Abstract: In some aspects the present invention provides methods for the treatment of B-cell lymphomas. Some such methods involve administration of HVEM ectodomain polypeptides, anti-HVEM antibodies, or anti-BTLA antibodies to subjects in need thereof. Some such methods involve use of CAR T cells, such as CD19-specific CAR T cells. The present invention also provides compositions useful in such methods. These and other embodiments of the present invention and described further herein.

Abstract: In some aspects the present invention provides methods for the treatment of B-cell lymphomas. Some such methods involve administration of HVEM ectodomain polypeptides, anti-HVEM antibodies, or anti-BTLA antibodies to subjects in need thereof. Some such methods involve use of CAR T cells, such as CD19-specific CAR T cells. The present invention also provides compositions useful in such methods. These and other embodiments of the present invention and described further herein.

Abstract: The present invention relates to the neurotoxicity that can occur as a side effect of the treatment of cancer patients with redirected T-cell therapies, such as chimeric antigen receptor (CAR) T cell therapies. The present invention provides various methods and compositions useful for treating and/or preventing such neurotoxicity, and/or for determining whether a subject is likely to develop such neurotoxicity, as well as a variety of other methods and compositions relating to the neurotoxicity associated with redirected T-cell therapies.

Abstract: Compounds are described with the general formula (I) wherein R1, R2, R3, R4, R5, R6, R7, R8, R9, R10, R11, R12, and n are defined as anywhere herein, which are useful for the treatment of cancer and other dysproliferative diseases.

Abstract: In some aspects the present invention provides methods for the treatment of B-cell lymphomas. Some such methods involve administration of HVEM ectodomain polypeptides, anti-HVEM antibodies, or anti-BTLA antibodies to subjects in need thereof. Some such methods involve use of CAR T cells, such as CD19-specific CAR T cells. The present invention also provides compositions useful in such methods. These and other embodiments of the present invention and described further herein.

Abstract: In some aspects the present invention provides methods for the treatment of B-cell lymphomas. Some such methods involve administration of HVEM ectodomain polypeptides, anti-HVEM antibodies, or anti-BTLA antibodies to subjects in need thereof. Some such methods involve use of CAR T cells, such as CD19-specific CAR T cells. The present invention also provides compositions useful in such methods. These and other embodiments of the present invention and described further herein.

Abstract: The present invention provides pluripotent and multipotent stem cells, including embryonic stem cells, induced pluripotent stem cells, adult stem cells and other progenitor cells, that have been modified to contain an inducible cancer-specific suicide gene construct that, upon induction, selectively kills stem- or progenitor-cell-derived cancerous cells without significant effect on healthy tissues or other (noncancerous) cells derived from such cells. This suicide gene construct expresses a dominant negative MYC-interfering protein (D-MIP) that acts as a tumor suppressor in cancer cells without significant deleterious effects on healthy cells and tissues. The suicide gene construct can also be used in gene therapies that produce cancers arising in association with the presence of the gene therapy vector and likewise discriminates between killing of cancerous cells and non-cancerous cells modified with a gene therapy vector.

Abstract: The invention relates generally to methods for diagnosis and treatment of follicular lymphoma or diffuse large B cell lymphoma. Specifically, the invention relates to detecting a lysine (K)-specific methyltransferase 2D (KMT2D) alteration to diagnose or treat follicular lymphoma or diffuse large B cell lymphoma.

Abstract: The present invention is directed to methods and compositions for treating cancer, including, hematologic malignancies, such as B-cell malignancies, with anti-tumor antibody-tumor suppressor fusion proteins in order to selectively restore tumor suppressor gene function to cancer cells in which such tumor suppressor gene function has been lost. The present invention is also directed to methods and compositions for diagnosing cancer and for predicting and assessing response to treatment.

Abstract: The present invention relates to microRNAs (miRNAs) which are associated with cancer, particularly including hematologic malignancies, and particularly T-cell acute lymphoblastic leukemia (T-ALL), and to the assessment and modulation thereof in the treatment and management of cancer. The present invention is directed to methods and compositions for diagnosing and treating cancer, particularly T-ALL, by modulating miRNAs, and the use of miRNAs and antagonists thereof, particularly antagomirs, for predicting and assessing response to treatment, in assays for isolating and selecting antagonists, and as compositions for the treatment and management of cancer. Methods and compositions are provided for treatment or alleviation of cancer, particularly T-ALL, with antagonists/antagomirs of miRNAs, particularly one or more of miR-19b, miR-20a, miR26, miR92, miR148 and miR223.

Abstract: The present disclosure identifies a novel subtype of follicular lymphoma (FL) characterized by dysregulation of the cyclin/CDK/RB proliferative pathway. This subtype of FL is associated with increased malignancy and mortality, relative to FL which is not associated with cell cycle dysregulation. Accordingly, this disclosure presents novel methods to subtype FL and stratify patient risk by detection of biomarkers associated with RB inactivation. This disclosure further presents novel therapies for the treatment of FL subtyped by inactivation of RB.

Abstract: The present disclosure identifies a novel subtype of follicular lymphoma (FL) characterized by dysregulation of the cyclin/CDK/RB proliferative pathway. This subtype of FL is associated with increased malignancy and mortality, relative to FL which is not associated with cell cycle dysregulation. Accordingly, this disclosure presents novel methods to subtype FL and stratify patient risk by detection of biomarkers associated with RB inactivation. This disclosure further presents novel therapies for the treatment of FL subtyped by inactivation of RB.

Abstract: The present invention provides pluripotent and multipotent stem cells, including embryonic stem cells, induced pluri-potent stem cells, adult stem cells and other progenitor cells, that have been modified to contain an inducible cancer-specific suicide gene construct that, upon induction, selectively kills stem- or progenitor-cell-derived cancerous cells without significant effect on healthy tissues or other (noncancerous) cells derived from such cells. This suicide gene construct expresses a dominant negative MYC-interfering protein (D-MIP) that acts as a tumor suppressor in cancer cells without significant deleterious effects on healthy cells and tissues. The suicide gene construct can also be used in gene therapies that produce cancers arising in association with the presence of the gene therapy vector and likewise discriminates between killing of cancerous cells and non-cancerous cells modified with a gene therapy vector.

Abstract: Methods are provided for identifying agents capable of modulating cap-dependent RNA translation by comparing translation efficiency in the presence and absence of the agent in an in-vitro or in-vivo translation system that comprises eIF4A and an mRNA having one or more eIF4A-dependent translation-controlling motifs. The modulation of translation in the presence of the agent indicates the agent as capable of modulating cap-dependent mRNA translation. The method can be used to identify anti-cancer agents and oncogenes that may be responsible for tumorigenesis.

Abstract: The present invention is directed to methods and compositions for treating cancer, including, hematologic malignancies, such as B-cell malignancies, with anti-tumor antibody-tumor suppressor fusion proteins in order to selectively restore tumor suppressor gene function to cancer cells in which such tumor suppressor gene function has been lost. The present invention is also directed to methods and compositions for diagnosing cancer and for predicting and assessing response to treatment.

Abstract: The present disclosure identifies a novel subtype of follicular lymphoma (FL) characterized by dysregulation of the cyclin/CDK/RB proliferative pathway. This subtype of FL is associated with increased malignancy and mortality, relative to FL which is not associated with cell cycle dysregulation. Accordingly, this disclosure presents novel methods to subtype FL and stratify patient risk by detection of biomarkers associated with RB inactivation. This disclosure further presents novel therapies for the treatment of FL subtyped by inactivation of RB.

Abstract: The present invention relates to microRNAs (miRNAs) which are associated with cancer, particularly including hematologic malignancies, and particularly T-cell acute lymphoblastic leukemia (T-ALL), and to the assessment and modulation thereof in the treatment and management of cancer. The present invention is directed to methods and compositions for diagnosing and treating cancer, particularly T-ALL, by modulating miRNAs, and the use of miRNAs and antagonists thereof, particularly antagomirs, for predicting and assessing response to treatment, in assays for isolating and selecting antagists, and as compositions for the treatment and management of cancer. Methods and compositions are provided for treatment or alleviation of cancer, particularly T-ALL, with antagonists/antagomirs of miRNAs, particularly one or more of miR-19b, miR-20a, miR26, miR92, miR148 and miR223.