This invention provides methods and compositions for preventing, treating or ameliorating one or more symptoms of a malignant tumor associated with KRAS mutation in a mammal in need thereof, by identifying a tumor cell in the mammal, the tumor cell comprising at least one of: (i) a mutation of the KRAS gene, and (ii) an aberrant expression level of KRAS protein; and administering to the mammal a therapeutically effective amount of a composition comprising one or more RNAi molecules that are active in reducing expression of GST-.

The present invention relates to a novel antibody against HERV-K envelope that targets a conserved region not affected by glycosylation or by native conformation, and its use in diagnostics and/or is therapy.

Kits, compositions, devices, and methods for administration of olanzapine are provided. Uses thereof to treat nausea and vomiting are also provided.

The invention provides monoclonal antibodies that specifically bind to TIGIT. The monoclonal antibodies have the capacity for substantial activation of T cells and natural killer cells by inhibiting binding of TIGIT to CD155. The monoclonal antibodies can be used for treatment of cancer and infectious disease, among other applications.

The present invention relates to compounds which bind and/or inhibit prostate-specific membrane antigen (PSMA) comprising at least one group electron dense substituent (EDS), and at least one moiety which is amenable to radiolabeling; and therapeutic and diagnostic uses thereof.

A method of treating CNS tumors such as gliomas is provided comprising delivering a -emitting radionuclide containing composition to the tumor via the cerebral vasculature.

Novel, antimitotic heteroaryl amides and pharmaceutically acceptable salts of Formula I where Ar, R.sup.5, R.sup.6, R.sup.8, R.sup.9, R.sup.11, X.sup.1, and X.sup.2 are as defined herein, as compounds for treatment and prevention of cancer and proliferative diseases and disorders. ##STR00001##

The invention relates to methods for gene therapy in a subject suffering from Pompe disease, comprising gene-editing of a glucosidase, acid, alpha gene (GAA) in said subject. The invention further relates to a cell culture of genetically changed, differentiated myogenic progenitor cells derived from a donor subject suffering from Pompe disease, to a vector for use in a method for gene-editing a eukaryotic cell, and to a myotube prepared from myogenic progenitor cells that have been genetically changed by gene-editing.

Methods for treating a proliferative disease in hematologic malignancy in a subject having a complex karyotype by administering an effective amount of an immunotherapy which includes a targeting agent for an epitope of CD33. The proliferative disease may be a hematological disease or disorder such as multiple myeloma, acute myeloid leukemia, myelodysplastic syndrome, and myeloproliferative neoplasm. The effective amount of the anti-CD33 targeting agent may be an amount sufficient to induce myeloconditioning or an amount to induce myeloablation. The methods may further include transplanting allogeneic stem cells to the patient after administration of the anti-CD33 targeting agent.

The present subject matter relates to a compound represented by the general formula (I) or (I) or a pharmacologically acceptable salt thereof; pharmaceutical compositions containing at least one of these compounds; methods of making at least one of these compounds; methods of using at least one of these compounds for treating and/or preventing various cancers and/or proliferation disorders; methods of using at least one of these compounds for monitoring the effectiveness of an anticancer therapy against various cancers. In one embodiment, the subject matter relates to compounds that bind with a level of specificity to heat shock protein 70 (Hsp70). In another embodiment, the subject matter relates to compounds that bind with a level of specificity to inhibit both heat shock protein 70 (Hsp70) and heat shock cognate protein 70 (Hsc70).