Takeshi Nishiwaki

A new record conversion efficiency of 24.7% was attained at the research level by using a heterojunction with intrinsic thin-layer structure of practical size (101.8 cm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> , total area) at a 98-μm thickness. This is a world height record for any crystalline silicon-based solar cell of practical size (100 cm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> and above). Since we announced our former record of 23.7%, we have continued to reduce recombination losses at the hetero interface between a-Si and c-Si along with cutting down resistive losses by improving the silver paste with lower resistivity and optimization of the thicknesses in a-Si layers. Using a new technology that enables the formation of a-Si layer of even higher quality on the c-Si substrate, while limiting damage to the surface of the substrate, the V <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">oc</sub> has been improved from 0.745 to 0.750 V. We also succeeded in improving the fill factor from 0.809 to 0.832.

The short arm of chromosome 3 is thought to contain multiple tumor suppressor genes, because one copy of this chromosomal arm frequently is missing in carcinomas that have arisen in a variety of tissues. We have isolated a novel gene encoding a 1755-amino acid polypeptide, through large-scale sequencing of genomic DNA at 3p21.3. Mutational analysis of this gene by reverse transcription-PCR revealed the lack of functional transcripts and an increase of nonfunctional RNA transcripts in a significant proportion (33%) of cancer cell lines and primary cancers (4 of 14 esophageal cancer cell lines, 2 of 2 renal cancer cell lines, 11 of 30 primary non-small cell lung cancers, and 3 of 10 primary squamous cell carcinomas of the esophagus). However, no alterations of the gene itself were detected in any of the cancers examined. Introduction of the cDNA significantly suppressed the growth of four different cancer cell lines, two of which produced no normal transcript on their own. No such effect occurred when antisense cDNA, cDNA corresponding to an aberrant transcript, or the vector DNA alone were transfected. These data suggest that aberrant transcription of this gene, designated DLC1 (deleted in lung cancer 1), may be involved in carcinogenesis of the lung, esophagus, and kidney.

Through a large-scale sequencing of genomic DNA at 3p22-->p21.3, we have isolated two human genes (ORCTL3 alias OCTL1 and ORCTL4 alias OCTL2) encoding novel members of the family of organic-cation transporter molecules. The predicted proteins revealed the highest similarities to recently- isolated organic-cation transporter proteins, rat OCT-1r, rat NLT and mouse NKT. The transcripts of both genes were expressed ubiquitously in various human tissues, but some tissue-specific transcripts were also observed in kidney, testis, or skeletal muscle. The two genes are clustered within a 52-kb region of genomic DNA and ORCTL4 lies about 27 kb telomeric to ORCTL3 in the genomic DNA sequence in a tail-to-head orientation.

Beta-catenin plays significant roles in cell-to-cell adhesion and the Wnt/Wg signal transduction pathway. Accumulation of this protein in the cytoplasm and nucleus as a result of mutations of the adenomatous polyposis coli tumor suppressor gene or of the beta-catenin gene itself is often seen in a wide variety of tumors including carcinomas of the colon, liver, uterus, and brain. Interaction of accumulated beta-catenin with Tcf/Lef transcription factors is known to deregulate expression of some downstream genes, but the precise mechanisms whereby beta-catenin contributes to carcinogenesis remain to be disclosed. Here we report isolation of a novel murine gene, Drctnnb1a (down-regulated by Ctnnb1, a), the expression of which was experimentally down-regulated in response to the activated form of beta-catenin. To investigate a possible role of DRCTNNB1A in cancers, we also isolated the human homologue, DRCTNNB1A, the deduced product of which was 91% identical to the murine protein. The transcript was expressed in all human tissues examined, and we assigned the genomic location of DRCTNNB1A to chromosomal band 7p15.3 by in situ hybridization. Expression of DRCTNNB1A in SW480 colon cancer cells was significantly increased in response to reduction of intracellular beta-catenin by adenovirus-mediated transfer of the beta-catenin-binding domain of the adenomatous polyposis coli gene into the cells. Furthermore, we documented reduced expression of DRCTNNB1A in 12 of 15 primary colorectal cancers examined, compared with corresponding adjacent noncancerous mucosae. Our results implied that DRCTNNB1A is one of the genes involved in the beta-catenin-Tcf/Lef signaling pathway, and that reduced expression of DRCTNNB1A may have some role in colorectal carcinogenesis.