9 (9)