机译:在神经性乳腺肿瘤中透明质酸的超量生产通过基质细胞募集促进血管生成
From the Department of Molecular Oncology,* Division of Molecular and Cellular Biology, Institute on Aging and Adaptation, Shinshu University Graduate School of Medicine, Nagano;
the Department of Surgery, Shinshu University School of Medicine, Nagano;
Biomedical Research Center,|| Department of Laboratory Medicine, Shinshu University Hospital, Nagano;
Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Saitama;
the Division of Pharmacotherapy, Department of Advanced Medicine, National Center for Geriatrics and Gerontology, Aichi;
Biochemistry and Molecular Biology Laboratory,¶ Aichi Prefectural College of Nursing and Health, Aichi;
Program of Molecular Pathology,** Aichi Cancer Center, Research Institute, Aichi;
and Institute for Molecular Science of Medicine, Aichi Medical University, Aichi, Japan;
机译:在神经元引起的乳腺肿瘤中透明质酸的过量生产通过基质细胞募集来加速血管生成:versican / PG-M的可能参与。
机译:持续的乳腺营养足以促进和同步ErbB2 | [sol] | Neu诱导的肿瘤的发展
机译:ErbB2 / Neu诱导的细胞周期蛋白D1依赖性转化在p27-Haploinsufficient乳腺上皮细胞中加速,但在p27-Null细胞中受损。
机译:基质细胞对肿瘤生长和血管生成影响的数值模拟
机译:阐明ErbB2 / Neu诱导的乳腺肿瘤发生的分子机制。
机译:在神经性乳腺肿瘤中透明质酸的超量生产通过基质细胞募集促进血管生成
机译:透明质酸在神经元诱导的乳腺肿瘤中的过度生产通过基质细胞募集促进血管生成:Versican / PG-M的可能参与
机译:骨髓源性干细胞在乳腺肿瘤血管生成,生长和转移中的作用以及VEGF-a和pIGF对其招募的影响