21 results about "Leukemia cell line" patented technology

A human chronic myeloid leukemia cell line and the use thereof. The human chronic myeloid leukemia cell line is the first cell line internationally established from chronic-phase leukemia cells of chronic myeloid leukemia, and was named human chronic myeloid leukemia cell YYXY-M6, which was deposited at the China Center for Type Culture Collection (Wuhan University, Wuhan, China) on July 24, 2023, under the deposit number of CCTCC NO: C2023219. The leukemia cell line exhibits primitive cell morphology and has three karyotypes, i.e. t(6:11)(q25:q23), del(11)(q23) and normal karyotype (46, XX); is BCR-ABL gene-negative; has good in-vitro proliferation ability; can be used as cellular material for the study of the mechanism of occurrence and development of the chronic phase of chronic myeloid leukemia, from the chronic phase thereof to the blastic phase thereof, and of BCR-ABL gene-negative chronic myeloid leukemia, and for the in-vitro study of individualized treatment; and can also be used for both in-vitro and in-vivo studies of drug screening and evaluation for the chronic phase of chronic myeloid leukemia, from the chronic phase thereof to the blastic phase thereof, and BCR-ABL gene-negative chronic myeloid leukemia, providing guidance for clinical medication.

The invention belongs to the technical field of biological detection, and provides a multiple cell factor detection kit in macrophage polarization and a preparation method and application thereof, and the detection kit comprises a capture antibody, a detection antibody, a mixed protein standard substance, a diluent and a washing buffer solution. The capture system is used for preparing a capture antibody coupled with a fluorescence coding microsphere by coupling a biotinylated antibody with a fluorescence microsphere coated with biotin, and the detection system is used for preparing a fluorescence labeled antibody by coupling derivatized phycoerythrin PE-SMCC with a specific thioether bond of a sulfhydrylated antibody. The mixed protein standard substance adopts a freeze-drying protection system containing BSA, trehalose and the like. The single hole of the kit can synchronously detect multiple cell factors, the sample dosage is only 25 microliters, the kit is suitable for in-vitro tests of mouse mononuclear macrophage leukemia cell lines RAW264.7, compared with a traditional ELISA method, the efficiency is improved by 10 times, the cost is reduced, and the kit has the remarkable advantages of being high in throughput, wide in linear range and high in stability.

This invention provides a method for preparing a non-natural humanized chimeric anti-human CD45RA antigen receptor, which specifically binds to the human CD45RA antigen by expressing CAR protein on T cells. Based on a humanized 3A4 antibody, this invention constructs a lentiviral expression vector pLenti / Hu3A4-4-1BB-3ζ. Compared with murine CAR, the humanized CAR significantly reduces immunogenicity, noticeably decreases the production of anti-scFv antibodies, and avoids the HAMA reaction. Research results show that Hu3A4CAR-T cells can specifically bind to the CD45RA-highly expressing myeloid leukemia cell line KG1a. Hu3A4CAR-T cells can target and kill 3A4-positive cell lines and leukemia cells, alleviate the human anti-mouse antibody response, and significantly reduce the production of anti-scFv antibodies, thereby ensuring the CAR's killing activity.

The invention provides application of small molecules ZQ-1-21 and derivatives thereof in prevention and treatment of leukemia brain metastasis. The invention finds that the small molecular compound ZQ-1-21 and the derivative thereof have a remarkable killing effect on various leukemia cell lines, especially drug-resistant leukemia cell lines, also have the capability of killing leukemia stem cells, and have a killing effect on human leukemia cell lines and primary leukemia cells of patients; and xenograft model leukemia derived from a patient can be treated. Furthermore, the ZQ-1-21 and the derivative thereof can effectively relieve leukemia cell infiltration of the brain of a leukemia brain metastasis model mouse, generate a treatment effect on leukemia brain metastasis or central nervous system leukemia, and have a good application prospect. In addition, it is found that ZQ-1-21 is a safe small molecule compound, and the cell viability and the clone forming ability of normal hematopoietic stem progenitor cells of people are not affected under the treatment dosage.

This invention belongs to the field of biomedical technology, specifically relating to the application of the RNA-binding protein RBM15B in MLL fusion gene leukemia (MLL-R). Using qRT-PCR technology, this invention detected significant high expression of RBM15B in a large number of leukemia patient samples, revealing a significant negative correlation between high RBM15B expression and patient survival rate. Further validation at the adult level was achieved by constructing mouse leukemia models using mouse MLL-AF9 cells and human MLL fusion gene leukemia cell lines. The results showed that knocking down RBM15B expression significantly inhibited the survival of MLL fusion gene leukemia cells and significantly prolonged the lifespan of the model mice. This indicates that RBM15B holds promise as a diagnostic marker and / or therapeutic target in MLL fusion gene leukemia.

The present invention relates to a novel compound having inhibitory activity against leukemia cell lines and a medical use thereof. The novel compound according to the present invention has excellent inhibitory activity against leukemia cell lines and thus can treat related diseases, and in particular, has an excellent therapeutic effect on acute myeloid leukemia (AML) and thus can be effectively used for treating leukemia as described above.

The invention belongs to the technical field of biological medicines, and particularly relates to application of FIS1 as a biomarker and a treatment target in NPM1 mutant leukemia. The mitochondrial fission enhancement phenomenon in the NPM1 mutant leukemia cell line is detected through a transmission electron microscope; then detecting the expression level of the mitochondrial fission gene by utilizing a qRT-PCR technology, and finding that the FIS1 is remarkably and highly expressed in the NPM1 mutant leukemia cell line; in addition, it is further verified that FIS1 is remarkably high in expression in clinical patients with NPM1 mutant leukemia through a western blot method, and the FIS1 can be used for indicating diagnosis of the disease. Subsequently, an in-vitro experiment further proves that the survival of NPM1 mutant leukemia cells can be remarkably inhibited by knocking down the expression of the FIS1. Therefore, a new target is provided for diagnosis, treatment and prognosis evaluation of the NPM1 mutant leukemia, and it is prompted that FIS1 has an important potential application prospect in diagnosis and treatment of the NPM1 mutant leukemia.

The invention provides a leukemia cell strain induced by an AVEN-NUTM1 fusion gene as well as an establishment method and application of the leukemia cell strain. The leukemia cell strain can stably express the AVEN-NUTM1 fusion gene, can be subcultured in vitro for a long time and maintain the multiplication capacity, and can induce leukemia after being transplanted into a receptor animal. The establishment method comprises the following steps: infecting hematopoietic stem / progenitor cells by using a virus vector carrying an AVEN-NUTM1 fusion gene, transplanting the infected cells into a receptor mouse body to induce leukemia, separating leukemia cells from the diseased mouse body, and culturing in vitro to finally obtain the stable cell strain. The cell strain established by the invention fills the blank of lack of stable and reliable experimental models in the research field of NUTM1 related leukemia, and provides a key tool and platform for analyzing pathogenesis of the leukemia, screening therapeutic drugs and developing new therapeutic strategies.

This invention relates to the field of pharmaceutical technology, specifically to the application of *Citrus aurantium* in the preparation of antitumor drugs. The invention uses *Citrus aurantium* as a raw material to obtain, for the first time, extracts with antitumor activity and novel compounds with extremely high activity. Furthermore, it provides a new natural method for obtaining *Citrus aurantium* alkaloids A, B, C, and D. The extracts and isolated monomeric compounds can effectively inhibit the growth of various tumor cell lines in vitro, including human colorectal cancer cells, human chronic myeloid leukemia cell lines, human gastric adenocarcinoma cell lines, human small cell lung cancer cell lines, and human liver cancer cell lines. The obtained extracts and monomeric compounds target a wide range of cancer cells, exhibiting significant effects on various cancer cells, thus achieving therapeutic effects and showing broad application prospects.

The invention provides a medicine for targeting early-stage precursor T cell acute lymphocytic leukemia (ETP-ALL) and application of the medicine. Dichloroacetic acid (DCA) is used for regulating mitochondrial oxidative phosphorylation, so that electron transport chain flux can be enhanced, ROS (reactive oxygen species) generation can be promoted, endoplasmic reticulum stress related pathways can be activated, the proliferation states of an ETP-ALL leukemia cell line and a primary patient sample can be influenced, and cell apoptosis can be induced. In cell line-derived and patient-derived xenograft models, DCA treatment can reduce leukemia load in bone marrow, spleen and peripheral blood and affect tumor formation characteristics. DCA shows good tolerance in normal hematopoietic system and other leukemia models. The method provides a treatment strategy based on metabolism targeted regulation, and provides a potential technical route and application reference for ETP-ALL research and drug development.

The invention discloses a triptolide peptide conjugate as well as a pharmaceutical composition and application thereof, and successfully designs and synthesizes the triptolide peptide conjugate which shows remarkable tumor cell proliferation inhibition activity. K-1 shows an excellent inhibition effect on a specific solid tumor cell strain; K-1 has particularly outstanding inhibition activity on a hepatoma cell strain HuH-7, a pancreatic cancer cell strain MIA PaCa-2 and a gastric cancer cell strain HGC-27; the compound shows broad-spectrum and high-efficiency anti-tumor characteristics as shown in the formula K-1, K-2 and K-3, and shows excellent inhibitory activity on a hepatoma cell line HepG2, an acute myelogenous leukemia cell line KG-1, a multiple myeloma cell line RPMI-8226 and a pancreatic cancer cell line MIA PaCa-2. The result not only proves the effectiveness of the K-3 on various solid tumors, but also highlights the strong inhibition effect of the K-3 on malignant tumors of a blood system, and shows the prospect of the K-3 as a broad-spectrum anti-tumor candidate drug. And a powerful guarantee is provided for subsequent deep development of potential antitumor candidate drug molecules and final realization of clinical application transformation.

The present invention provides the use of a traditional Chinese medicine monomer, rhamnosine, or a solvate, hydrate, or salt thereof, in the preparation of a drug for treating or alleviating leukemia. The present invention explores the anti-tumor activity of rhamnosine from multiple levels, including in vitro and in vivo levels. Experiments have shown that the traditional Chinese medicine monomer, rhamnosine, can inhibit the proliferation of leukemia cell lines, induce cell apoptosis, and enhance the effect of cytarabine in inhibiting leukemia; in vivo, rhamnosine can inhibit the growth of leukemia subcutaneous transplanted tumors and prolong the survival of tumor-bearing mice. Further experiments revealed the biological mechanism by which rhamnosine inhibits leukemia proliferation and promotes apoptosis by regulating the PI3K‑AKT signaling pathway, indicating that it has certain prospects in the treatment of leukemia.

The invention provides a novel application of elaifolin, and belongs to the technical field of acute myelogenous leukemia treatment. In particular to application of the elaifolin compound or pharmaceutically acceptable salt thereof in preparation of drugs for treating acute myelogenous leukemia, and when the elaifolin compound is used for treating an acute myelogenous leukemia cell line, the elaifolin compound has excellent effects of killing cells and remarkably inhibiting cell proliferation; in a PDX mouse model of AML, the elaifolin compound can significantly inhibit tumor growth and prolong the lifetime; when the compound is combined with a BCL-2 inhibitor Venetoclax, the compound shows a synergistic anti-AML effect, and the drug resistance risk can be reduced. Therefore, the elaifolin compound can be effectively used as a pharmaceutical composition for preventing or treating acute myelogenous leukemia.

The invention discloses a medicine for treating leukemia. It is found for the first time that CPI-0610 can effectively promote apoptosis of leukemia cell lines and leukemia patient cells and enhance the activity of imatinib, existing treatment problems are expected to be solved, a new path is developed for treatment of leukemia, the treatment effect is remarkably improved, and the life of a patient is prolonged.

The application belongs to the technical field of biological medicine, and particularly relates to application of a small peptide PEARL in diagnosis and targeted treatment of acute myeloid leukemia. The application detects samples of leukemia patients and leukemia cell lines, and finds that the small peptide PEARL is significantly lowly expressed in patients with acute myeloid leukemia. Meanwhile, it is found through research that PROSER2-AS1 does not play a role by itself, but plays a function through the coded small peptide PEARL. Further through a mouse leukemia model experiment, it is found that overexpression of the small peptide PEARL can significantly inhibit survival of acute myeloid leukemia cells, and significantly prolong the survival cycle of model mice. Finally, through mechanism research, it is found that overexpression of PEARL significantly increases endoplasmic reticulum stress of acute myeloid leukemia cells, activates UPR response, and thus affects functions of the acute myeloid leukemia cells. Therefore, the application can provide a new precise judgment or treatment strategy for diagnosis or targeted treatment of acute myeloid leukemia.

This useful solution refers to a procedure for isolating and purifying the compound kaempterol-3-O-rhamnoside from the bark of the medicinal tree Schima wallichii (DC.) Korth., which exhibits cytotoxic activity against HL-60 leukemia cells. The process according to the solution includes the following steps: a) preparing the raw material from the bark of the medicinal plant *Euphorbia hirta*; b) extracting the powdered raw material with 70% ethanol to obtain the ethanol extract labeled VT-E; c) dissolving the VT-E extract in hot water to obtain a liquid mixture; d) partition extraction with n-hexane to obtain the n-hexane extract labeled VT-H; e) partition extraction with dichloromethane to obtain the dichloromethane extract labeled VT-DCM; f) partition extraction with ethyl acetate to obtain the ethyl acetate extract labeled VT-EA. g) Isolating the fraction containing kaempferol-3-O-rhamnoside from the VT-EA extract using silica gel column chromatography to obtain the fraction labeled VT-EA-6; h) Purifying the VT-EA-6 fraction using column chromatography to obtain the fraction labeled VT-EA-6-3; i) Purifying the VT-EA-6-3 fraction using silica gel column chromatography to obtain the kaempferol-3-O-rhamnoside compound with formula (1). The compound kaempferol-3-O-rhamnoside obtained by the utility solution procedure exhibited significant cytotoxic activity against HL60 leukemia cell line under in vitro conditions.

Use of a compound of general formula (A) which is a CFS-IR kinase inhibitor or a pharmaceutically acceptable salt thereof in the preparation of medicaments for treating diseases related to CSF-1R kinase signal transduction pathway or medicaments for regulating immunization. In vivo and in vitro studies show that the compound can significantly inhibit CSF-IR kinase activity; significantly inhibits the proliferation of a CSF-1 / CSF-1R-driven mouse myeloid leukemia cell line, inhibits the survival of macrophages induced by CSF-1 and reverses M2 polarization phenotype of macrophages, and has an effect superior to that of the marketed medicament Pexidartinib. In a TAM enriched tumor model (MC38 model), the compound significantly antagonizes the tumor immunosuppressive microenvironment and exhibits significant anti-tumor efficacy. The compound has inhibitory effects on tumors that are not sensitive to immune checkpoint drugs, and can enhance the efficacy of immune checkpoint drugs, and has good clinical application prospects.

The invention discloses an application of an anti-malarial drug primaquine phosphate in preparation of drugs for treating BCR-ABL positive leukemia and breast cancer and a drug combination composition, and discovers that the anti-malarial drug primaquine phosphate has obvious effects of resisting BCR-ABL + leukemia and breast cancer, and has obvious anti-BCR-ABL + leukemia and breast cancer in the cellular level. The PRQ can significantly inhibit the growth of a BCR-ABL + leukemia cell line and an imatinib drug-resistant BCR-ABL + leukemia cell line, significantly inhibit the growth of breast cancer cells and induce ferroptosis of the breast cancer cells, and further researches find that the PRQ can degrade wild or mutant BCR-ABL proteins in a targeted manner. At the patient level, the PRQ is found to be capable of inhibiting the formation ability of primary cell colonies of wild-type or mutant patients with the BCR-ABL + leukemia, and at the animal level, the PRQ is found to have an obvious inhibiting effect on the progress of the BCR-ABL + leukemia.

The present invention discloses the use of 1,3-dicyclohexylbarbituric acid combined with dexamethasone in the preparation of a drug for treating leukemia. Experimental testing shows that 1,3-dicyclohexylbarbituric acid can increase the sensitivity of leukemia to dexamethasone. In vitro testing using the glucocorticoid-resistant acute T lymphocytic leukemia cell line Jurkat reveals that 1,3-dicyclohexylbarbituric acid and dexamethasone have a significant synergistic effect on Jurkat cells, and 1,3-dicyclohexylbarbituric acid can enhance the sensitivity of Jurkat cells to dexamethasone in a concentration- and time-dependent manner. The combination of 1,3-dicyclohexylbarbituric acid and dexamethasone can induce G1 arrest in Jurkat cells and regulate GR / BIM and JAK2 / STAT3 signal transduction to activate the caspase cascade reaction, thereby inducing Jurkat cell apoptosis. The 1,3-dicyclohexylbarbituric acid of the present invention has the potential to become a dexamethasone sensitizer, and also provides a research basis for the development of drugs to overcome glucocorticoid resistance.

The invention belongs to the field of molecular biology, and relates to design and application of ASO drugs, in particular to antisense oligonucleotide for inhibiting MYB gene expression and application of the antisense oligonucleotide in leukemia treatment. The ASO for inhibiting the expression of the MYB gene is an ASO of a target MYB or an ASO of an enhancer lncRNA of the target MYB, and the expression of the MYB gene is inhibited by targeting the MYB or the enhancer lncRNA of the target MYB. The ASO of the targeted MYB or the ASO of the enhancer lncRNA of the targeted MYB specifically inhibits MYB gene expression, so that the expression level of the MYB in a leukemia cell line can be effectively reduced, the proliferation and migration capabilities of leukemia cells are remarkably inhibited, and a way is provided for treating malignant tumors.

The application belongs to the technical field of biological medicine, and particularly relates to application of circular RNA (circRNA) CIRC8341 in leukemia. The application proves that the circular RNA CIRC8341 is stably present in leukemia cells and is generally highly expressed in leukemia cell lines through RNase R experiments and qRT-PCR experiments. Meanwhile, it is found through research that targeting CIRC8341 can significantly inhibit the growth of leukemia cells; the test results of a mouse leukemia model show that knocking down the expression of CIRC8341 can significantly inhibit the survival of leukemia cells and significantly prolong the survival cycle of model mice. The above results show that CIRC8341 can play a role in leukemia as a therapeutic target.