337 results about "Cadherin" patented technology

Compositions and methods for diagnosing, treating and / or preventing cancers characterized by CDH17 overexpression based on the detection of CDH17 or the use of CDH17 as a target for therapeutic intervention or prophylactic intervention are provided. Methods for diagnosing and / or monitoring liver cancers using the expressing of CDH17 involve detecting and / or quantitating the CDH17 protein or encoding nucleic acids (DNA or RNA) in a biological sample such as urine from the subject. Methods for treating liver cancers using CDH17 as a target and of sensitizing cells with aberrant expression of CDH17 have also been developed. The methods include suppression or knockdown of the expression of CDH17 by administering an effective amount of a CDH17 inhibitor.

The present invention relates to methods of modulating epithelial stem cell lineage by regulating the expression of Lef1 or a BMP inhibitor and / or the stability of β-catenin or the expression of a Wnt; regulating the expression or activity of GATA-3; or regulating BMPR1A activity either at the level of receptor expression or at the level of pathway activation. Methods of regulating E-cadherin, GATA-3, BMPR1A and HK1-hair keratin and methods of identifying agents which modulate the epithelial stem cell lineage are further provided. Such agents are useful for inhibiting or stimulating inner root sheath development or hair follicle formation.

A methylation state information about CpG island in the promoter region of the gene associated with primary liver cancer, its use and the method and reagent kit for detecting primary liver cancer aredisclosed. Said reagent kit contains the methylation-specific restriction endonuclease and the promoter CpG island-specific primer pair of the gene associated with liver cancer, or the reagent for transforming the methylation cytosine to uracil and the primer for the promoter CpG island of the gene associated with liver cancer. Said genes are also disclosed.

Modulating agents for inhibiting or enhancing nonclassical cadherin mediated cell adhesion are provided. The modulating agents comprise one or more of: (a) a peptide sequence that is at least 50% identical to a nonclassical cadherin CAR sequence; (b) a non-peptide mimetic of a nonclassical cadherin CAR sequence; (c) a substance, such as an antibody or antigen-binding fragment thereof, that specifically binds a nonclassical cadherin CAR sequence; and / or (d) a polynucleotide encoding a polypeptide that comprises a nonclassical cadherin CAR sequence or analogue thereof. Methods for using such modulating agents for modulating nonclassical cadherin-mediated cell adhesion in a variety of contexts are also provided.

The invention provides a variety of reagents for use in the diagnosis and management of cancer, particularly breast cancer. cDNA microarray technology was used to identify genes whose expression profile across a large group of tumor samples correlates with that of cytokeratin 5 and cytokeratin 17, markers for basal cells of the normal mammary lactation gland. The invention demonstrates that tumors that express cytokeratin 5 / 6 and / or 17 have a poor prognosis relative to tumors overall. The invention provides basal marker genes and their expression products and uses of these genes for diagnosis of cancer and for identification of therapies for cancer. In particular, the invention provides basal marker genes including cadherin3, matrix metalloproteinase 14, and cadherin EGF LAG seven-pass G-type receptor 2. The invention provides antibodies to the polypeptides expressed by these genes and methods of use thereof.

This invention provides methods, processes, compounds and compositions for modulating the gene expression and modulating the secretion, expression, or synthesis of adhesion proteins or their receptors to cure disease, wherein the modulating comprises positive and negative regulating; wherein comprises inhibiting cancer growth, wherein the adhesion proteins or receptors comprise fibronectin, integrins family, Myosin, vitronectin, collagen, laminin, Glycosylation cell surface proteins, polyglycans, cadherin, heparin, tenascin, CD 54, CAM, elastin and FAK; wherein the methods, processes, compounds and compositions are also for anti-angiogenesis; wherein the cancers comprise breast cancer, leukocyte cancer, liver cancer, ovarian cancer, bladder cancer, prostate cancer, skin cancer, bone cancer, brain cancer, leukemia cancer, lung cancer, colon cancer, CNS cancer, melanoma cancer, renal cancer or cervix cancer.

Modulating agents for inhibiting or enhancing desmosomal cadherin mediated cell adhesion are provided. The modulating agents comprise one or more of: (a) a peptide sequence that is at least 50% identical to a desmosomal cadherin CAR sequence; (b) a non-peptide mimetic of a desmosomal cadherin CAR sequence; (c) a substance, such as an antibody or antigen-binding fragment thereof, that specifically binds a desmosomal cadherin CAR sequence; and / or (d) a polynucleotide encoding a polypeptide that comprises a desmosomal cadherin CAR sequence or analogue thereof. Methods for using such modulating agents for modulating desmosomal cadherin-mediated cell adhesion in a variety of contexts are also provided.

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.

We examined IQGAP1 copy gain and its relationship with clinicopathologic outcomes of thyroid cancer and investigated its role in cell invasion and molecules involved in the process. We found IQGAP1 copy number (CN) gain ?3 in 1 of 30 (3%) of benign thyroid tumor, 24 of 74 (32%) follicular variant papillary thyroid cancer (FVPTC), 44 of 107 (41%) follicular thyroid cancer (FTC), 8 of 16 (50%) tall cell papillary thyroid cancer (PTC), and 27 of 41 (66%) anaplastic thyroid cancer, in increasing order of invasiveness of these tumors. A similar tumor distribution trend of CN ?4 was also seen. IQGAP1 copy gain was positively correlated with IQGAP1 protein expression. It was significantly associated with extrathyroidal and vascular invasion of FVPTC and FTC and, remarkably, a 50%-60% rate of multifocality and recurrence of BRAF mutation-positive PTC (P=0.01 and 0.02, respectively). The siRNA knock-down of IQGAP1 dramatically inhibited thyroid cancer cell invasion and colony formation. Co-immunoprecipitation assay showed direct interaction of IQGAP1 with E-cadherin, a known invasion-suppressing molecule, which was upregulated when IQGAP1 was knocked down. IQGAP1, through genetic copy gain, plays an important role in the invasiveness of thyroid cancer and represents a useful prognostic marker and therapeutic target for this and other cancers.

A method for diagnosing, or differentially diagnosing, an increased risk of pre-term birth (PTB) involves detecting or measuring increased expression of a biomarker Soluble E-cadherin (SE-CAD) in a biological sample from a mammalian subject, particularly in the urine, cervicovaginal fluid or blood. An increased level of expression of SE-CAD above the level of expression in the same sample of a healthy mammalian subject is an indication of a diagnosis of increased risk of PTB. Such diagnosis may further involve identify other clinical symptoms of PTB or PTL. Additionally the method may use additional biomarkers, such as fetal fibronectin.

The subject invention pertains to the use of peptide fragments of cadherins (including cadherin-like proteins). The subject invention includes a cell (and use thereof) comprising a polynucleotide that expresses the peptide fragment. The subject invention includes methods of feeding the peptides to insects. In preferred embodiments, the peptides are fed to target insects together with one or more insecticidal proteins, preferably (but not limited to) B.t. Cry proteins. When used in this manner, the peptide fragment can not only enhance the apparent toxin activity of the Cry protein against the insect species that was the source of the receptor but also against other insect species. Preferably, the cadherin is a Bacillus thuringiensis (B.t.) insecticidal crystal protein (Cry) toxin receptor. Preferably, the peptide fragment is a binding domain of the receptor. In some preferred embodiments, the peptide is the binding domain nearest to the membrane proximal ectodomain. Corresponding domains are identifiable in a variety of B.t. toxin receptors.

Methods and therapeutic compositions for the treatment of cancer are disclosed. Specifically, peptides including beta-catenin binding domains and polynucleotide sequences encoding same, such as cadherins and o-catenins and polynucleotide sequences encoding same, effective in methods and compositions for treating cancers associated with abnormally high levels of beta-catenin, such as colon cancers and melanomas.

A method of predicting CNS metastasis of a non-neuronal cancer in a subject is disclosed. The method comprises determining a level and / or activity of N-cadherin (CDH2), in a sample of the subject wherein an increase in the CDH2 with respect to an unaffected sample is indicative of the CNS metastasis of the non-neural cancer. The method further comprises determining a level and / or activity or kinesin family member C1 (KIFC1) and / or Fetal Alzheimer Antigen (FALZ1) in the sample wherein an increase in KIFC1 and a decrease in FALZ with respect to an unaffected sample is further indicative of the CNS metastasis of the non-neural cancer. The method may be used for selection of a treatment regimen. In addition, kits for prediction CNS metastasis are disclosed.

[Problem] To provide a cell culture substrate, and a cell culturing method using the substrate and a method for inducing differentiation of pluripotent stem cells using the substrate, which allow culturing of pluripotent stem cells and allow differentiation of pluripotent stem cells into a specified cell species, particularly neural and neural progenitor cells, at a high purity.[Means for Solution] A cell culture substrate, characterized in that, onto the surface, one or more selected from the group consisting of N-cadherin, a fusion protein comprising an entire or partial region of N-cadherin, and a fusion protein comprising an entire or partial region of a protein homologous to N-cadherin are immobilized or coated.

Described is a method of modulating E-cadherin mediated cell adhesion. More specifically, described is the use of hECRep1a and homologues thereof to modulate and / or control tumor cell invasiveness.

It is an object of the present invention to provide an anti-cadherin antibody having a high internalization capacity and provide an anti-cadherin antibody-drug conjugate that effectively kills cadherin-expressing cancer cells with the use of such antibody. The present invention provides an anti-cadherin antibody which recognizes a cadherin domain 1 (EC1) of cadherin and exhibits a high internalization capacity.

Compounds, particularly compounds having activity as modulators of cadherin-mediated cell adhesion having the following structure:or a pharmaceutically acceptable salt, stereoisomer or prodrug thereof,wherein R1, R2, R3, R4, R5, R6, A, X, Y, Z, m and n are as defined herein. Methods associated with preparation and use of the same, as well as pharmaceutical compositions containing the same, are also disclosed.

The present invention provides methods of diagnosis, providing a prognosis and a therapeutic target for the treatment of cancers that overexpress N-cadherin and Ly6-E, including prostrate and bladder cancers. The invention further provides methods of drug discovery to identify pharmaceutical agents that inhibit or prevent the binding of N-cadherin and Ly6-E to its receptor, which are useful when used alone or in combination with known chemotherapeutics, immunotherapeutics, and radiotherapy for the reversal of resistance, tumor progression, and metastasis of cancers associated with the overexpession of N-cadherin and Ly6-E.

The present invention provides methods of diagnosis, providing a prognosis and a therapeutic target for the treatment of cancers that express N-cadherin, including prostrate and bladder cancers.

This invention is directed to coral scaffolds seeded with precursor cells in culture in the presence of a chelator and uses thereof in inducing or enhancing bone and / or cartilage formation in a subject, and kits related thereto. This invention is also directed to use of cadherin-upregulating coral for treating cancer or inhibiting cancer progression. This invention is also directed to use of aragonite or calcite-producing species for in vivo calcium release, and its application to the treatment of skin diseases, disorders or conditions.

Modulating agents and methods for enhancing or inhibiting classical cadherin-mediated functions are provided. The modulating agents comprise at least a tryptophan-containing cell adhesion recognition sequence of a classical cadherin molecule, a conservative analogue or peptidomimetic thereof, or an antibody or fragment thereof that specifically binds to such a cell adhesion recognition sequence. Modulating agents may additionally comprise one or more cell adhesion recognition sequences recognized by cadherins and / or other adhesion molecules. Such modulating agents may, but need not, be linked to a targeting agent, pharmaceutically active substance and / or support material.

Methods and compositions are provided for the isolation, culture and use of highly regenerative somatic mammalian cells. The cells are very small, and have an undefined nuclear structure. The cells may be isolated from fetal or adult tissues, and are found in tissue including, without limitation, fetal dermal tissue, blood, and bone marrow. The cells are characterized as expressing one or more markers selected from E-cadherin, integrin β1, CXCR4, CD90 and CD34, and may be selected on the basis of such expression patterns.

The present disclosure related to isolated laminin-521, methods for making recombinant laminin-521, host cells that express recombinant laminin-521, and compositions containing laminin-521. Laminin-521 can maintain stem cells in vitro pluripotency, enable self-renewal, and enable single cell survival of human embryonic stem cells. When pluripotent human embryonic stem cells are cultured on plates coated with recombinant laminin-521 (laminin-11), in the absence of differentiation inhibitors or feeder cells, the embryonic stem cells proliferate and maintain their pluripotency. It has also been discovered that human recombinant laminin-521 (laminin-11) provides single cell survival of stem cells after complete dissociation into a single cell suspension. Useful cell culture mediums containing at most 3.9 ng / ml of beta fibroblast growth factor (bFGF) are also described herein.

Peptidomimetics of cyclic peptides, and compositions comprising such peptidomimetics are provided. The peptidomimetics have a three-dimensional structure that is substantially similar to a three-dimensional structure of a cyclic peptide that comprises a cadherin cell adhesion recognition sequence HAV. Methods for using such peptidomimetics for modulating cadherin-mediated cell adhesion in a variety of contexts are also provided.

The present invention provides methods of diagnosing a cancer or providing a prognosis for a cancer by analyzing the level of expression of a marker that is a downstream target of N-cadherin.

This application discloses anti-P-cadherin antibodies, antigen binding fragments thereof, and antibody drug conjugates of said antibodies or antigen binding fragments. The invention also relates to methods of treating cancer using the antibodies, antigen binding fragments, and antibody drug conjugates. Also disclosed herein are methods of making the antibodies, antigen binding fragments, and antibody drug conjugates, and methods of using the antibodies and antigen binding fragments as diagnostic reagents.

The present invention relates to methods and compositions for monitoring, diagnosis, prognosis, and determination of treatment regimens in subjects suffering from or suspected of having a renal injury. In particular, the invention relates to using assays that detect one or more biomarkers selected from the group consisting of Tumor necrosis factor receptor superfamily member 1OB, Cadherin-16, Caspase-9, Bcl2 antagonist of cell death, Caspase-1, Cadherin-1, Poly [ADP-ribose] polymerase 1, Cyclin-dependent kinase inhibitor 1, Cadherin-5, Myoglobin, Apolipoprotein A-II, Mucin-16, Carcinoembryonic antigen-related cell adhesion molecule 5, and Cellular tumor antigen p53 as diagnostic and prognostic biomarker assays in renal injuries.

The present application provides fully human antibodies against N-Cadherin for therapeutic and diagnostic methods in cancer.