Methods for determination of risk, previous history and/or presence of a betaretrovirus infection in a subject are described herein. Said methods may comprise incubating a biological sample from the subject, the biological sample comprising immune effector-producing cells, with one or more betaretrovirus-specific epitopes, the betaretrovirus-specific epitopes comprising at least 7 contiguous amino acids according to any one of SEQ ID Nos. 1-36, and measuring the production of immune effectors by the immune effector-producing cells, wherein production of the immune effectors by the immune effector-producing cells determines risk and/or presence of betaretrovirus infection in the subject. Isolated peptides and kits for carrying out the methods are also described.

A method of identifying a subject having cancer who is likely to be responsive to a treatment compound, comprising administering the treatment compound to the subject having the cancer; obtaining a sample from the subject; determining the level of a biomarker in the sample from the subject; and diagnosing the subject as being likely to be responsive to the treatment compound if the level of the biomarker in the sample of the subject changes as compared to a reference level of the biomarker; wherein the treatment compound is a compound of Formula I:

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Markers of acute myeloid leukemia stem cells (AMLSC) are identified. The markers are differentially expressed in comparison with normal counterpart cells, and are useful as diagnostic and therapeutic targets.

The present disclosure relates to methods of early identification and detection of neurotoxicity associated with the administration of chimeric antigen receptor (CAR) T cell therapy and mitigation strategies to reduce the occurrence and/or severity of treatment associated neurotoxicity.

High affinity antibodies capable of binding to a single-chain variable fragment (scFv) of anti-CD19 antibody FMC63, for example, the scFv expressed on cell surface as a portion of a chimeric antigen receptor (CAR). Also provided herein are methods for producing such anti-scFv antibodies and methods of using the antibodies disclosed herein for detecting, for example, T cells expressing an anti-CD19 CAR that comprise the scFv as an extracellular domain.

Applicant discloses an anti-idiotypic antibody to MOR202, which when fused to human albumin, shifted the anti-body in IFE thus mitigating any potential interference of MOR202 with the M-protein clinical assessment.

Compositions and methods are provided for classification and treatment of MYC-driven cancers, i.e. causally dependent on MYC as a result of, over-expression of MYC, constitutive expression of MYC, chromosomal translocation resulting in overactive MYC, and the like. Specifically, the methods comprising determining the MYC status of the cancer, and in a cancer that is determined to be driven by MYC activation, administering a composition of an effective dose of one or both of activated natural killer (NK) cells and a type 1 interferon.

A normal set of cells is characterized using flow cytometry. A centroid and radius are defined for a set of clusters in an n-dimensional space corresponding to a normal maturation for a cell lineage in the normal set of cells. A test set of cells is characterized using flow cytometry and the characterization is compared to the defined set of clusters. Support Vector Machine (SVM) subroutines are employed to identify reference populations of interest by generating multidimensional boundary definitions. These boundary definitions may be used to identify reference populations to use in defining or refining a centroid line or a radius or radii defining a set of normal clusters, and to characterize and compare a test set of cells to the defined set of normal clusters.

The disclosure provides for humanized antibodies, and fragments thereof, that are capable of binding to and killing human myeloma and ovarian cancer cells. The antibodies and their fragments are useful for therapeutic, diagnostic, and research purposes.

Applicant discloses an anti-idiotypic antibody to MOR202, which when fused to human albumin, shifted the antibody in IFE thus mitigating any potential interference of MOR202 with the M-protein clinical assessment.