Abstract: The invention discloses oncogenic fusion proteins. The invention provides methods for treating gene-fusion based cancers.

Abstract: Disclosed herein are methods for identifying subjects, diagnosed as having glioblastoma (GBM), as likely responders to treatment with a programmed death protein 1 (PD-1) blockade. In some embodiments, the subjects are identified by determining the level of phosphorylated extracellular-signal-regulated kinase (p-ERK) in a GBM tumor sample from the subject. In some embodiments, the GBM is recurrent. Also disclosed herein are methods of treating GBM subjects, whereby the methods include (1) identifying the subject as a likely responder to PD-1 blockade, and (2) administering a PD-1 inhibitor and/or a programmed death-ligand 1 (PD-L1) inhibitor.

Abstract: The invention discloses oncogenic fusion proteins. The invention provides methods for treating gene-fusion based cancers.

Abstract: The invention discloses oncogenic fusion proteins. The invention provides methods for treating gene-fusion based cancers.

Abstract: The invention relates to inhibitory nucleotide signal sequences or “INS” sequences in the genomes of lentiviruses. In particular the invention relates to the AGG motif present in all viral genomes. The AGG motif may have an inhibitory effect on a virus, for example by reducing the levels of, or maintaining low steady-state levels of, viral RNAs in host cells, and inducing and/or maintaining in viral latency. In one aspect, the invention provides vaccines that contain, or are produced from, viral nucleic acids in which the AGG sequences have been mutated. In another aspect, the invention provides methods and compositions for affecting the function of the AGG motif, and methods for identifying other INS sequences in viral genomes.

Abstract: The invention discloses oncogenic fusion proteins. The invention provides methods for treating gene-fusion based cancers.

Abstract: Systems and methods for predicting a sensitivity of the cancer to an anti-programed cell death 1 (PD-1) immunotherapy are disclosed. The method can comprise determining a presence of at least one mutation in at least one target gene/protein in a sample of the cancer, wherein the target gene can include a PTEN, a PTPN11, and/or a BRAF gene/protein. If the PTPN11 or BRAF gene/protein includes at least one mutation and/or the PTEN gene/protein is a wild type PTEN gene/protein, then the cancer can be predicted to be sensitive to the PD-1 immunotherapy.

Abstract: The invention discloses oncogenic fusion proteins. The invention provides methods for treating gene-fusion based cancers.

Abstract: The invention discloses oncogenic fusion proteins. The invention provides methods for treating gene-fusion based cancers.

Abstract: The invention discloses oncogenic fusion proteins. The invention provides methods for treating gene-fusion based cancers.

Abstract: Techniques for treating a subject with M-GBM and recurrent GBM are provided. Example methods include obtaining at least two M-GBM tumor samples from different locations within a patient, extracting genomic DNA from each of the tumor samples, and determining whether the subject has a mutation in PI3K-AKT-mTOR (PAM) pathway in both DNA samples. If a mutation in PAM pathway is present in each of the isolated DNA samples, the method can further include treating the subject with an effective amount of an agent that inhibits the PAM pathway. Pharmaceutical agents and kits for use in the treatment of M-GBM and recurrent GBM are also provided.

Abstract: The invention relates to inhibitory nucleotide signal sequences or “INS” sequences in the genomes of lentiviruses. In particular the invention relates to the AGG motif present in all viral genomes. The AGG motif may have an inhibitory effect on a virus, for example by reducing the levels of, or maintaining low steady-state levels of, viral RNAs in host cells, and inducing and/or maintaining in viral latency. In one aspect, the invention provides vaccines that contain, or are produced from, viral nucleic acids in which the AGG sequences have been mutated. In another aspect, the invention provides methods and compositions for affecting the function of the AGG motif, and methods for identifying other INS sequences in viral genomes.

Abstract: Whole exome sequencing of 12 tumor-normal DNA pairs, RNAseq analysis and targeted deep sequencing identified new genetic alterations in PTCL transformation. These analyses identified highly recurrent epigenetic factor mutations in TET2, DN-MT3A and IDH2 as well as a new highly prevalent RHOA p.Gly17Val (NM_001664) mutation present in 22/35 (67%) of angioimmunoblastic T-cell lymphomas (AITL) and in 8/44 (18%) not otherwise specified PTCL (PTCL NOS) samples. Mechanistically, the RHOA Gly17Val protein interferes with RHOA signaling in biochemical and cellular assays, an effect potentially mediated by the sequestration of activated Guanine Exchange Factor (GEF) proteins. In addition, new and recurrent, genetic defects are described including mutations in FYN, ATM, B2M and CD58 implicating SRC signaling, impaired DNA damage response and escape from immune surveillance mechanisms in the pathogenesis of PTCL.

Abstract: The invention relates to inhibitory nucleotide signal sequences or “INS” sequences in the genomes of lentiviruses. In particular the invention relates to the AGG motif present in all viral genomes. The AGG motif may have an inhibitory effect on a virus, for example by reducing the levels of, or maintaining low steady-state levels of, viral RNAs in host cells, and inducing and/or maintaining in viral latency. In one aspect, the invention provides vaccines that contain, or are produced from, viral nucleic acids in which the AGG sequences have been mutated. In another aspect, the invention provides methods and compositions for affecting the function of the AGG motif, and methods for identifying other INS sequences in viral genomes.

Abstract: This disclosed subject matter relates to methods for predicting drug based on genomic and transcriptomic data. The methods prioritize genetic and gene expression features of cancer cell lines that predict drug response, by integrating genomic/pharmaceutical data, protein-protein interaction network, and prior knowledge of drug-targets interaction with the techniques of network propagation.

Abstract: The invention discloses oncogenic fusion proteins. The invention provides methods for treating gene-fusion based cancers.

Abstract: Whole exome sequencing of 12 tumor-normal DNA pairs, RNAseq analysis and targeted deep sequencing identified new genetic alterations in PTCL transformation. These analyses identified highly recurrent epigenetic factor mutations in TET2, DN-MT3A and IDH2 as well as a new highly prevalent RHOA p.Gly17Val (NM_001664) mutation present in 22/35 (67%) of angioimmunoblastic T-cell lymphomas (AITL) and in 8/44 (18%) not otherwise specified PTCL (PTCL NOS) samples. Mechanistically, the RHOA Gly17Val protein interferes with RHOA signaling in biochemical and cellular assays, an effect potentially mediated by the sequestration of activated Guanine Exchange Factor (GEF) proteins. In addition, new and recurrent, genetic defects are described including mutations in FYN, ATM, B2M and CD58 implicating SRC signaling, impaired DNA damage response and escape from immune surveillance mechanisms in the pathogenesis of PTCL.

Abstract: The present invention relates to hairy cell leukemia biomarkers and methods of utilizing these biomarkers to diagnose and/or treat hairy cell leukemia.

Abstract: The invention is based on the discovery of certain new somatic single nucleotide substitution mutations of NT5C2 gene variants found in some Acute Lymphoblastic Leukemia (ALL) relapse subjects. Techniques include obtaining a biological sample taken from a subject having ALL, and detecting the presence or absence in the biological sample of a biomarker selected from the group consisting of an NT5C2 gene mutation, an mRNA transcribed from the NT5C2 gene mutation, or a protein encoded by the NT5C2 gene mutation. The method also includes determining that the subject has increased resistance to treatment with 6-mercaptopurine or 6-thioguanine, if the biomarker is detected. In some embodiments, the method still further includes treating the subject with a nucleoside analog other than 6-mercaptopurine or 6-thioguanine if the biomarker is detected.

Abstract: The invention discloses oncogenic fusion proteins. The invention provides methods for treating gene-fusion based cancers.