Provided herein are methods and articles of manufacture for use with cell therapy for the treatment of diseases or conditions, e.g., cancer, including for predicting and treating a toxicity. In some embodiments, the toxicity is related to cytokine release syndrome (CRS). The methods generally involve assessing a change in a factor indicative of tumor burden prior to administration of a cell therapy in a subject that is associated with and/or correlate to a risk of developing toxicity. In some aspects, the methods can be used to determine if the subject is at risk or likely at risk for developing a toxicity following administration of the cell therapy. Also provided are methods for treating a subject having a disease or condition, in some cases involving administration of the cell therapy, based on assessment of risk of developing a toxicity following administration of the therapy. Also provided herein are reagents and kits for performing the methods.

The present invention is directed to methods for detecting a plasma cell dyscrasia like myeloma or MGUS, methods for determining whether a plasma cell dyscrasiais stable or progressive, methods for determining a risk for disease relapse, and methods for determining a response by a subject having a plasma cell dyscrasia to a therapy.

The present invention contemplates that complement receptor 1 and 2 may play a role in the induction of regulatory B cells under inflammatory conditions that accompany immune-mediated diseases. For example, long noncoding RNA may regulation transcription of the complement receptor I gene, thereby resulting in an induction and/or suppression of regulatory B cells. Such long noncoding RNA in mature B cells may be specifically targeted to modify complement receptor 1 levels and induce or suppress the generation of antigen-specific regulatory B cells, thereby modifying the course of immune mediated diseases including, but not limited to, autoimmune disease, cancer, and infection.

Introduced here is an approach to improving the automatic identification of hematological malignancies by taking advantage of established databases through transfer learning. At a high level, this approach attempts to address the cross-domain gap by preserving knowledge of the source domain for better optimization of the target domain.

Methods for detection, diagnosis, prognosis, theragnosis, and targeted therapy of a PRSS21-overexpressing condition (e.g., cancer), in particular, PRSS21-overexpressing acute myeloid leukemia of the AMKL subtype.

The present invention relates to a chimeric antigen receptor (CAR) which comprises an antigen-binding domain which selectively binds TCR beta constant region 1 (TRBC1) or TRBC2; cells; such a T cells comprising such a CAR; and the use of such cells for the treatment of a T-cell lymphoma or leukaemia in a subject.

The present invention is directed to a method of treating a hematologic malignancy such as acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS), including hematologic malignancies that are refractive to chemotherapeutic and/or hypomethylating agents. The method concerns administering a CD123×CD3 bispecific binding molecule to a patient in an amount effective to stimulate the killing of cells of said hematologic malignancy in said patient. The present invention is particularly directed to the embodiment of such method in which a cellular sample (Z from the patient prior to such administration evidences an expression of one or more target genes that is increased relative to a baseline level of expression of such genes, for example, a baseline level of expression of such genes in a reference population of individuals who are suffering from the hematologic malignancy, or with respect to the level of expression of a reference gene.

The invention relates to new nucleophosmin protein (NPM) mutants, corresponding gene sequences and relative uses thereof for diagnosis, monitoring of minimal residual disease, prognostic evaluation and therapy of acute myeloid leukaemia (AML).

The present invention relates to an antibody specific for CD22 and uses thereof, and more particularly to an antibody that specifically binds to CD22, a chimeric antigen receptor comprising the antibody, a CAR-T cell expressing the chimeric antigen receptor, and a pharmaceutical composition for preventing or treating diseases mediated by cells expressing CD22 including the same.

It was confirmed that the antibody selected in the present invention specifically recognized CD22-expressing cells, and the chimeric antigen receptor (CAR) and CAR-T cells targeting CD22 using the CD22-specific antibody not only effectively bound to CD22, but also activated CAR-T cells bound to CD22. In addition, since it was confirmed that the CAR-T cells of the present invention effectively kill CD22-expressing cells, the CD22-specific antibody, the chimeric antigen receptor targeting CD22, and CAR-T cells of the present invention can be usefully used as a composition for preventing or treating diseases relating to CD22 expression.

Described herein are agents that inhibit CBL autoinhibition, agents that activate CBL, SLAP and/or SLAP2 mimetics, and recombinant SLAP and/or SLAP2 or variants and/or fragments thereof that inhibit CBL autoinhibition. Also described are fusion proteins comprising these molecules as well as methods of inhibiting CBL autoinhibition and related uses thereof.