Abstract: A diagnostic method for predicting whether a human tumor will be sensitive or resistant to treatment with tivozanib (AV-951) is disclosed. The method is based on measurement of macrophage content in a tissue sample from a tumor. Measurement of macrophage content can be based on analysis of macrophage marker gene expression, e.g., by RNA analysis or immunohistochemistry.

Abstract: Chimeric nonhuman mammals useful as inducible spontaneous cancer models are disclosed. The nonhuman mammals are obtained by introducing one or more genetically modified embryonic stem (ES) cells into an early stage embryo, and then implanting the manipulated embryo into a surrogate mother. The ES cells contain a recombinant oncogene, and also may contain a genetic mutation that deletes or inactivates a tumor suppressor gene. Models of different types of cancer are produced by introducing different combinations of genetic mutations into the ES cells that are introduced into the early stage embryo.

Abstract: A diagnostic method for predicting quantitatively whether a human tumor will be responsive or resistant (non-responsive) to treatment with the VEGF inhibitor, tivozanib (AV-951), is disclosed. The test is based on application of an algorithm to measurements of expression levels of the genes in a predictive gene set.

Abstract: A method of producing a tumorigenic mouse cell, the tumorigenicity of which depends on a recombinant gene of interest is disclosed. The method involves: (a) providing a conditionally tumorigenic mouse cell containing a recombinant oncogene operably linked to an inducible promoter, wherein (i) expression of the recombinant oncogene is necessary and sufficient for the tumorigenicity of the tumorigenic mouse cell, and (ii) the inducible promoter is in the uninduced state; and (b) introducing into the cell a recombinant gene of interest that functionally complements the oncogene, thereby restoring tumorigenicity without expression of the inducible recombinant oncogene. Also disclosed is a method of testing a compound for anti-tumor effects.

Abstract: DNA sequences encoding endothelial cell-leukocyte adhesion molecules ELAMs, methods for producing such molecules, and ELAMs (including the specific molecules ELAM1 and VLAM1 and 1b) essentially free of normally associated animal proteins are disclosed.DNA sequences encoding molecules involved in leukocyte adhesion (MILAs), methods for producing such molecules and MILAs (including the specific molecule, CDX) essentially free of normally associated animal proteins are also disclosed. Antibody preparations which are reactive for MILAs and also disclosed.Methods for identifying molecules which inhibit binding of leukocytes to endothelial cells, methods for inhibiting leukocyte binding to endothelial cells, and methods for detecting acute inflammation are disclosed.

Abstract: Human lipocortins III, IV, V and VI, DNA sequences and recombinant DNA molecules that are characterized in that they code for these human lipocortins. Hosts transformed with these sequences may be employed in the processes of this invention to produce the human lipocortin molecules of this invention. These polypeptides possess anti-inflammatory activity and are useful in the treatment of arthritic, allergic, dermatologic, ophthalmic and collagen diseases.

Abstract: DNA sequences encoding vascular cell adhesion molecules 1 and 1b ("VCAM1" and "VCAM1B"), recombinant DNA molecules comprising those sequences, and unicellular hosts transformed with those recombinant DNA molecules.

Abstract: There is provided highly purified tobacco putrescine N-methyltransferase, a process for its purification, and production of PMT DNA sequence. The purification process includes the step of applying a tobacco root extract to an anion exchange medium and specifically eluting putrescine N-methyltransferase with an elution buffer comprising putrescine.

Abstract: This invention relates to E2 trans-activation repressors which interfere with normal functioning of the native full-length E2 transcriptional activation protein of the papillomavirus. Native full-length E2 trans-activation protein activates transcription of papillomavirus only through binding to DNA, and it binds to DNA only in the form of a pre-formed homodimer--a pair of identical polypeptide subunits held together by non-covalent interactions. The E2 trans-activation repressors of this invention are proteins, polypeptides or other molecules that dimerize with full-length native E2 polypeptides to form inactive heterodimers, thus interfering with the formation of active homodimers comprising full-length native E2 polypeptides, thereby repressing papillomavirus transcription and replication. The E2 trans-activation repressors of this invention are advantageously used in the treatment of papillomavirus infections and their associated diseases.