39 results about "Lymphoid tissue hyperplasia" patented technology

The invention concerns the use of recombinant clonotypic immunoglobulins (Ig) as a vaccine in the treatment of HCV-related and non HCV-related lymphoproliferations, in particular the use of recombinant proteins with immunogenic properties derived from protein segments VK3-20 and VK3-15 of Ig light chains derived from patients with lymphoproliferations.

The present invention provides chimeric and humanized versions of anti-CD22 mouse monoclonal antibody, HB22.7. The anti-CD22 antibodies of the invention comprise four human or humanized framework regions of the immunoglobulin heavy chain variable region (“VH”) and four human or humanized framework regions of the immunoglobulin light chain variable region (“VK”). The invention further comprises heavy and/or light chain FW regions that contain one or more backmutations in which a human FW residue is exchanged for the corresponding residue present in the parental mouse heavy or light chain. Human or humanized VH framework regions of antibodies of the invention may comprise one or more of the following residues: a valine (V) at position 24 of framework region 1, a glycine (G) at position 49 of framework region 2, and an asparagine (N) at position 73 of framework region 3, numbered according to Kabat. The invention further relates to pharmaceutical compositions, immunotherapeutic compositions, and methods using therapeutic antibodies that bind to the human CD22 antigen and that preferably mediate human ADCC, CDC, and/or apoptosis for: the treatment of B cell diseases and disorders in human subjects, such as, but not limited to, B cell malignancies, for the treatment and prevention of autoimmune disease, and for the treatment and prevention of graft-versus-host disease (GVHD), humoral rejection, and post-transplantation lymphoproliferative disorder in human transplant recipients.

Pharmaceutical compositions and compounds are provided. The compounds of the invention demonstrate anti-proliferative activity, and may promote apoptosis in cells lacking normal regulation of cell cycle and death. In one embodiment of the invention, pharmaceutical compositions of the compounds in combination with a physiologically acceptable carrier are provided. The pharmaceutical compositions are useful in the treatment of hyperproliferative disorders, which disorders include tumor growth, lymphoproliferative diseases, angiogenesis. The compounds of the invention are substituted pyrazoles and pyrazolines.

The present disclosure provides methods for genetically modifying lymphocytes and methods for performing adoptive cellular therapy that include transducing T cells and/or NK cells without prior ex vivo stimulation. The methods typically include engineered signaling polypeptides that can include a lymphoproliferative element, and/or a chimeric antigen receptor (CAR), for example a microenvironment restricted CAR. Additional elements of such engineered signaling polypeptides are provided herein, as well as vectors, such as retroviral vectors, packaging cell lines and methods of making the same. Furthermore, recombinant retroviruses and methods of making the same are provided. Numerous controls are provided, including riboswitches that are controlled, for example in vivo, by nucleoside analogues.

Disclosed is a method of diagnosing and treating myeloproliferative or lymphoproliferative cell disorders, such as cancer, with chlorotoxin and/or derivatives, analogs or fragments thereof, which are effective to bind to an inhibit abnormal myeloid or lymphoid cell growth.

A method of treatment of lymphoproliferative and autoimmune disorders with a new composition of four boswellic acids including β-boswellic acid, 3-O-acetyl-β-boswellic acid, 11-keto-β-boswellic acid, and 3-O-acetyl-11-keto-β-boswellic acid. Boswellic acids of invention have been obtained in a novel industrial process from the gum resin of Boswellia serrata tree, providing standardized composition which inhibits DNA, RNA and protein synthesis of the target cell without cytotoxic effects. The composition of invention provides advantage of irreversible cytostatic therapy, equivalent to biological effects of a cytotoxic therapy without killing body cells.

Pharmaceutical compositions and compounds are provided. The compounds of the invention have anti-proliferative activity, and may promote apoptosis in cells lacking normal regulation of cell cycle and death. In one embodiment of the invention, formulations of the compounds in combination with a physiologically acceptable carrier are provided. The pharmaceutical formulations are useful in the treatment of hyperproliferative disorders, which disorders include tumor growth, lymphoproliferative diseases, angiogenesis. The compounds of the invention are 1,2,3-thiadiazoles having the structure:

and including stereoisomers, solvates, and pharmaceutically acceptable salts thereof, wherein each of R¹, R²2 , R³ and R⁴ is independently selected from hydrogen, R⁵R⁶, and R⁷, R⁵ is selected from alkyl, heteroalkyl, aryl and heteroaryl; R⁶ is selected from (R⁵)_n-alkylene, (R⁵)_n-heteroalkylene, (R⁵)_n-arylene and (R⁵)_n-heteroarylene; R⁷ is selected from (R⁶)_n-alkylene, (R⁶)_n-heteroalkylene, (R⁶)_n-arylene, and (R⁶)_n-heteroarylene; and n is selected from 0, 1, 2, 3, 4 and 5, where R¹ and R² may together form a heterocyclic structure including the nitrogen to which they are both attached, and R³ and R⁴ may together form a heterocyclic structure including the nitrogen to which they are both attached; and each of L¹ and L² is independently selected from -A1-A2-A3- where each of Al, A2, and A3 is independently selected from a direct bond, alkylene, heteroalkylene, arylene and heteroarylene.

Human T-cell lymphotropic virus type-1 (HTLV-1) infects and transforms CD4⁺ lymphocytes and causes Adult T-cell Leukemia/Lymphoma (ATLL), an aggressive, often fatal, lymphoproliferative disease. A conserved HTLV-1 3+ regulatory domain, pX, encodes at least five non-structural proteins, including the alternative splice-variant p30^II. HTLV-1 p30^II may enhance the transforming activity of Myc and transcriptionally activate the human cyclin D2 promoter, dependent upon its conserved Myc-responsive enhancer elements, associated with markedly increased S-phase entry and multi-nucleation. Enhancement of Myc transforming activity by HTLV-1 p30^II may be dependent upon the transcriptional coactivators, TRRAP/p434^6-8 and TIP60, require TIP60 histone acetyltransferase activity, and strongly correlate with interactions between HTLV-1 p30^II and Myc-TIP60 complexes in HTLV-1-infected ATLL patient-derived lymphocytes. Thus, p30^II may function as a novel retroviral modulator of Myc-transforming interactions that may prominently contribute to adult T-cell leukemogenesis. Thus, the present invention provides methods and compositions for screening and identifying agents that interfere with transformation.

A transgenic zebrafish animal model for the study of haemopoietic cell differentiation, control, and screening of therapeutic agents.

This invention relates to the treatment of lymphoproliferative cancers, such as myeloma and lymphoma, using UDP-glucosylceramide synthase inhibitors, such as eliglustat tartrate. Methods, uses and inhibitors for use are provided.

A method of (a) treating a lymphoproliferative disease in a subject in need thereof; (b) slowing the progression of lymphoproliferative disease in a subject who has been diagnosed with a lymphoproliferative disease; or (c) preventing or delaying development of a lymphoproliferative disease in a subject who is at risk of developing a lymphoproliferative disease. The method generally comprises administering to the individual an effective amount of a combination therapy comprising: i) at least one autophagy modulating agent, or a derivative, pharmaceutically acceptable salt thereof, or prodrug thereof; and ii) at least one CDK inhibitor agent, or a derivative, pharmaceutically acceptable salt thereof, or prodrug thereof, wherein the i) agent and the ii) agents are administered in amounts sufficient to enhance the cytotoxicity of the combination relative to the CDK inhibitor agent treatment alone.

Material and method for using 4-1BB agonizes to treat or prevent autoimmune disorders, lymphoproliferative diseases, and allergies are provided.

The present invention relates to novel methods for the diagnosis and therapy of lymphoproliferative diseases. Specifically, the present invention relates to novel methods for the diagnosis and therapy taking advantage of the detection of chromosomal breakpoints in chromosome 12 and/or translocation of chromosomal material from chromosome 12, said chromosomal breakpoints and/or translocation(s) being associated with lymphoproliferative diseases, such as primary cutaneous T-cell lymphomas (CTCL). The present invention further relates to the use of neuron navigator 3 gene (NAV3) or an equivalent or functional fragment thereof involved in chromosomal breakpoints in chromosome 12 and/or translocations thereof, said gene and/or translocations thereof being associated with lymphoproliferative diseases, such as primary cutaneous T-cell lymphomas (CTCL), as a diagnostic and therapeutic agent. The present invention also relates to the development of therapy.

The present invention provides chimeric and humanized versions of anti-CD22 mouse monoclonal antibody, HB22.7. The anti-CD22 antibodies of the invention comprise four human or humanized framework regions of the immunoglobulin heavy chain variable region (“VH”) and four human or humanized framework regions of the immunoglobulin light chain variable region (“VK”). The invention further comprises heavy and/or light chain FW regions that contain one or more backmutations in which a human FW residue is exchanged for the corresponding residue present in the parental mouse heavy or light chain. Human or humanized VH framework regions of antibodies of the invention may comprise one or more of the following residues: a valine (V) at position 24 of framework region 1, a glycine (G) at position 49 of framework region 2, and an asparagine (N) at position 73 of framework region 3, numbered according to Kabat. The invention further relates to pharmaceutical compositions, immunotherapeutic compositions, and methods using therapeutic antibodies that bind to the human CD22 antigen and that preferably mediate human ADCC, CDC, and/or apoptosis for: the treatment of B cell diseases and disorders in human subjects, such as, but not limited to, B cell malignancies, for the treatment and prevention of autoimmune disease, and for the treatment and prevention of graft-versus-host disease (GVHD), humoral rejection, and post-transplantation lymphoproliferative disorder in human transplant recipients.

Covalently reactive antigen analogs are disclosed herein. The antigens of the invention may be used to stimulate production of catalytic antibodies specific for predetermined antigens associated with particular medical disorders. The antigen analogs may also be used to permanently inactivate endogenously produced catalytic antibodies produced in certain autoimmune diseases as well as in certain lymphoproliferative disorders.

The invention provides human AML-specific binding compounds that are able to bind a cell surface component of AML cells. Therapeutic uses of binding compounds against AML are also provided.

Clinical diagnosis and newborn screening for primary immunodeficiencies (PIDDs) is described. The PIDDs include X-linked chronic granulomatous disease (X-CGD), X-linked lymphoproliferative syndrome (XLP1; SH2D1A deficiency), familial hemophagocytic lymphohistiocytosis 2 (FHL2), ataxia telangiectasia (AT), common variable immunodeficiency (CVID; B-cell dysfunctions), severe combined immunodeficiency (SCID), adenosine deaminase (ADA) deficiency, and dedicator of cytokinesis 8 (DOCKS) deficiency. Additionally, cell specific markers for platelets (CD42), natural killer (NK) cells (CD56), and T cells (CD3epsilon and CD3delta) can be used as secondary markers to provide support for diagnosis of disease.