115 results about "T-cell lymphoma" patented technology

The invention is directed to a method of prognosing in an individual a transformation from follicular lymphoma to diffuse large B-cell lymphoma (DLBCL) by measuring changes and/or lack of changes in certain groups of related clonotypes, referred to herein as “clans,” in successive clonotype profiles of the individual. A clan may arise from a single lymphocyte progenitor that gives rise to many related lymphocyte progeny, each possessing and/or expressing a slightly different immunoglobulin receptor due to somatic mutation(s), such as base substitutions, inversions, related rearrangements resulting in common V(D)J gene segment usage, or the like. A higher likelihood of transformation from follicular lymphoma to DLBCL is correlated with the persistence of clans in successive clonotype profiles whose clonotype membership fails to undergo diversification over time.

Provided is pyrazole derivatives as a TNIK (Traf2- and NCK-interacting kinase), IKKε (I-kappa-B kinase epsilon) and TBK1 (TANK-binding kinase 1) inhibitor; the pyrazole derivative according to the present invention effectively inhibits TNIK, IKKε and TBK1, and thus is useful not only as an anticancer agent for the treatment of various cancers including colorectal cancer, breast cancer, CNS cancer, colon cancer, non-small cell lung cancer, kidney cancer, prostate cancer, ovarian cancer, uterus cancer, stomach cancer, liver cancer, skin cancer, lung cancer, brain cancer, bladder cancer, esophageal cancer, pancreatic cancer, thyroid cancer, head and neck cancer, squamous cell carcinoma, osteosarcoma, B-cell or T-cell lymphoma, acute or chronic leukemia and multiple myeloma, but as a therapeutic agent for chronic inflammation.

Certain cells, including types of cancer cells such as B-cell lymphomas, T cell lymphomas, Hodgkin's disease and myeloid leukemias, are capable of expressing Toll-like Receptor 9 (TLR9) or Toll-like Receptor 10 (TLR10) mRNA. Immunotargeting using TLR9 or TLR10 polypeptides, nucleic acids encoding for TLR9 or TLR10 polypeptides and anti-TLR9 or anti-TLR10 antibodies provides a method of killing or inhibiting that growth of cancer cells that express the TLR9 or TLR10 protein. Methods of immunotherapy and diagnosis of disorders associated with TLR9 or TLR10 protein-expressing cells, such as B-cell lymphoma, T cell lymphoma, acute myeloid leukemia, Hodgkin's disease, B cell leukemia, chronic lymphocytic leukemia, chronic myelogenous leukemia and myelodysplastic syndromes, are described.

The OX-40 antigen is characterized and claimed together with variants and derivatives thereof. Also described are binding agents for the antigen and the use of these in diagnosis and therapy. Examples of such use include a method for the selective depletion of activated CD4+ T-cells in vivo by using immunotoxins comprising an OX-40 antibody conjugated to a toxic molecule (such as Ricin-A chain). The administration of these specific immunotoxins is used therapeutically to deplete autoimmune reactive CD4+ T-cells which have been implicated in diseases including Multiple Sclerosis, Rheumatoid Arthritis, Sarcoidosis, and Autoimmune Uveitis as well as inflammatory bowel disease and graft-versus-host disease. This type of therapy is also beneficial for eradicating CD4+ T-cell lymphomas and alloreactive CD4+ T-cells involved with a transplantation reaction. The use of the human form of the OX-40 antibody will also help in the early diagnosis of all the diseases mentioned above.

The present disclosure provides a compound of formula (I) and the use thereof for the therapeutic treatment of human cancers including B-cell lymphoma and autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis.

T cell lymphoma is treated by administering to a patient suffering from T cell lymphoma a therapeutically effective amount of 10-propargyl-10-deazaaminopterin. Remission is observed in human patients, even with drug resistant T cell lymphoma at weekly dosages levels as low as 30 mg/m². In general, the 10-propargyl-10-deazaaminopterin is administered in an amount of from 30 to 275 mg/m² per dose.

A method and composition for treatment of advanced cutaneous T cell lymphoma is provided which involves administration of recombinant interleukin-12.

Provided are 7-azaindole or 4,7-diazaindole derivatives as an IKKε (I-kappa-B kinase epsilon) and TBK1 (TANK-binding kinase 1) inhibitor. The 7-azaindole or 4,7-diazaindole derivative effectively inhibits IKKε and TBK1, and thus is useful not only as an anticancer agent for the treatment of various cancers including colorectal cancer, breast cancer, CNS cancer, colon cancer, non-small cell lung cancer, kidney cancer, prostate cancer, ovarian cancer, uterus cancer, stomach cancer, liver cancer, skin cancer, lung cancer, brain cancer, bladder cancer, esophageal cancer, pancreatic cancer, thyroid cancer, head and neck cancer, squamous cell carcinoma, osteosarcoma, B-cell or T-cell lymphoma, acute or chronic leukemia and multiple myeloma, but as a therapeutic agent for chronic inflammation.

The invention relates to a molecular mark (p-Akt and/or YB-1) for selecting treatment scheme and/or prognostic evaluation of diffuse large b-cell lymphomas and an application therefore, and relates to a method for selecting treatment scheme and/or prognostic evaluation of diffuse large b-cell lymphomas. The molecular mark p-Akt and/or YB-1 can simply and correctly judge the prognosis of diffuse large b-cell lymphomas, to select objective treatment scheme for patients, thereby improving the prognosis effect of treatment scheme and saving medical cost.

The invention relates to a combined medicine with a synergistic action for treating T cell lymphomata. The combined medicine comprises bortezomib and SAHA, wherein the proportion of the bortezomib to the SAHA is 5-10nM:1-2.0 mu M. The invention also provides an application of the combined medicine in preparing a medicine for treating lymphomata diseases, wherein the lymphomata is T cell lymphomata. By using the combined medicine, the synergistic action of the two medicines is exerted, and the growth and the multiplication of T lymphomata cells can be synergically suppressed. By combining the two medicines, the curative effect is enhanced, and the cost can also be greatly lowered.

The invention relates to a method for building the animal model of external nose shape NK/T lymphocyte cancer, which comprises: a, seeding, b, generating, c, checking, while it optimizes the parameters of each step, to overcome the defects of prestn technique. The invention has short generating time, with high on-time seeding success ratio. Compared with present technique, it can build the animal model of external nose shape NK/T lymphocyte cancer. And the model can replay the key biological character of external nose shape NK/T lymphocyte cancer, with stable growing period and wider application.

Uses of anti-CS1 antibodies, alone or in combination with other agents, for the treatment of rare lymphomas, such as NK lymphomas, NK/T-cell lymphomas, and angioimmunoblastic lymphomas.

A method for diagnosing a lymphoid proliferative disorder (such as lymphoma, T-cell lymphoma or leukemia) in a subject or determining the risk of a subject for a lymphoid proliferative disorder recurrence after transient remission, which includes high throughput T-Cell Receptor β (TCRβ) sequencing tests to identify dominant oncogenic clones in the subject suffering from the lymphoid proliferative disorder. Oligonucleotides primer compositions and kits associated with the above-described methods are also provided herein. Said subject includes living organisms, such as mammals (e.g., dogs, cats, pigs, cows, horses, goats, rabbits, humans), non-mammalian vertebrates, such as birds (e.g., chicken, ducks), fish (e.g., sharks), or frogs, and transgenic species thereof.

The invention discloses an antigen epitope peptide. Amino acid sequences of the antigen epitope peptide contain an amino acid sequence shown as SEQ ID NO.2 or SEQ ID NO.3, or an amino acid sequence formed by adding one or more amino acids to the amino acid sequence shown as SEQ ID NO.2 or SEQ ID NO.3, deleting one or more amino acids from the amino acid sequence shown as SEQ ID NO.2 or SEQ ID NO.3 or substituting one or more amino acids. The antigen epitope peptide can be used for producing antigen-presenting cells, major histocompatibility antigen complexes or cytotoxic T lymphocyte inducers, and can be further used for preparing drugs for treating cancer such as NK/T-cell lymphoma.

The invention belongs to the technical field of biology, and particularly relates to a gene mutation site group of NK/T cell lymphoma and a kit and application thereof. The invention provides a gene mutation site group of NK/T cell lymphoma, which can be used for evaluating molecular typing of NK/T cell lymphoma, predicting prognosis of a patient and guiding medication of the patient. According tothe kit, an IlluminaMiseq sequencing platform and performance sequencing are adopted, a series of mutant genes related to NK/TCL diseases can be efficiently and accurately detected, the detection period is short, the detection cost is low, the application range is wide, and the accuracy is high.

Compounds, pharmaceutical compositions including the compounds, and methods of preparation and use thereof are disclosed. The compounds are noscapine analogs. The compounds and compositions can be used to treat and/or prevent a wide variety of cancers, including drug resistant cancers. While the antitussive plant alkaloid, noscapine, binds tubulin, displays anticancer activity, and has a safe pharmacological profile in humans, structure-function analyses pointed to a proton at position 9 of the isoquinoline ring that can be modified without compromising tubulin binding activity. Noscapine analogs with various functional moieties at position 9 on the isoquinoline ring kill human cancer cells resistant to other anti-microtubule agents, such as vincas and taxanes. Representative analogs include the 9-nitro, 9-bromo-, 9-iodo-, and 9-fluoro-noscapines, which bind tubulin and induce apoptosis selectively in tumor cells (ovarian and T-cell lymphoma) resistant to paclitaxel, vinblastine and teniposide. Surprisingly, treatment with one of the analogs, 9-nitro-nos, at doses as high as 100 μM, did not affect the cell cycle profile of normal human fibroblasts. This selectivity for cancer cells represents a unique edge over the other available antimitotics. The compounds can perturb the progression of cell cycle by mitotic arrest, followed by apoptotic cell death associated with increased caspase-3 activation and appearance of TUNEL-positive cells. Thus, the compounds are novel therapeutic agents for a variety of cancers, including ovarian and T-cell lymphoma cancers, even those that have become drug-resistant to currently available chemotherapeutic drugs.

The invention belongs to the technical field of animal tumor model construction and specifically relates to an immunodeficiency nude mouse model constructed by a lymphoma cell line and capable of being stably passed and a constructing method thereof. The immunodeficiency nude mouse model constructed by the lymphoma cell line and capable of being stably passed is constructed by using an NK cell lymphoma cell line, a T cell lymphoma cell line or a B cell lymphoma cell line; and the immunodeficiency nude mouse model constructed by the lymphoma cell line and capable of being stably passed comprises processes such as corresponding pre-treatment of an object of inoculation and the lymphoma cell line, preparation of a tumor suspension and injection of a nude mouse and tumor cell passage. The constructing method for constructing a lymphoma animal model by using the NK cell lymphoma cell line, the T cell lymphoma cell line or the B cell lymphoma cell line, provided by the invention, has the advantages that a lymphoma cell can be fixed under the skin by using a fixing effect of matrigel so as to guarantee the tumor formation rate of the nude mouse; technical advantages of fast tumor formation and high tumor formation rate are shown; and on the other hand, in the passage process, the lymphoma animal model for passage can be resuscitated at any time and can be directly constructed under the coordination of freezing operation of relevant tumor tissue culture solution.

A method for detecting T-cell lymphoma characterized in that gene mutations of at least one base selected from a group comprising base numbers 50, 331, 334, and 482 or gene mutations of base numbers 49 to 51 in the base sequence of an RHOA gene collected from a subject are analyzed, and the analysis results and T-cell lymphoma are associated with each other.

The present invention includes a method to reverse the trend towards progressive resistance to consecutive treatments for T-cell lymphoma in a patient. This method includes selecting a patient having T-cell lymphoma, wherein the patient has had at least one prior treatment for T-cell lymphoma, wherein the prior treatment comprises non-10-propargyl-10-deazaaminopterin; and administering to the patient a composition comprising a therapeutically effective amount of 10-propargyl-10-deazaminopterin, whereby the trend towards progressive resistance is reversed.