106 results about "Vimentin" patented technology

Neural stem cells which can be provided stably and which are free from the problem of compatibility in transplantation are disclosed. The stem cells are separated from human amniotic mesenchymal cell layer and express vimentin, nestin and BrdU which are markers of neural stem cells. The stem cells can also be differentiated to cells expressing alkaline phosphatase, that is, osteocytes, and to cells expressing collagen type II, that is, chondrocytes.

The invention discloses a circulating tumor cell identification kit and a circulating tumor cell identification method. The circulating tumor cell identification kit comprises a detection probe for detecting mRNA of an epithelial cell marking gene and/or mRNA of a mesenchymal cell marking gene, wherein the epithelial cell marking gene is selected from one or more of CDH2, VIMENTIN, FN1 and AKT2. Multiple RNA probes are adopted in the identification method, specific genes of a plurality of circulating tumor cells (CTCs) can be marked at the same time and are divided into genes I (epithelial genes), genes II (epithelial-mesenchymal genes) and genes III (mesenchymal genes), and false positive results caused by lack of part of the specific genes of the CTCs in a process that the CTCs enter peripheral blood for circulation are reduced; the method can be finished within eight hours, and a single copied mRNA hybridization probe is combined with a corresponding fluorescent probe by virtue of a signal amplification system, so that the detection sensitivity of in-situ RNA (Ribonucleic Acid) hybridization is remarkably improved.

The present invention provides methods and materials related to the detection of colorectal neoplasm-specific markers (e.g., markers associated with colorectal cancer, markers associated with adenoma) in or associated with a subject's stool sample. In particular, the present invention provides methods and materials for identifying mammals (e.g., humans) having a colorectal neoplasm by detecting the presence and level of indicators of colorectal neoplasia such as, for example, long DNA (e.g., quantified by Alu PCR) and the presence and level of tumor-associated gene alterations (e.g., mutations in KRAS, APC, melanoma antigen gene, p53, BRAF, BAT26, PIK3CA) or epigenetic alterations (e.g., DNA methylation) (e.g., CpG methylation) (e.g., CpG methylation in coding or regulatory regions of bmp-3, bmp-4, SFRP2, vimentin, septin9, ALX4, EYA4, TFPI2, NDRG4, FOXE1) in DNA from a stool sample obtained from the mammal.

The present invention provides diagnostic and prognostic methods for predicting the effectiveness of treatment of a cancer patient with inhibitors of EGFR kinase, PDGFR kinase, or FGFR kinase. Based on the surprising discovery that tumors cells after having undergone an EMT, while being mesenchymal-like, still express characteristics of both epithelial and mesenchymal cells, and that such cells have altered sensitivity to inhibition by receptor protein-tyrosine kinase inhibitors, in that they have become relatively insensitive to EGFR kinase inhibitors, but have frequently acquired sensitivity to inhibitors of other receptor protein-tyrosine kinases such as PDGFR or FGFR, methods have been devised for determining levels of specific epithelial and mesenchymal biomarkers that identify such “hybrid” tumor cells (e.g. determination of co-expression of vimentin and epithelial keratins), and thus predict the tumor's likely sensitivity to inhibitors of EGFR kinase, PDGFR kinase, or FGFR kinase. Improved methods for treating cancer patients with EGFR, PDGFR or FGFR kinase inhibitors that incorporate such methodology are also provided.

The invention discloses loop-mediated isothermal amplification (LAMP) primers, a kit and a detection method for detecting common carbapenemase genes of gram negative bacilli. In the LAMP primers disclosed by the invention, klebsiella pneumoniae carbapenemase (KPC) and new delhi metallo-b-lactamase (NDM) primer groups can detect all subtypes except for NDM-10; hypoxanthine nucleotide (IMP) and vimentin (VIM) primer groups can detect common subtypes at home and abroad. The LAMP kit built by the invention is applied to joint detection of KPC, NDM, IMP and VIM genes, can cover the common carbapenemase genes of non-fermentative bacteria and enterobacteriaceae, can accurately and quickly screen the common carbapenemase genes, and has great clinical significance for timely detecting and further controlling fulminant epidemic caused by propagation of the carbapenemase genes in enterobacteriaceae. The kit disclosed by the invention is high in detection sensitivity and the minimum detection limits of the KPC, NDM, IMP and VIM genes can reach 100 CFU/reaction.

The present invention provides diagnostic methods for predicting the effectiveness of treatment of a cancer patient with an EGFR kinase inhibitor. These methods are based on the surprising discovery that the effectiveness of treatment with an EGFR kinase inhibitor is predicted by whether a patient's tumor cells express a high or a low level of the biomarkers vimentin and E-cadherin, such that patients whose tumors express a high level of at least one of the biomarkers vimentin and E-cadherin have a longer overall survival and progression free survival than patients whose tumors express a low level of both vimentin and E-cadherin. The present invention further provides a method for treating tumors or tumor metastases in a patient, comprising the steps of diagnosing a patient's likely responsiveness to an EGFR kinase inhibitor by assessing whether tumor cells express a high level of at least one of the biomarkers vimentin and E-cadherin, and administering to said patient a therapeutically effective amount of an EGFR kinase inhibitor (e.g. erlotinib), particularly when effectiveness of the inhibitor is predicted.

The invention discloses separation, purification and identification methods of human amnion mesenchymal stem cells. The separation method of hAMSCs (human amnion mesenchymal stem cells) comprises the following steps: fragmentating human amnion; and carrying out two-step rotating digestion with trypsin of EDTA (ethylene diamine tetra-acetic acid) and collagenase of DNaseI, filtering with a steel mesh and collecting cell filtrate namely separated original hAMSCs. The purification method of hAMSCs comprises the following steps: incubating original hAMSCs with an LG (low glucose)-DMEM (dulbecco modified eagle medium) culture medium in a CO2 incubator; removing amnion epithelial cells which do not perform complete adherence growth under an inverted microscope; replacing a new culture medium on the third day; digesting with a trypsin-EDTA solution after cell converge degree reaches 80-90%; and collecting cells so as to obtain high-purity hAMSCs. The identification method of hAMSCs comprises the following steps: identifying hAMSCs and the amnion epithelial cells by adopting immunocytochemical staining vimentin and CK19; and detecting expressions of CD29, CD44, CD166, CD34 and CD45 by adopting a flow cytometry. The separation and purification methods disclosed by the invention have the advantages of high yield, high activity and high purity of hAMSCs; and the identification method is simple, convenient and precise.

The invention relates to an idiopathic pulmonary fibrosis urine protein marker, and application of the same to diagnosis and prognosis. Specifically, the invention relates to application of a urine protein marker obtained by using an idiopathic pulmonary fibrosis model and mass spectrometry to early-stage diagnosis, pathogenesis monitoring and curative effect assessment of human pulmonary fibrosis. The urine protein marker comprises collagen alpha-1(I) chain, vimentin, protein RUFY3, keratin type-II skeleton 8, a sodium-hydrogen exchange regulation factor NHE-RF2, a threonine synthase sample 2, zinc-actin binding repeat protein 2, low-density lipoprotein receptor-associated protein 4, alpha-11 of a guanine nucleotide binding protein subunit, an alpha-1 chain of tropomyosin, mitochondrial stress-70 protein, NSFL1 cofactor P47, ubiquitin carboxyl-terminal hydrolase isozyme L1, etc.

The present invention includes the discovery of cell-surface vimentin as a novel biomarker to detect and isolate mesenchymal and epithelial-mesenchymal transformed circulating tumor cells from blood of cancer patients. In addition, an antibody specific for the detection of cell-surface vimentin on circulating tumor cells and the use the antibody to detect, enumerate, and isolate CTC are provided.

Disclosed are methods for detecting multidrug resistance in neoplastic or damaged cells or multidrug resistant (MDR) neoplastic or damaged cells by detecting an increase in the cell surface expression of vimentin protein in such cells as compared to the level of cell surface expression of vimentin protein in a normal cell or a non-MDR neoplastic cell.

This application describes methods and compositions for detecting and treating vimentin-associated neoplasia. Differential methylation of the vimentin nucleotide sequences has been observed in vimentin-associated neoplasia such as colon neoplasia.

Cellular markers indicating a poor prognosis for ovarian cancer patients are disclosed. In particular, the invention relates to methods utilizing the frequency of a subset of cells in ovarian tumor tissue expressing vimentin, cMyc, or HE4, or any combination thereof, to predict an ovarian cancer patient will relapse.

The present invention relates to methods for screening and modulating the bioavailability of extracellular secretory vimentin. In particular, the present invention provides inhibitors and activators of secretory vimentin including antibodies, small interfering RNAs, and antisense oligonucleotides. The present invention thus provides novel drug targets for enhanced anti-microbial response, and methods of using such modulators to beneficially alter the pathophysiologic effects of secretory vimentin.

Provided herein is technology relating to detecting cancer and particularly, but not exclusively, to methods for detecting colorectal cancer by evaluating multiple markers in paired plasma and stool samples. In particular, the technology relates to CRC screening by assaying plasma for methylated Septin 9 and assaying stool DNA for methylated vimentin, NDRG4, BMP3, and/or TFPI2.

Methods of identifying specific target molecules for design of anti-angiogenic and vascular targeting approaches are disclosed. Transcriptional profiles of tumor endothelial cells were compared with that of normal resting endothelial cells, normal but angiogenically activated placental endothelial cells, and cultured endothelial cells. Although the majority of transcripts were classified as general angiogenesis markers, 17 genes were identified that show specific overexpression in tumor endothelium. Antibody targeting of four cell-surface expressed or secreted products (vimentin, CD59, HMGB1 and IGFBP7) inhibited angiogenesis in vitro and in vivo. Finally, targeting endothelial vimentin in a mouse tumor model significantly inhibited tumor growth and reduced microvessel density. The results demonstrate the utility of the identification and subsequent targeting of specific tumor endothelial markers for anticancer therapy.

The present invention provides for a mass spectrometry proteomic approach to distinguishing Spitz nevi from Spitzoid malignant melanoma. Histology directed mass spectral profiling allows for targeted analysis of sites of melanocytic lesion within formalin-fixed, paraffin embedded excisional biopsies. The classification system identified 5 peptide peaks, of which two have been identified as originating from vimentin and actin. A sensitivity and specificity for Spitz nevi of 97% and 90%, respectively, were achieved.

A mini-peptide and its analogs have been found to target gene products to tumors. The peptide, named Carcinoma Homing Peptide (CHP), increased the tumor accumulation of the reporter gene products in five independent tumor models, including one human xenogeneic model. A CHP-IL-12 fusion gene was also developed using CHP and the p40 subunit of IL-12. The product from CHP-IL-12 fusion gene therapy increased accumulation of IL-12 in the tumor environment. In three tumor models, CHP-IL-12 gene therapy inhibited distal tumor growth. In a spontaneous lung metastasis model, inhibition of metastatic tumor growth was improved compared to wild-type IL-12 gene therapy, and in a squamous cell carcinoma model, toxic liver lesions were reduced. The receptor for CHP was identified as vimentin. CHP can be used to improve the efficacy and safety of targeted cancer treatments.

The invention discloses a method for screening a donor cell line based on blastocyst gene expression level. The method comprises the steps of: detecting expression levels of TCF7, DGCR8, SENP7, DNMT3B, Vimentin, IFI6, EFNA2, F5, IRAK1, PRICKLE1, TNFRSF1A, ARG2, NEK6, OCT4, NANOG, SOX2, CDX2, XIST and IGF2R at a blastula stage after carrying out nuclear transferring on the donor cell lines from different individuals; and selecting the donor cell line which is not significant in difference of all expression levels of these genes on cloned blastocysts and the expression level of normally growing in vitro fertilization blastocyst as a nuclear donor cell. The cloning efficiency of bovine somatic cells can be significantly improved.

Rheumatoid arthritis and other autoimmune diseases are diagnosed by multiplex assays for antibodies to a panel of antigens that includes cyclic citrullinated peptide and at least five members of a list that includes BRAF1 506-525, BRAF2 656-675, Vimentin (protein) citrullinated, Vimentin 415-433 cit cyclic, Vimentin 58-77 cit3 cyclic, Clusterin 231-250 cit sm1 cyclic, Fibrinogen A 556-575 cit sm cyclic, Fibrinogen A 616-635 cit sm cyclic, Histones2A H2A/a 1-20 cit sm2 cyclic, Filaggrin 48-65 cit2v1 cyclic, BRAF (catalytic domain from v raf murine sarcoma viral oncogene homologue B1, amino acids 416-766).

The present invention describes a method to inhibit replication of the human immunodeficiency virus (HIV) by negatively modulating or altering the cytoskeleton, more precisely the proteins forming the intermediate cytoskeletal filaments, wherein the said proteins are vimentin and/or keratin-10. The replication of the virus is inhibited in human cells by intervening in the structure of these proteins. The present invention is also related to the use of agents, which comprise peptides and/or interfering RNA and/or lipidic compounds, said agents producing a negative modulation or alteration of the cytoskeleton to prevent or to treat the HIV infection. The invention provides means and methods for altering the cytoskeleton/filament structure of cells, as a result of which the infection of human cells by HIV is disturbed and can even be completely inhibited. The cytoskeleton is altered by reducing the amount of vimentin and/or keratin (e.g. by transcriptional control using interfering RNA) or by using peptides that disrupt the cytoskeleton.