Abstract: In order to identify the molecules involved in esophageal carcinogenesis and those to be useful for diagnostic markers as well as targets for new drugs and immunotherapy, a cDNA microarray representing 32,256 genes was constructed to analyze the expression profiles of 19 esophageal squamous-cell carcinomas (ESCCS) purified by laser-capture microdissection. A detailed genome-wide database for sets of genes that are significantly up- or down-regulated in esophageal cancer is disclosed herein. These genes find use in the development of therapeutic drugs or immunotherapy as well as tumor markers. Additionally, genes associated with lymph-node metastasis and post-surgery recurrence are disclosed herein. Among the candidate molecular target genes, ECT2, CDC45L and DKK1 are further characterized. Treatment of ESCC cells with small interfering RNAs (siRNAs) of ECT2 or CDC45L suppressed growth of the cancer cells.

Abstract: Described herein are antibodies and antibody fragments capable of treating or preventing cancers associated with the over-expression and/or up-regulation of DKK1. Also disclosed are methods of treating or preventing cancer using the antibody and methods and kits utilized to diagnosing cancer. The herein described products and methods find utility in the context of a variety of cancers, such as pancreatic cancer, gastric cancer, liver cancer, prostate cancer, breast cancer, cervical cancer, bile duct cancer, lung cancer and esophageal cancer.

Abstract: The present invention provides peptides comprising the amino acid sequence of SEQ ID NO: 8, 67, 89, as well as peptides comprising the above-mentioned amino acid sequences in which 1, 2, or several amino acids are substituted, deleted, or added, and having cytotoxic T cell inducibility. The present invention also provides drugs for treating or preventing tumors comprising these peptides. The peptides of the present invention can also be used as vaccines.

Abstract: Peptide vaccines against cancer are described herein. In particular, epitope peptides derived from the C6orf167 gene that elicit CTLs are provided. Antigen-presenting cells and isolated CTLs that target such peptides, as well as methods for inducing the antigen-presenting cell, or CTL are also provided. The present invention further provides pharmaceutical compositions containing peptides derived from C6orf167 or polynucleotides encoding the polypeptides as active ingredients. Furthermore, the present invention provides methods for the treatment and/or prophylaxis of (i.e., preventing) cancers (tumors), and/or the prevention of postoperative recurrence thereof, as well as methods for inducing CTLs, methods for inducing anti-tumor immunity, using the peptides derived from C6orf167, polynucleotides encoding the peptides, or antigen-presenting cells presenting the peptides, or the pharmaceutical compositions of the present invention.

Abstract: The present invention provided methods for treating lung cancers using therapeutic agents for lung cancers comprising erbB receptor inhibitors as active ingredients. Methods for examining the responsiveness of lung cancer patients to erbB receptor inhibitors by using blood amphiregulin (AREG) as an indicator were provided. Furthermore, methods for treating lung cancers in which responsiveness to an erbB receptor inhibitor is determined based on blood AREG concentration, and in which therapeutic agents are selectively administered to patients expected to be responsive, were also provided. Advanced therapeutic effects can be expected by administering an erbB receptor inhibitor to patients predicted to be responsive. The present invention contributes to the improvement of therapeutic effects of gefitinib (Product name: Iressa®) and such on lung cancers.

Abstract: In order to identify the molecules involved in esophageal carcinogenesis and those to be useful for diagnostic markers as well as targets for new drugs and immunotherapy, a cDNA microarray representing 32,256 genes was constructed to analyze the expression profiles of 19 esophageal squamous-cell carcinomas (ESCCS) purified by laser-capture microdissection. A detailed genome-wide database for sets of genes that are significantly up- or down-regulated in esophageal cancer is disclosed herein. These genes find use in the development of therapeutic drugs or immunotherapy as well as tumor markers. Additionally, genes associated with lymph-node metastasis and post-surgery recurrence are disclosed herein. Among the candidate molecular target genes, ECT2, CDC45L and DKK1 are further characterized. Treatment of ESCC cells with small interfering RNAs (siRNAs) of ECT2 or CDC45L suppressed growth of the cancer cells.

Abstract: The present invention relates to the roles played by the TBC1D7 genes in cancer, in particular, lung cancer or esophageal cancer, or carcinogenesis and features a method for treating and/or preventing cancer, in particular, lung cancer or esophageal cancer by administering a double-stranded molecule against one or more of the TBC1D7 genes or a composition, vector or cell containing such a double stranded molecule. The present invention also features methods for diagnosing lung or assessing/determining the prognosis of a patient with lung, especially NSCLC or SCLC, or esophageal cancer, using one or more over-expressed genes selected from among TBC1D7. To that end, TBC1D7 may serve as a novel biomarker for lung cancer or esophageal cancer. Also, disclosed are methods of identifying compounds for treating and preventing lung or esophageal cancer, using as an index for their effect on the over-expression of one or more of TBC1D7 in the lung cancer or esophageal cancer.

Abstract: Disclosed herein is a method for determining a kinase activity of ERK for CDCA5 and methods of screening for modulators of this kinase activity. Also disclosed are methods and pharmaceutical compositions for preventing and/or treating lung cancer or esophageal cancer that use or include such modulators.

Abstract: The invention features methods for detecting lung cancer or esophageal cancer, by detecting over-expression of ECT2 compared the normal organs. Also disclosed are methods of identifying compounds for treating and preventing lung cancer or esophageal cancer, based on the over-expression of ECT2 in the lung cancer or esophageal cancer, the cell proliferation function of ECT2. Also, provided are a method for treating lung cancer or esophageal cancer by administering a double-stranded molecule against the ECT2 gene or an antibody against ECT2 protein. The invention also provides products, including the double-stranded molecules and vectors encoding them, as well as compositions comprising the molecules or vectors, useful in the provided methods.

Abstract: The present invention features methods for diagnosing cancer or assessing or determining the prognosis of a patient with lung cancer, by detecting the expression level of Nectin-4. The present invention also features double-stranded molecules against the Nectin-4 gene, vectors encoding them, compositions comprising them and methods comprising the step of administering them into a subject, which are useful for treating or preventing cancer. Also, disclosed are methods of identifying candidate compounds for treating and preventing cancer, using the Nectin-4 polypeptide or cells expressing the Nectin-4 gene.

Abstract: In order to identify the molecules involved in esophageal carcinogenesis and those to be useful for diagnostic markers as well as targets for new drugs and immunotherapy, a cDNA microarray representing 32,256 genes was constructed to analyze the expression profiles of 19 esophageal squamous-cell carcinomas (ESCCS) purified by laser-capture microdissection. a detailed genome-wide database for sets of genes that are significantly up- or down-regulated in esophageal cancer is disclosed herein. these genes find use in the development of therapeutic drugs or immunotherapy as well as tumor markers. additionally, genes associated with lymph-node metastasis and post-surgery recurrence are disclosed herein. among the candidate molecular target genes, ECT2 and CDC45L and DKK1 are further characterized. treatment of ESCC cells with small interfering RNAs (siRNAs) of ECT2 or CDC45L suppressed growth of the cancer cells.

Abstract: The present invention relates to the roles played by the SYNGR4 genes in lung cancer carcinogenesis and features a method for treating or preventing lung cancer by administering a double-stranded molecule against one or more of the SYNGR4 genes or a composition, vector or cell containing such a double stranded molecule and antibody. The present invention also features methods for diagnosing lung cancer or assessing/determining the prognosis of a patient with lung cancer, especially NSCLC or SCLC, using one or more over-expressed genes selected from among SYNGR4. To that end, SYNGR4 may serve as a novel serological biomarker for lung cancer. Also, disclosed are methods of identifying compounds for treating and preventing lung cancer, using as an index their effect on the over-expression of one or more of SYNGR4 in the lung cancer.

Abstract: The present invention is based on the observation that the co-activation of CDCA1 and KNTC2, and their cognate interactions, play significant roles in lung-cancer progression and that methods of inhibiting the complex can be used to treat non-small-cell lung cancer.

Abstract: The present invention provides the method of predicting an non-small cell lung cancer (NSCLC) prognosis.

Abstract: Disclosed are methods for detecting non-small cell lung cancer (NSCLC) using differentially expressed genes KIF11, GHSR1b, NTSR1, and FOXM1. Also disclosed are methods of identifying compounds for treating and preventing NSCLC, based on the interaction between KOC1 and KIF11, or NMU and GHSR1b or NTSR1.

Abstract: Disclosed are methods for detecting non-small cell lung cancer (NSCLC) using differentially expressed genes KIF11, GHSR1b, NTSR1, and FOXM1. Also disclosed are methods of identifying compounds for treating and preventing NSCLC, based on the interaction between KOC1 and KIF11, or NMU and GHSR1b or NTSR1.

Abstract: The present invention relates to the roles played by OIP5 genes in lung and/or esophageal cancer carcinogenesis and features a method for treating and/or preventing lung and/or esophageal cancer by administering a double-stranded molecule against the OIP5 genes or a composition, vector or cell containing such a double-stranded molecule and antibody. The present invention also features methods for detecting and/or diagnosing lung and/or esophageal cancer, or assessing/determining the prognosis of and/or monitoring the efficacy of a cancer therapy in a patient with lung and/or esophageal cancer by detecting OIP5. Also, disclosed are methods of identifying compounds for treating and preventing cancer relating to OIP5.

Abstract: The invention features methods for detecting cancers, especially lung cancer and/or esophageal cancer, using over-expressed gene; CDCA5, EPHA7, STK31 or WDHD1 compared the normal organs. Also disclosed are methods of identifying compounds for treating and preventing cancers, based on the over-expression or the biological activity of CDCA5, EPHA7, STK31 or WDHD1 in the cancers, especially the interaction between EPHA7 and EGFR. Also, features are a method for treating cancers by administering a double-stranded molecule against CDCA5, EPHA7, STK31 or WDHD1 gene. The invention also features products, including the double-stranded molecules and vectors encoding them, as well as compositions comprising the molecules or vectors, useful in the provided methods.

Abstract: The present invention relates to methods for treating or preventing lung cancer by administering a double-stranded molecule against one or more of EBI3, DLX5, NPTX1, CDKN3 or EF-I delta genes or compositions, vectors or cells containing such a double-stranded molecule. The present invention also features methods for diagnosing lung cancer, especially NSCLC or SCLC, using one or more over-expressed genes selected from among EBI3, DLX5, NPTX1, CDKN3 and/or EF-I delta. Also disclosed are methods of identifying compounds for treating and preventing lung cancer, using as an index their effect on the over-expression of one or more of EBI3, DLX5, CDKN3 and/or EF-I delta in the lung cancer, the cell proliferation function of one or more of EBI3, DLX5, NPTX1, CDKN3 and/or EF-I delta or the interaction between CDKN3 and VRS, EF-I beta, EF-I gamma and/or EF-I delta.

Abstract: The present invention is based on the observation that the co-activation of CDCA1 and KNTC2, and their cognate interactions, play significant roles in lung-cancer progression and that methods of inhibiting the complex can be used to treat non-small-cell lung cancer.