22 results about "Non malignant" patented technology

This disclosure provides: (i) a method of using an anticeramide antibody or an antigen-binding fragment thereof to improve hematopoietic stem cell transplantation for the treatment of various non-malignant and malignant diseases; and (ii) a composition for such treatment.

A method for selectively targeting tumor cells for a given strain of cancer includes providing amino acids shown to discourage promotion of tumor growth for the given strain of cancer. The method may include determining the amino acids by identifying extracellular vesicles (EVs) involved in cell-cell signaling for tumor development, quantifying relative abundance of amino acids present in patient samples, comparing the relative abundance of the amino acids from the patient sample to a known distribution of the individual amino acids present in a nonmalignant sample, and comparing the abundance of the amino acids in the patient sample to the nonmalignant sample to determine the plurality of amino acids suitable for treating the given strain of cancer. The method may include supplementing the combination of the plurality of amino acids with a chemotherapy drug.

T-cell malignancies are a broad, heterogenous group of diseases and include T-cell lymphomas and T-cell leukemias. T-cell lymphomas are a heterogeneous group of malignancies involving T lymphocytes and generally characterized by a poor prognosis. Among them, cutaneous T-cell lymphomas involve primarily the skin. Mycosis fungoides and Sézary syndrome are the most frequent cutaneous T-cell lymphomas. The inventors showed that both circulating malignant and non-malignant T cells express CD51 in patients with Sézary syndrome. CD51 therefore appears as a useful diagnostic, prognostic and follow-up marker, and as a potential therapeutic target in T-cell lymphomas.

The present invention relates to means and methods to prevent and / or treat Epstein-Barr virus (EBV) and EBV-induced diseases, such as EBV infection, infectious mononucleosis (IM), malignant or non-malignant post-transplant lymphoproliferative disorder (PTLD) and other EBV-associated diseases. In particular, the invention provides a SQAPLPCVL peptide that can be used in a treatment or a method of treatment to induce an EBV-specific immune response in a subject. The SQAPLPCVL can be used in a treatment or method of treatment as a vaccine against EBV and EBV-induced diseases. It is preferred herein that Epstein-Barr virus (EBV) and / or EBV-induced diseases are prevented.

It has been discovered that differential methylation in DNA can be used to distinguish between malignant and non-malignant skin lesions. Seven genes, 3 that are hypermethylated in melanoma, 1 that is hypermethylated in melanocytes and remains methylated in melanoma, and 3 that are hypermethylated in all tissues are provided as biomarkers. The panel demonstrates a 93% sensitivity, 97% specificity and an AUC of 95% in distinguishing between melanoma and benign lesions. Thus provided herein are melanoma biomarkers and methods of detecting them and using them to diagnose and guide treatment of subjects with the same, and monitor melanoma tumor dynamics during and after treatment.

Immunotherapeutic Monoclonal Antibody Complexes or Conjugates (IMAC) comprising readily accessible antibodies designed and approved for clinical use are provided using a one-step method that combines killing of existing cancer cells in parallel with induction of long-lasting anti-cancer vaccination. Methods for their use, alone or in combination with cancer killer cells including intentionally mismatched donor T cells, NK cells concomitantly with additional anti-cancer or immune activating agents, or activation of patient's own immune system for personalized treatment of cancer and elimination of undesirable non-malignant cells are also provided. In addition, treatment method based on IMAC can be applied for in vivo vaccination against cancer using an existing malignant lesion as internal anti-cancer vaccine by engagement of patients antigen presenting cells for induction of long-lasting anti-cancer vaccination in situ against residual or recurrent disease.

Immunotherapeutic Monoclonal Antibody Complexes or Conjugates (IMAC) comprising readily accessible antibodies designed and approved for clinical use are provided using a one-step method that combines killing of existing cancer cells in parallel with induction of long-lasting anti-cancer vaccination. Methods for their use, alone or in combination with cancer killer cells including intentionally mismatched donor T cells, NK cells concomitantly with additional anti-cancer or immune activating agents, or activation of patient's own immune system for personalized treatment of cancer and elimination of undesirable non-malignant cells are also provided. In addition, treatment method based on IMAC can be applied for in vivo vaccination against cancer using an existing malignant lesion as internal anti-cancer vaccine by engagement of patient's antigen presenting cells for induction of long-lasting anti-cancer vaccination in situ against residual or recurrent disease.

The present invention provides gene or RNA therapeutic vectors for use in the treatment of non-malignant CNS disorders, which are to be injected into the pons by convection-enhanced delivery (CED). The invention also provides a method for treating non-malignant CNS disorders, comprising injecting a gene or RNA therapeutic vector into the pons of a subject in need (CED), and a method for distributing a gene therapy agent throughout the nervous system, wherein a viral vector transported anterograde and retrogradely is injected into the pons and middle cerebellar peduncle of a subject from a cannula inserted from the cerebellum and middle cerebellar peduncle into the pons.

The application provides an application of a sensitizer of PARPi in treatment of malignant tumors, and particularly relates to the field of biological medicine technology.The application proves for the first time that TRMT10A is crucial for the recruitment of BRCA1 to DNA damage sites, thereby promoting HR repair.A loss of TRMT10A inhibits HR repair, making tumor cells more sensitive to PARPi.It is revealed that the expression of TRMT10A is up-regulated in mCRPC and is regulated by ubiquitin-specific peptidase 10 (USP10).Spautin-1 significantly leads to the lack of TRMT10A and makes tumors sensitive to PARPi in patient-derived xenografts (PDX) and cell-derived xenografts (CDX).Our research reveals the important role of the ATM-TRMT10A-BRCA1 axis in PARP inhibitor sensitization and provides a new perspective for exploring synthetic lethality.This mechanism can be therapeutically utilized through the combination of PARPi and Spautin-1, which may benefit a wider range of non-BRCA malignant tumor patients and has important clinical significance.

Disclosed is an antibody or an antigen binding fragment thereof comprising a heavy chain 5 variable region comprising CDR-H1 of SEQ ID NO:1, CDR-H2 of SEQ ID NO:2, CDR- H3 of SEQ ID NO:3, and a light chain variable region comprising CDR-L1 of SEQ ID NO:4, CDR-L2 of SEQ ID NO:5, CDR-L3 of SEQ ID NO:6, or an amino acid sequence having at least 80% sequence identity with these sequences, wherein the antibody or antigen binding fragment binds to CD137 antagonistically. Also disclosed is a method of 0 treating a cancer or a non-malignant disease in a subject in need thereof, comprising administering to the subject the antibody or antigen binding fragment thereof as disclosed herein.

Novel chimeric and / or humanized forms of the anti-CD45 BC8 antibody are described. The disclosed chimeric or humanized antibodies can be used as research, diagnostic, or therapeutic tools against CD45-related disorders, such as hematologic malignancies including acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), other myeloid and lymphoid disorders, other cancers, as well as non-malignant disorders, such as autoimmune disorders, infections, inherited blood disorders, and metabolic disorders.

A method and system for determining whether at least one indeterminate pulmonary nodule identified in a subject is likely to be malignant or likely not to be malignant are disclosed herein.

Various methods of treating a disease or condition, such as cancer, autoimmune disease, or any disease involving cellular proliferation are presented herein comprising administering to the subject an effective amount of an HPDL inhibitor compound or pharmaceutical composition as described herein.

To provide a method for depleting hematopoietic stem cells of a subject, and a method for treating a subject afflicted with a non-cancerous disorder treatable via genetically edited cell therapy.SOLUTION: This invention provides a method for depleting a subject's hematopoietic stem cells that includes administering to the subject an effective amount of a radiolabeled antibody against CD34, CD117, or CD135, where preferred radiolabels include 131I and 225Ac. This invention also provides a method for treating a subject afflicted with a non-cancerous disorder treatable via genetically edited cell therapy, where the method includes (i) administering to the subject an amount of the radiolabeled antibody effective to deplete the subject's hematopoietic stem cells, and (ii) after a suitable time period, performing the therapy on the subject to treat the subject's disorder. Finally, this invention provides articles of manufacture for performing the subject methods.

A three dimensional (3D) model of a tumor made of a synthetic material and a plurality of cell types, including malignant cells and non-malignant cells of the tumor, having a full HLA match, such that the synthetic material and the plurality of cell types are arranged in high matchability to a 3D image of the tumor, is provided. Methods of forming the 3D tumor model by bioprinting are also provided, as well as systems in which the 3D tumor model can be perfused and fluidly connected to a medium containing immune cells and / or other cells and factors present in the tumor's microenvironment. Methods utilizing the 3D tumor model or the system in, for example, personalized therapy, are also provided.

A system and method for identifying genomic regions with higher fragmentation rates than the local and global backgrounds as part of diagnosing early stage cancer is provided. The method includes steps of: de-novo characterizing genome-wide cell-free DNA fragmentation regions with higher fragmentation rates than the local and global backgrounds from whole-genome sequencing by weighing the fragment coverages in each region by a ratio of average fragment sizes in the region versus that in the whole chromosome to generate a score; and identifying DNA fragmentation regions of interest based upon comparing the score with a threshold. The system and method can utilize identified DNA fragmentation hotspots for the detection and localization of multiple early-stage cancers (or certain other non-malignant disease).

There is described herein methods for assessing survival risk of a human subject with haematological cancer or an age-related non-malignant disease. The method comprises analysis of at least 1000 of the 31744 differentially methylated regions (DMRs) set forth in Table 1 by determining an epigenetically stable loci (ESL) profile based on the methylation status of the at least 1000 DMRs; and categorizing the subject as having either low survival risk or high survival risk, each being associated with high DNA methylation instability (DMI) or low DMI respectively, wherein the subject has high DMI if the ESL profile has methylated DMRs exceeding a predetermined threshold and the subject has low DMI if the ESL profile has methylated DMRs below the predetermined threshold.

A method of analysing a tumour sample comprising tumour cells and immune cells is described. The method comprises obtaining single cell gene expression profiles for a plurality of cells from the tumour sample, the single cell gene expression profiles comprising gene expression measurements for a set of genes: using a deep learning model to identify a respective latent variable representation of the single cell gene expression profiles in the sample; and identifying a respective one of one or more latent space clusters of cells that the cells in the sample belong to, wherein the clusters of cells correspond to cells from different cell types. The deep learning algorithm is selected from deep learning algorithms trained to identify a latent variable representation of single cell gene expression profiles from cells in tumour samples that have not been purified to select tumour microenvironment cells, from cells identified as non-malignant in tumour samples that have not been purified to select tumour microenvironment cells and / or cells from samples comprising purified tumour microenvironment cells, or using cell type labels associated with clusters of cells in the latent space of the such deep learning models. Related methods, systems and products are also described.

An orally active, brain penetrant first-in-class small molecule midkine inhibitor for use in the treatment of triple-negative breast cancer, brain tumors (including glioblastoma, medulloblastoma, and NF1-mutant optic pathway gliomas), ovarian and endometrial cancers, lung cancer, as well as gynecologic non-malignant conditions such as endometriosis, uterine fibroids, and preterm birth, in which tumor cells and / or pathological cells exhibit heightened midkine signaling and express multiple midkine receptors.

An isolated immune cell, a method for preparing such modified immune cell, a method of treating a living being suffering or at risk of suffering from cancer or non-malignant diseases, an oligonucleotide and a use thereof.

Dose-limiting toxicity poses a major limitation to the clinical utility of targeted cancer therapies, often arising from target engagement in non-malignant tissues. This obstacle can be minimized by targeting cancer dependencies driven by proteins with tissue- and / or tumor-restricted expression. Here, the inventors show that in acute myeloid leukemia (AML), suppression of the myeloid-restricted PIK3CG / p110γ-PIK3R5 / p101 axis blocks AKT signaling, compromises cell fitness, and sensitizes to established AML therapies. Importantly, the inventors find that existing small molecule inhibitors against PIK3CG are insufficient to achieve a sustained longterm anti-leukemic effect. To address this concern, the inventors developed a proteolysis- targeting chimera (PROTAC) heterobifunctional molecule that specifically degrades PIK3CG and potently suppresses AML progression alone and in combination with venetoclax in human AML cell lines, primary AML patient samples, and syngeneic mouse models.

The invention provides methods, compositions, and combinations for treating cancer or a non-malignant disease or condition in which αv and / or α5 (e.g., α5β1 ) integrin is expressed or implicated in pathogenesis or progression. The methods include administration of a bispecific antibody that specifically binds αv integrin and α5 (e.g., α5β1 ) integrin and a Src inhibitor to provide treatment for the cancer or non-malignant disease or condition.