125 results about "CD24" patented technology

Human breast tumors contain hetrogeneous cancer cells. using an animal xenograft model in which human breast cancer cells were grown in immunocompromised mice we found that only a small minority of breast cancer cells had capacity to form new tumors. The ability to form new tumors was not a slochastic property, rather certain populations of cancer cells were depleted for the ability to form new tumors, while other populations were enriched for the ability to form new tumors. Tumorigenic cells could be distinguished from non-tumorigenic cancer cells based on surface marker expression. We prospectively identified and isolated the tumorigenic cells as CD44³⁰CD24^−/lowLINEAGE A few as 100 cells from this population were able to form tumors the animal xenograft model, while tens of thousands of cells from non-tumorigenic populations failed to form tumors. The tumorigenic cells could be serially passaged, each time generating new tumors containing and expanded numbers of CD44^+CD24 Lineage tumorigenic cells as well as phenotypically mixed populations of non-tumorigenic cancer cells. This is reminiscent of the ability of normal stem cells to self-renew and differentiate. The expression of potential therapeutic targets also differed between the tumorigenic and non-tumorigenic populations. Notch activation promoted the survival of the tumorigenic cells, and a blocking antibody against Notch 4 induced tumorigenic breast cancer cells to undergo apoptosis.

The present invention relates to a method for prognosing cancer in a subject with triple negative (TN) breast cancer, whose tumors lack expression of the estrogen receptor (ER), the progesterone receptor (PR) and normal (not amplified) levels of the human epidermal growth factor receptor 2 (HER2). Methods and biomarkers are disclosed that are useful for predicting the overall survival (OS) potential of cancer in a subject with triple negative breast cancer or for predicting metastatic disease in a subject with triple negative breast cancer. For example, the method comprises detecting in a sample from a subject one or more biomarkers selected from the group consisting of ANK3, CD24, EIF1, KLF6, KRAS, KRT1, MAP2K4, SDC4, SLC2A3, STK3, TFAP2C, and WRN. An increase or decrease in one or more biomarkers as compared to a standard is prognostic of OS of TN breast cancer. Likewise, in another example, the method comprises detecting in a sample from a subject one or more biomarkers selected from the group consisting of ANG, DICER1, EIF1, and MSH6. An increase or decrease in one or more biomarkers as compared to a standard is prognostic of metastasis of TN breast cancer.

Gene expression profiling and hierarchial clustering analysis readily distinguish normal ovarian epithelial cells from primary ovarian serous papillary carcinomas. Laminin, tumor-associated calcium signal transducer 1 and 2 (TROP-1/Ep-CAM; TROP-2), claudin 3, claudin 4, ladinin 1, S100A2, SERPIN2 (PAI-2), CD24, lipocalin 2, osteopontin, kallikrein 6 (protease M), kallikrein 10, matriptase and stratifin were found among the most highly overexpressed genes in ovarian serous papillary carcinomas, whereas transforming growth factor beta receptor III, platelet-derived growth factor receptor alpha, SEMACAP3, ras homolog gene family, member I (ARHI), thrombospondin 2 and disabled-2/differentially expressed in ovarian carcinoma 2 (Dab2/DOC2) were significantly down-regulated. Therapeutic strategy targeting TROP-1/Ep-CAM by monoclonal chimeric/humanized antibodies may be beneficial in patients harboring chemotherapy-resistant ovarian serous papillary carcinomas. Claudin-3 and claudin-4 being receptors for Clostridium Perfringens enterotoxin, this toxin may be used as a novel therapeutic agent to treat ovarian serous papillary tumors.

Methods and kits for diagnosing cancer or a pre-malignant lesion by determining the presence and/or level of circulating CD24 of a subject are provided. Also provided are methods and kits for determining if a subject is predisposed to gastrointestinal cancer by the determining the presence or absence, in a homozygous or heterozygous form of cancer associated genotype(s) in the CD24 and/or APC nucleic acid sequences. Also provided are methods and kits for monitoring efficacy of cancer therapy by determining the presence and/or level of circulating CD24 of a subject.

Provided herein is a method of treating rheumatoid arthritis using a CD24 protein. The CD24 protein may include mature human or mouse CD24, as well as a N- or C-terminally fused portion of a mammalian immunoglobulin.

A method of diagnosing cancer or a pre-malignant lesion is disclosed. The method comprises determining a level of CD24 expressed on peripheral blood cells of a subject in need thereof, wherein the level of CD24 above a predetermined threshold is indicative of the cancer or the pre-malignant lesion.

The present invention relates to a method to inhibit cancer by targeting CD24, more precisely a method to inhibit cancer by using CD24 expressed in most cancer cells as a target of an antibody therapeutic agent or by inhibiting the interaction between CD24 and P-selectin. CD24 is over-expressed in most cancer cells and CD24 accumulated in cytoplasm accelerates metastasis. Therefore, the method to inhibit cancer of the invention by targeting CD24 can be effectively used for the treatment of cancer by inhibiting the progress of various cancers over-expressing CD24.

The invention relates to a monoclonal anti-human CD24 antibody, for example, a single-chain variable region fraction which includes a VH having the amino acid represented as the SEQ ID NO.5 and a VL having the amino acid represented as the SEQ ID NO.6; the invention also relates to a chimeric antigen receptor fusion protein, which includes, from a N-terminal to a C-terminal: (i) the single-chain variable region fraction in the invention; (ii) a transmembrane structural domain; (iii) at least one co-stimulus structural domain; and (iv) an activation domain.

Anti-CD24 antibodies and adjuvant combinations thereof with chemotherapeutic agents or toxins, which can be used to inhibit growth of CD24-expressing cancer cells and prevent and treat cancer are provided.

The invention belongs to the technical field of genetic engineering antibodies, and particularly relates to a preparation and application of a bispecific antibody targeting a CD24 (cluster of differentiation 24) and activating NK cells (natural killer cells). According to the preparation and application of the bispecific antibody, an anti-CD24 humanized chimeric antibody cG7 and an MICA molecule capable of recruiting and activating the activity of the NK cells are connected through flexible peptide (Gly4Ser) and are stably transferred to a CHO-s eukaryotic expression system, and a stable high-expression cell strain is selected for propagation and expression of cG7-MICA; the bispecific antibody cG7-MICA utilizes the function of remodeling the MICA by utilizing the targeting effect of the cG7 to selectively display the MICA on the surface of a CD24+ tumor cell, the immune surveillance effect of the NK cells is induced, in addition, the NK cells are further activated through the effect ofan Fc part, and the antibody-dependent cell-mediated cytotoxicity (ADCC) is achieved; and through experimental verification, the immunocompetence of killing the CD24+ hepatocellular carcinoma cells is achieved in vitro and vivo.

There are disclosed methods and compositions for the diagnosis, prevention, and treatment of tumors and cancers in mammals, for example, humans, utilizing the CTSZ and CD24 genes, which are amplified colon cancer and/or ovarian cancer and/or breast cancer genes. The CTSZ and CD24 genes, their expressed protein products and antibodies are used diagnostically or as targets for cancer therapy or vaccine; they also are used to identify compounds and reagents useful in cancer diagnosis, prevention, and therapy.

The present invention is directed to methods of treating a primary brain tumor and preventing the migratory spread of a primary brain tumor in a subject. These methods involve utilizing the CD24 surface protein selectively expressed on tumor progenitor cells as a therapeutic target as well as a means for directing oncolytic therapeutics directly to the tumor site. The present invention further relates to methods of diagnosing the presence of a brain tumor and monitoring the status of the brain tumor in a subject based on CD24 expression in tumor progenitor cells.

The invention belongs to the field of pharmacy, and relates to an application of a TCM monomer of apigenin to prepare a medicine for treating the pancreatic cancer. A CCK-8 method for evaluation, repeated screening and optimization, and a pharmacodynamic test for inhibiting proliferation of pancreatic cancer SW1990 cells are adopted to screen an effective monomer, having a strong anti-tumor effect, of apigenin. Moreover, an equipment of apigenin for interfering a Sonic Hedgehog signal channel of human pancreatic cancer SW1990 stem cells is carried out. The result shows that apigenin can obviously inhibit proliferation of pancreatic cancer stem cells, lower the ratio of pancreatic cancer stem cells, and reduce self-renewable ability of pancreatic cancer stem cells. The ratio of CD24+CD44+ cells is obviously lowered through flow cytometry; the amount of cancer stem cells cultured free of serum decreases; and expression of members in the Sonic Hedgehog signal channel at mRNA and protein levels is obviously lowered. The TCM monomer of apigenin can be taken as an individual unique active component for preparing the medicine for treating the pancreatic cancer.

The invention belongs to the technical field of genetic engineering antibodies, and particularly relates to a preparation method and application of CD24 antibody fusion protein. The preparation method includes that genetic engineering technology is utilized to connect CD24 single-strand antibody rG7S with MICA extracellular 1-3 zones through G4S flexible peptide, and a mammal eukaryotic expression system stably expresses rG7S-MICA; the CD24 antibody fusion protein rG7S-MICA can be combined with CD24 molecules on the surface of tumor cells and an activated receptor NKG2D on the surface of NK cells at the same time, and can remodel immunological surveillance effect, on CD24+tumor cells, of NK cells induced through an NKG2D path to finally achieve the objective of activating a body autoimmune system to effectively kill the CD24+tumor cells.

The invention relates to an osteosarcoma stem cell molecular marker CD24 and application thereof. The molecular marker comprises a CD24 gene or CAD24 protein. The molecular marker CD24 is used as an osteosarcoma stem cell molecular marker, a product for detecting CD gene expression is used for detecting the CD24 gene expression level in a to-be-measured osteosarcoma tissue sample, the CD24 gene expression level in the to-be-measured osteosarcoma tissue sample is compared with that in the normal para-carcinoma tissue, the progression of the osteosarcoma disease is diagnosed, assessment and prognosis are conducted, the marker has good specificity and high sensitivity, and a brand-new approach is provided for osteosarcoma diagnosis and/or treatment.

The invention provides a kit for detecting the invasiveness of circulating tumor cells (CTC). The kit is characterized by comprising antibody-oligonucleotide probes obtained by coupling CD133, CD24 and CD44 antibodies with different oligonucleotides, respectively, an amplification primer and a buffering solution which are used for carrying out PCR (Polymerase Chain Reaction) amplification on the antibody-oligonucleotide probes, and a fluorescent probe. According to the kit provided by the invention, the CD133, the CD24 and the CD44 are used as markers of cancer stem cells (CSC) and the content of each antigen in the CTC can be detected in parallel, so that the expression amount of the CSC in the CTC is obtained, and the invasiveness of the CTC is analyzed. The kit provided by the invention is low in detection cost and high in sensitivity, and has very strong practicability.

The invention relates to the field of gene detection technologies and biomedicine, in particular to a breast cancer patient recurrence risk 20 gene prediction model based on breast cancer single-celltranscriptome sequencing analysis and an establishment method and application thereof. The model is composed of 20 genes of CEBPD, SERPINA1, CD24, ERRFI1, BCL3, DSTN, BTG2, SERTAD1, SPINT1, BAMBI, LIMCH1, NFIA, SKP1, DHRS7, ODF3B, KRT7, ZFP36, CEBPB, BHLHE40 and UGDH. The breast cancer patient recurrence risk 20 gene prediction model provided by the invention provides more accurate judgment for long-term prognosis of a breast cancer patient, and provides a basis for selection of a postoperative adjuvant therapy scheme of the patient, so that individualized accurate treatment is realized, and meanwhile, a new research perspective is provided for research of breast cancer tumor stem cells.