Abstract: The present invention relates to a novel combination of (1) a substance that suppresses or inhibits the function of extracellular TCTP (translationally controlled tumor protein), especially released from tumor cells, and (2) a cancer immunotherapeutic agent for the treatment of cancer. Preferably, such a cancer immunotherapeutic agent is an immune checkpoint inhibitor. The substance that suppresses or inhibits the function of extracellular TCTP functions as an activator or enhancer of anti-tumor immune cells including T cells and natural killer (NK) cells and/or an antagonist of immunosuppressive cells, such as myeloid-derived suppressor cells (MDSCs), in the tumor immune microenvironment (TIME). The combination according to the present invention is useful for treating or preventing cancer. The combination according to the present invention is also useful for alleviating, reverting, or preventing immune suppression in the tumor immune microenvironment.

Abstract: The present invention is intended to identify a modulatory substance of the tumor immune microenvironment, and to provide a therapeutic utilization method of the modulatory substance. Specifically, the present invention relates to an inhibitor of the accumulation of myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TIME), wherein the inhibitor comprises, an active ingredient, a substance that suppresses or inhibits the function of an immunomodulator released from dead tumor cells. More specifically, the present invention relates to the aforementioned inhibitor comprising a substance that suppresses or inhibits the function of, for example, TCTP (translationally controlled tumor protein).

Abstract: Disclosed is a recombinant plasmid having a gene which encompasses at least the entire coding region of human fibroblast interferon messenger RNA and a method for preparing such plasmid.

Abstract: Provided are an inhibitor of activation of an immune response mediated by an HMGB protein, the inhibitor containing at least one compound selected from the group consisting of a phosphorothioate oligonucleotide and a derivative thereof, and a method of screening for an inhibitor or enhancer of activation of an immune response mediated by an HMGB protein.

Abstract: Provided are an inhibitor of activation of an immune response mediated by an HMGB protein, the inhibitor containing at least one compound selected from the group consisting of a phosphorothioate oligonucleotide and a derivative thereof, and a method of screening for an inhibitor or enhancer of activation of an immune response mediated by an HMGB protein, the method including a mixing step of mixing an HMGB protein and a labeled nucleic acid in the presence and absence of a test substance; a quantifying step of quantifying the HMGB protein bound to the labeled nucleic acid; and a determination step of determining that the test substance is an inhibitor of activation of an immune response mediated by the HMGB protein when the amount of the HMGB protein bound to the labeled nucleic acid in the presence of the test substance is less than the amount of the HMGB protein bound to the labeled nucleic acid in the absence of the test substance and determining that the test substance is an enhancer of activation of an i

Abstract: A gene coded for a polypeptide which possesses interleukin-2 is isolated, and connected with a vector DNA which is capable of replicating in a procaryotic or eucaryotic cell at a position downstream of a promoter gene in the vector obtaining a recombant DNA, with which the cell is transformed to produce interleukin-2.

Abstract: The present invention relates to a polypeptide, p43, which is associated with the interleukin-2 receptor (IL-2R). It binds specifically to the &bgr; and &ggr; subunits of IL-2R and is further capable of binding NAD+. The invention is further related to nucleic acid molecules coding for p43 and to antibodies specifically binding to p43.

Abstract: A recombinant DNA molecule coding for a protein having the activity of an interferon regulatory factor-1 (IRF-1).

Abstract: The present invention relates, in general, to a method of diagnosing tumorigenic mammalian cells or the propensity of a mammalian cell to become tumorigenetic. Additionally, the present invention relates to a cloned cDNA or genomic DNA for reducing the propensity of a cell to become tumorigenic or suppressing tumorigenic phenotype of a cell; a method of reducing the propensity of a cell to become tumorigenic or suppressing the tumorigenic phenotype of a cell; a method of treating a patient suffering from or predisposed to subsequent cancer development; and a method of diagnosing tumorigenic tissue of a human or tissue predisposed to become tumorigenic.

Abstract: A gene coded for a polypeptide which possesses interleukin-2 is isolated, and connected with a vector DNA which is capable of replicating in a procaryotic or eucaryotic cell at a position downstream of a promoter gene in the vector obtaining a recombinant DNA, with which the cell is transformed to produce interleukin-2.

Abstract: A gene coded for a polypeptide which possesses interleukin-2 is isolated, and connected with a vector DNA which is capable of replicating in a procaryotic or eucaryotic cell at a position downstream of a promoter gene in the vector obtaining a recombinant DNA, with which the cell is trans-formed to produce interleukin-2.

Abstract: A plasmid containing a recombinant DNA molecule coding for a protein having the activity of an interferon regulatory factor-1 (IRF-1) and promoter and regulator sequences thereof, are described.

Abstract: A method of producing a recombinant protein having the activity of an interferon regulatory factor-1 (IRF-1) or a target protein, are described.

Abstract: Interferon regulatory factor-1 (IRF-1) is implicated in the regulation of type I interferons (IFN) and cell growth. The invention is a mutant mouse lacking expression of the IRF-1 gene. Mice lacking IRF-1 did not differ from normal mice in size, behaviour, or reproductive ability. With fibroblasts derived from these mutant mice, it was shown that type I IFN induction is dramatically reduced when cells are induced by poly(I):poly(C). In contrast, no differences were found when cells are induced by New Castle Disease Virus (NDV), or induced by poly(I):poly(C) with prior treatment of IFN-.beta.. On the other hand, the induction levels of IFN-inducible genes such as MHC class I and 2'-5' oligoadenylate synthetase (2'5'OAS) were not affected. Collectively, these results illustrate an IRF-1 independent mechanism of gene induction for type I IFN and these IFN-inducible genes. The critical role of IRF-1 in the immune system has been documented for the first time by the observation that the number of TcR.alpha..beta..

Abstract: Recombinant human Interleukin-2 (IL-2) polypeptides are provided. The polypeptides are produced by expression of suitable nucleic acid molecules in transformed host cells such as E. coli.

Abstract: The transcription factors, IRF-1 and IRF-2 are induced by interferons (IFNs) and a variety of other cytokines. IRF-1 functions as an activator whereas IRF-2 represses IRF-1 action by competing for binding to the same cis-elements. Recently, it has been shown that balanced expression between these two factors is critical for maintaining normal restraints on cell growth. Mutant mice deficient for IRF-2 were prepared by homologous recombination. In mutant cells, infection by Newcastle disease virus (NDV) resulted in the induction of type I IFN (IFN-.alpha. and IFN-.beta.) mRNAs, the levels of which were significantly higher than in wild type cells; whereas, such a difference was not found upon induction by poly(I):poly(C). Unlike the IRF-1 deficient mutant mice, the IRF-2 deficient mice of the invention exhibit multiple phenotypes of physical vulnerability, including lethality to lymphocytic choriomeningitis virus (LCMV).

Abstract: The present invention relates to a method of altering the phenotype of cells expressing an oncogene by expressing a nucleic acid encoding interferon regulatory factor 1 (IRF-1).

Abstract: The present invention relates, in general, to a method of diagnosing tumorigenic mammalian cells or the propensity of a mammalian cell to become tumorigenetic. Additionally, the present invention relates to a cloned cDNA or genomic DNA for reducing the propensity of a cell to become tumorigenic or suppressing tumorigenic phenotype of a cell; a method of reducing the propensity of a cell to become tumorigenic or suppressing the tumorigenic phenotype of a cell; a method of treating a patient suffering from or predisposed to subsequent cancer development; and a method of diagnosing tumorigenic tissue of a human or tissue predisposed to become tumorigenic.

Abstract: The present invention concerns a novel molecular marker useful for diagnosing hematopoietic disorders, including cancers and precancerous conditions. The invention is based on the unexpected discovery that inactivation of the IRF-1 tumor suppressor gene can occur via an altered splicing pattern of the IRF-1 primary transcript. This altered splicing pattern leads to mRNAs lacking exon 2 or exons 2 and 3. The relative amounts of full-length RNA and shortened RNA molecules are significantly different in samples obtained from patients suffering from certain cancers and precancerous conditions as compared to healthy donors.

Abstract: A gene coded for a polypeptide which possesses interleukin-2 is isolated, and connected with a vector DNA which is capable of replicating in a procaryotic or eucaryotic cell at a position downstream of a promoter gene in the vector obtaining a recombinant DNA, with which the cell is transformed to produce interleukin-2.