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AXIN1 mutations in hepatocellular carcinomas, and growth suppression in cancer cells by virus-mediated transfer of AXIN1
Adenovirus mediated gene transfer of wild-type AXIN1 induced apoptosis in hepatocellular and colorectal cancer cells that had accumulated β-catenin as a consequence of either APC, CTNNB1 orAXIN1 mutation, suggesting that axin may be an effective therapeutic molecule for suppressing growth of hepato cellular andcolorectAL cancers.
Overexpression of β1-chain-containing laminins in capillary basement membranes of human breast cancer and its metastases
Similar to high-grade brain gliomas, the expression of laminin-8 (and lamin in-10) in breast cancer tissue may be a predictive factor for tumor neovascularization and invasion and suggest that laminationin-2, laminine-8, and laminIn-10 are important components of tumor microvessels and may associate with breast tumor progression.
Isolation of a novel human gene, APCDD1, as a direct target of the beta-Catenin/T-cell factor 4 complex with probable involvement in colorectal carcinogenesis.
Data suggest that APCDD1 is directly regulated by the beta-catenin/Tcf complex and that its elevated expression is likely to contribute to colorectal tumorigenesis.
Up-regulation of the ectodermal-neural cortex 1 (ENC1) gene, a downstream target of the beta-catenin/T-cell factor complex, in colorectal carcinomas.
- M. Fujita, Y. Furukawa, T. Tsunoda, T. Tanaka, M. Ogawa, Y. Nakamura
- BiologyCancer research
- 1 November 2001
Examination of expression profiles of LoVo cells infected with either adenoviruses expressing wild-type AXIN1 or those expressing a control gene, and results suggest that ENC1 is regulated by the beta-catenin/Tcf pathway, suggest that it may contribute to colorectal carcinogenesis by suppressing differentiation of colonic cells.
Identification of AF17 as a downstream gene of the beta-catenin/T-cell factor pathway and its involvement in colorectal carcinogenesis.
The results suggest that the AF17 gene product is likely to be involved in the beta-catenin-T-cell factor/lymphoid enhancer factor signaling pathway and to function as a growth-promoting, oncogenic protein.
Brain tumor tandem targeting using a combination of monoclonal antibodies attached to biopoly(beta-L-malic acid).
Antisense inhibition of laminin-8 expression reduces invasion of human gliomas in vitro.
The results show that laminin-8 may contribute to glioma progression and recurrence not only as part of the neovascularization process but also by directly increasing the invasive potential of tumor cells.
Inhibition of brain tumor growth by intravenous poly(β-l-malic acid) nanobioconjugate with pH-dependent drug release
- Hui Ding, S. Inoue, J. Ljubimova
- Biology, ChemistryProceedings of the National Academy of Sciences
- 15 September 2010
The availability of a systemically active polymeric drug delivery system that passes through the BTB, targets tumor cells, and inhibits glioma growth gives hope for a successful strategy ofglioma treatment.
Polycefin, a new prototype of a multifunctional nanoconjugate based on poly(beta-L-malic acid) for drug delivery.
In vitro experiments using two human glioma cell lines U87MG and T98G demonstrated that Polycefin was delivered into the tumor cells by a receptor-mediated endocytosis mechanism and was able to inhibit the synthesis of laminin-8 alpha4 and beta1 chains at the same time.
Polymalic acid-based nanobiopolymer provides efficient systemic breast cancer treatment by inhibiting both HER2/neu receptor synthesis and activity.
The characterization of a novel, targeted, nanobiopolymeric conjugate based on biodegradable, nontoxic, and nonimmunogenic PMLA offers a preclinical proof of concept for use of the PMLA nanoplatform for combination cancer therapy.