Abstract: The present invention provides peptides containing the BIG3 polypeptide-binding site in a PHB2 polypeptide, which inhibit the binding between a PHB2 polypeptide and a BIG3 polypeptide, and pharmaceutical compositions containing the peptide. The peptides of the present invention have the ability to bind not to PHB2, whose expression is found in organs throughout the human body, but to BIG3, which is a protein highly expressed specifically in particularly estrogen receptor-positive cancer, and have excellent growth suppressive effects on BIG3-positive cancer cells. Accordingly, the peptides of the present invention are useful as therapeutic agents for breast cancer which can avoid expression of side effects.

Abstract: The present invention provides peptides having a structure in which portions of a dominant-negative peptide of BIG3 which inhibits the interaction between BIG3 and PHB2 are replaced by at least two stapling structures. The peptides of the present invention have excellent cell growth inhibiting activity. The cell growth inhibiting activity lasts longer, compared to a single-stapled peptide. Therefore, the peptides of the present invention have a feature suitable for clinical applications in cancer therapy.

Abstract: The present invention provides peptides having a structure in which portions of a dominant-negative peptide of BIG3 which inhibits the interaction between BIG3 and PHB2 are replaced by at least two stapling structures. The peptides of the present invention have excellent cell growth inhibiting activity. The cell growth inhibiting activity lasts longer, compared to a single-stapled peptide. Therefore, the peptides of the present invention have a feature suitable for clinical applications in cancer therapy.

Abstract: The present invention provides peptides containing a structure in which a portion of the dominant negative peptide of BIG3 which inhibits the interaction between BIG3 and PHB2 is substituted with stapling structure(s). Peptides of the present invention have excellent cell growth inhibitory actions. Furthermore, their cell growth inhibitory actions continue for a longer time than the actions of peptides without stapling structures. Therefore, these peptides have features suitable for clinical applications in cancer therapy.

Abstract: The present invention provides peptides containing a structure in which a portion of the dominant negative peptide of BIG3 which inhibits the interaction between BIG3 and PHB2 is substituted with stapling structure(s). Peptides of the present invention have excellent cell growth inhibitory actions. Furthermore, their cell growth inhibitory actions continue for a longer time than the actions of peptides without stapling structures. Therefore, these peptides have features suitable for clinical applications in cancer therapy.

Abstract: Provided is a novel cancer-treating agent which can be used as a novel choice for the treatment of cancer. Specifically provided are: a peptide that inhibits binding of ERAP1 polypeptide to PHB2 polypeptide, which comprises a binding site of the ERAP1 polypeptide to the PHB2 polypeptide, and a pharmaceutical composition comprising the peptide. In addition, provided is a method for screening a drug candidate for treating and/or preventing cancer using inhibition of the binding of the ERAP1 polypeptide to PP1? polypeptide, PKA polypeptide or PKB polypeptide as an index.

Abstract: Methods of detecting synovial sarcoma using differentially expressed genes are disclosed. Also disclosed are methods of identifying agents for treating synovial sarcoma. Further, a method for treating or preventing a disease that is associated with Frizzled homolog 10 (FZD10) in a subject is provided.

Abstract: The present application provides novel human genes A7322, whose expression is markedly elevated in breast cancer. The present application also provides human genes F3374 whose expression is markedly elevated in breast cancer. These genes and polypeptides encoded thereby can be used, for example, in the diagnosis of breast cancer, and as target molecules for developing drugs against breast cancer. The invention features methods of screening for modulators of the kinase activity of PBK/TOPK. The invention further provides methods of screening for agents to prevent or treat cancer, such as breast cancer.

Abstract: The present invention relates to an antibody or a fragment thereof which is capable of binding to a Frizzled homologue 10 (FZD10) protein, such as a mouse monoclonal antibody, a chimeric antibody and a humanized antibody. Also, the present invention relates to a method for treating and/or preventing FZD10-associated disease; a method for diagnosis or prognosis of FZD10-associated disease; and a method for in vivo imaging of FZD10 in a subject.

Abstract: The present invention provides therapeutic agents and methods for treating cancer using the polypeptides composed of an amino acid sequence which includes a polypeptide fragment of DEPDC1. The polypeptides of the present invention can be introduced into cancer cells by modifying the polypeptides with transfection agents such as poly-arginine. Furthermore, the present invention provides methods of screening for therapeutic agents or compounds useful in inhibition of the DEPDC1/ZN-F224 complex formation or the treatment of cancer. The present invention also provides siRNAs targeting the ZNF224 gene, which are suggested to be useful in the treatment of bladder cancer.

Abstract: Methods of detecting synovial sarcoma using differentially expressed genes are disclosed. Also disclosed are methods of identifying agents for treating synovial sarcoma. Further, a method for treating or preventing a disease that is associated with Frizzled homologue 10 (FZD10) in a subject is provided.

Abstract: Methods of detecting synovial sarcoma using differentially expressed genes are disclosed. Also disclosed are methods of identifying agents for treating synovial sarcoma. Further, a method for treating or preventing a disease that is associated with Frizzled homologue 10 (FZD10) in a subject is provided.

Abstract: The present application provides novel human genes A7322, whose expression is markedly elevated in breast cancer. The present application also provides human genes F3374 whose expression is markedly elevated in breast cancer. These genes and polypeptides encoded thereby can be used, for example, in the diagnosis of breast cancer, and as target molecules for developing drugs against breast cancer. The invention features methods of screening for modulators of the kinase activity of PBK/TOPK. The invention further provides methods of screening for agents to prevent or treat cancer, such as breast cancer.

Abstract: The present application provides novel human gene B7330N whose expression is markedly elevated in breast cancers. The gene and polypeptide encoded by the gene can be used, for example, in the diagnosis of breast cancers, as target molecules for developing drugs against the disease, and for attenuating cell growth of breast cancer.

Abstract: Provided is a novel cancer-treating agent which can be used as a novel choice for the treatment of cancer. Specifically provided are: a peptide that inhibits binding of ERAP1 polypeptide to PHB2 polypeptide, which comprises a binding site of the ERAP1 polypeptide to the PHB2 polypeptide, and a pharmaceutical composition comprising the peptide. In addition, provided is a method for screening a drug candidate for treating and/or preventing cancer using inhibition of the binding of the ERAP1 polypeptide to PP1? polypeptide, PKA polypeptide or PKB polypeptide as an index.

Abstract: Methods of detecting synovial sarcoma using differentially expressed genes are disclosed. Also disclosed are methods of identifying agents for treating synovial sarcoma. Further, a method for treating or preventing a disease that is associated with Frizzled homologue 10 (FZD10) in a subject is provided.

Abstract: Objective methods for detecting and diagnosing bladder cancer (BLC) are described herein. In one embodiment, the diagnostic method involves determining the expression level of a BLC-associated gene that discriminates between BLC cells and normal cells. The present invention further provides means for predicting and preventing bladder cancer metastasis using BLC-associated genes having unique altered expression patterns in bladder cancer cells with lymph-node metastasis. The present invention provides methods of screening for therapeutic agents useful in the treatment of bladder cancer, methods of treating bladder cancer and method for vaccinating a subject against bladder cancer. Specifically, the present application provides novel human genes C2093, B5860Ns and C6055s whose expression is markedly elevated in bladder cancers.

Abstract: The present application provides novel human genes A7322, whose expression is markedly elevated in breast cancer. The present application also provides human genes F3374 whose expression is markedly elevated in breast cancer. These genes and polypeptides encoded thereby can be used, for example, in the diagnosis of breast cancer, and as target molecules for developing drugs against breast cancer. The invention features methods of screening for modulators of the kinase activity of PBK/TOPK. The invention further provides methods of screening for agents to prevent or treat cancer, such as breast cancer.

Abstract: Methods of detecting synovial sarcoma using differentially expressed genes are disclosed. Also disclosed are methods of identifying agents for treating synovial sarcoma. Further, a method for treating or preventing a disease that is associated with Frizzled homologue 10 (FZD10) in a subject is provided.

Abstract: The present invention relates to an antibody or a fragment thereof which is capable of binding to a Frizzled homologue 10 (FZD10) protein, such as a mouse monoclonal antibody, a chimeric antibody and a humanized antibody. Also, the present invention relates to a method for treating and/or preventing FZD10-associated disease; a method for diagnosis or prognosis of FZD10-associated disease; and a method for in vivo imaging of FZD10 in a subject.