20 results about "B-cell lymphoma" patented technology

The invention discloses a method for screening a B-cell lymphoma biomarker, and belongs to the technical field of bioinformatics. The invention aims to provide a more accurate and simple method for screening the B-cell lymphoma biomarker. The invention provides a method for screening a B cell lymphoma biomarker. The relation between the infiltration ratio of all cell subgroups of T / NK and myeloid cells and the lifetime of a patient is screened out by utilizing scRNA-seq data of Burki lymphoma, diffuse large B cell lymphoma, follicular lymphoma and spleen marginal region lymphoma and bulk RNA-seq data of a Burki lymphoma and diffuse large B cell lymphoma database. And a theoretical basis is provided for screening survival analysis of lymphoma diseases.

The application discloses a kind of bispecific anti-CD3 / CD20 antibodies and its application in B cell lymphoma, belong to the field of biological medicine technology.The bispecific antibody uses "tandem type" molecular structure, by the single-chain antibody (scFv) of anti-CD20 and the nanometer antibody (VHH) of anti-CD3 are fused by flexible connecting peptide.The high-purity bispecific antibody BsAb-20S3V is obtained by CHO cell stable expression system, and it has nanomolar level affinity to CD20+ and CD3+ cells.Experiments in vitro prove that the antibody can effectively mediate T cell specific killing to Raji cell, and the maximum killing rate can reach 75%-90%.In vivo pharmacodynamic evaluation shows that in tumor-bearing mouse model, high-dose group can significantly inhibit tumor growth and induce tumor negative growth.The antibody has good potential to prepare B cell lymphoma treatment drugs.

The present disclosure relates generally to mutations in B cell lymphoma, and methods of use of the mutations in T cell therapy.

The present disclosure relates generally to mutations in B cell lymphoma, and methods of use of the mutations in T cell therapy.

Described are the compounds, compositions and methods of treating a cancer characterized by aberrant B-cell lymphoma 6 (BCL6) activity.

The application discloses a trispecific antibody combining CD3, CD19 and BCMA and application thereof. The trispecific antibody comprises a first antigen binding domain combining CD3, a second antigen binding domain combining CD19, a third antigen binding domain combining BCMA and a heterodimeric Fc region. The application recruits and activates T cells through the CD3 binding domain, and realizes broad-spectrum recognition and combination of the whole abnormal B cell lineage from early B cells to terminally differentiated plasma cells through the CD19 and BCMA double binding domains, can more thoroughly eliminate pathological B cells, overcomes the antigen escape or drug resistance problems possibly existing in single target treatment by using multiple synergies, and provides a novel antibody drug for diseases such as multiple myeloma, B cell lymphoma and B cell related autoimmune diseases.

The invention discloses an application of a small molecule compound in preparation of a medicine for treating lymphoma, and the small molecule compound is resazurin sodium or 2-(3, 4-dihydroxybenzoyloxy) ethyl 3, 4-dihydroxybenzoyloxy. The application of the small molecule compound in preparation of the medicine for treating the lymphoma is characterized in that the small molecule compound is resazurin sodium or 2-(3, 4-dihydroxybenzoyloxy) ethyl 3, 4-dihydroxybenzoyloxy. Deoxyribose nucleic acid (DNA) methylation abnormity is one of important mechanisms of tumor generation and development, existing researches show that CDCA7 is highly expressed in lymphoma, CDCA7 knock-down can damage the invasion ability of lymphoma cells in vitro, and another research shows that CDCA7 protein is a key factor for maintaining methylation. According to the application disclosed by the invention, CDCA7 of a mouse B cell lymphoma cell line CH12F3 is knocked out, and the methylation degree of a Microsallite DNA region is found to be reduced, while the methylation degree of the Microsallite DNA region is also reduced when CH12F3 cells of which CDCA7 is not knocked out are cultured by using the small molecule compound disclosed by the invention. Therefore, the small molecule compound has a wide prospect in application to preparation of drugs for treating lymphoma.

The invention discloses application of a DNTTIP1 gene in preparation of acute leukemia treatment medicines, and belongs to the technical field of biological medicines. The problem of providing a new scheme for preparing acute leukemia treatment medicines is solved. The DNTTIP1 gene is used as a drug target of a biomarker, an inhibitor MS-275 of an interaction protein HDAC1 of the DNTTIP1 and a simulant ABT199 of a downstream target gene BMF are jointly applied to preparation of a drug for treating acute leukemia, and deletion of the interaction protein 1 gene DNTTIP1 at the tail end of deoxynucleotidyl transferase can damage recruitment of histone deacetylase 1 HDAC1 to chromatin. According to the present invention, with the application of the BMF promoter, the high acetylation of the histone H3 lysine 27 on the BMF promoter of the B cell lymphoma 2 modification factor is caused, the BMF is reactivated, and the reactivated BMF competitively destroys the BCL2 mediated survival pathway so as to trigger the coordinated autophagy and apoptosis;

The invention discloses application of NK4 as a target spot in preparation of a product for diagnosing or preventing and treating B-cell lymphoma, and belongs to the technical field of biological medicine. By inhibiting the expression or function of NK4, a Rap1 signal channel is blocked, so that the proliferation of tumor cells is inhibited, and the apoptosis of the tumor cells is induced. The invention provides that NK4 can induce B cell lymphoma, and block NK4 can treat diffuse large B cell lymphoma (DLBCL) by reducing proliferation of the B cell lymphoma and increasing apoptosis of the B cell lymphoma; and NK4 is also a mark of the DLBCL. NK4 and a downstream Rap1 signal channel thereof can be used as diagnosis, treatment and drug development targets of B cell lymphoma.

The application discloses an antibody against human CD180 and application thereof. The antibody against human CD180 A24C9 and C12F11 provided by the application has strong affinity with human CD180 protein, and the Kd values are 0.4748 nM and 78.19 nM respectively; meanwhile, the antibody has strong binding specificity and can specifically recognize human CD180 positive acute myeloid leukemia (AML) cell lines (OCI-AML2, MV4-11, THP1) and human CD180 positive B cell lymphoma cell lines (Daudi, BJAB, Nalm6); and the antibody has no cross reaction with various human CD180 negative cell lines (K562, NB4, Kasumi1, TF1, NK92, Jurkat, SupT1 and MM1S). The antibody can be used for detecting expression of human CD180 protein, and can be used in immunotherapy alone or in combination with other methods, and has diagnostic and therapeutic values in tumors, autoimmune diseases, graft-versus-host diseases and inflammatory diseases.

The invention discloses an EB virus related B cell lymphoma diagnostic kit based on GNAS methylation detection. The invention provides a new marker for diagnosis of EB virus related B cell lymphoma, provides a matched and verified special detection primer, and performs functional reverse verification of 5-aza-2 '-deoxycytidine drug intervention. According to the invention, the potential value of the marker in the aspect of curative effect prediction is defined, and a possible molecular basis is provided for implementing individualized demethylation treatment clinically.

Described are the compounds, compositions and methods of treating a cancer characterized by aberrant B-cell lymphoma 6 (BCL6) activity.

The invention belongs to the technical field of tumor immunotherapy, and relates to a method for enhancing killing of B cell lymphoma by CD19 CAR-T through an ITK inhibitor Soquelitzinib. The background is as follows: the existing CAR-T cell faces the problems of insufficient in-vivo amplification, poor persistence, T cell depletion and the like when being used for treating B cell lymphoma, and the curative effect is influenced. According to the content of the invention, it is found for the first time that Soquitzinib inhibits a CAR-T depletion process by regulating an ITK / PLC gamma signal channel. The CAR-T cell pretreated by the Soquitinib is transfused back into the body of a B-cell lymphoma tumor-bearing mouse, and the Soquitinib is continuously administered by oral administration, so that the tumor load can be relieved and the lifetime of the mouse can be prolonged by combining the Soquitinib and the CAR-T. An in-vitro experiment shows that the Soquitinib can be used for improving the killing effect of the CAR-T on tumor cells. The technical effects are as follows: the epigenetic status of CAR-T is regulated and controlled through the targeted ITK / PLC gamma pathway, and (1) the survival and killing capabilities of CAR-T cells in a tumor microenvironment are enhanced; (2) the treatment effect bottleneck caused by CAR-T cell depletion is broken through; and (3) a new safe and efficient combined treatment strategy is provided for patients with B-cell lymphoma.

Disclosed herein is a platform technology for designing T cell engagers. Examples of such T cell engagers and nucleic acids (e.g., mRNAs) encoding same as well as lipid nanoparticles comprising nucleic acids (e.g., mRNAs) encoding the T cell engagers are provided. Such T cell engagers can be used to treat cancers such as FCRH5+, GPRC5D+, and / or BCMA+ cancers, including hematological malignancies such as multiple myeloma (e.g., advanced MM, RRMM), B cell lymphoma, and myeloid cancers.

The present invention provides a method of treating CD20 positive B cell lymphoma with Usutuzumab, involving the rate of administration of Usutuzumab. In some embodiments, the methods comprise an intravenous drip infusion at 1000 mg of ustuzumab olbabine each administration, and are administered in two or more cycles at a specific administration rate.

The invention is related to a chimeric checkpoint receptor (CCR) fusion protein, a nucleic acid molecule encoding said fusion protein, a vector comprising said nucleic acid molecule, a host cell comprising said nucleic acid molecule and / or expressing the fusion protein, a method for providing said host cell, a pharmaceutical composition comprising said fusion protein, nucleic acid molecule or host cell, and said products for use as a medicament and in the treatment of B cell lymphoma.

Chimeric antigen receptor (CAR) T cell therapies have revolutionized the treatment of B cell malignancies, but a significant proportion of patients with large B cell lymphoma (LBCL) experience primary resistance or relapse after CAR T cell treatment. As disclosed herein, anti-inflammatory macrophages suppress CAR-T cell expansion, induce death, and reduce CAR expression. Disclosed is a method for enhancing anti-tumor efficacy of immune effector cells, such as CAR-T cells, in a subject that involves administering to the subject a nitric oxide synthase (NOS) inhibitor.

The present invention relates to a compound of formula (I), or its pharmaceutically acceptable salt. The compound, or its pharmaceutically acceptable salt, is useful as a PI3K inhibitor and therefore in therapy. In particular, the compound, or its pharmaceutically acceptable salt, has utility in the treatment of B cell lymphoma.

Provided are adoptive cell therapy involving the administration of doses of cells for treating subjects with certain B cell malignancies, and related methods, compositions, uses and articles of manufacture. The cells generally express recombinant receptors such as chimeric antigen receptors (CARs). In some embodiments, the disease or condition is a large B cell lymphoma (LBCL) relapsed or refractory to first-line chemoimmunotherapy.