160 results about "Colony formation" patented technology

Pharmaceutical compositions and methods of using them. Lipid formulations of a glutathione analog and methods of manufacturing them. Their use to stimulate hematopoiesis, protect hematopoietic cells from damage caused by radiation or chemotherapy, or potentiate the stimulatory action of one or a combination of cytokines on colony formation by hematopoietic progenitor cells, protect a subject from a destructive effect of a chemotherapeutic agent or irradiation, or to potentiate the effect of a chemotherapeutic agent.

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.

This invention provides an agonist antibody to a human thrombopoietin receptor (alias: human c-Mpl). More particularly, this invention provides an agonist antibody to a human thrombopoietin receptor, wherein the agonist antibody comprises: antibody constant regions comprising (1) amino acid sequences in a heavy chain constant region and a light chain constant region of a human antibody, (2) an amino acid sequence of a heavy chain constant region with a domain substituted between human antibody subclasses, and an amino acid sequence of a light chain constant region of a human antibody, or (3) amino acid sequences comprising a deletion(s), substitution(s), addition(s), or insertion(s) of one or several amino acid residues in the amino acid sequences of (1) or (2) above; and antibody variable regions capable of binding to and activating a human thrombopoietin receptor; and wherein the agonist antibody has the properties: (a) that the antibody induces colony formation at a concentration of 10,000 ng / ml or lower as determined by the CFU-MK colony formation assay using human umbilical-cord-blood-derived CD34+ cells; and (b) that the antibody has a maximal activity at least 50% higher than that of PEG-rHuMGDF and an 50% effective concentration (EC50) of 100 nM or less in the cell proliferation assay using UT7 / TPO cell. Also provided is a pharmaceutical composition for treating thrombocytopenia comprising said antibody.

The present invention provides methods, compositions, and kits wherein nanomaterials are used for inhibiting cancer stem cell division, colony formation, spheroid formation and self-renewal. The present invention also provides methods, compositions, and kits wherein nanomaterials are used for treating cancer, coating tumors, and inhibiting metastasis. The present invention also provides methods, compositions, and kits wherein nanomaterials are used for inducing cells to go into stasis. The present invention further provides methods for isolating tumors, inhibiting bleeding, and marking margins of tumors and organs during surgery with a nanomaterial.

The present invention relates to a mesenchymal stem cell-derived microparticle that has corneal epithelial stem cell and / or corneal epithelial cell growth-promoting activity, undifferentiated cornealepithelial stem cell maintenance activity, corneal epithelial stem cell colony formation-promoting activity, or a corneal epithelium protection effect.

The present invention relates to methods and compositions designed for the treatment, management, or prevention of cancer, particularly, metastatic cancer. In one embodiment, the methods of the invention comprise the administration of an effective amount of an antibody that binds to EphA2 and agonizes EphA2, thereby increasing EphA2 phosphorylation and decreasing EphA2 levels. In other embodiments, the methods of the invention comprise the administration of an effective amount of an antibody that binds to EphA2 and inhibits cancer cell colony formation in soft agar, inhibits tubular network formation in three-dimensional basement membrane or extracellular matrix preparation, preferentially binds to an EphA2 epitope that is exposed on cancer cells but not non-cancer cells, and / or has a low Koff, thereby, inhibiting tumor cell growth and / or metastasis. The invention also provides pharmaceutical compositions comprising one or more EphA2 antibodies of the invention either alone or in combination with one or more other agents useful for cancer therapy.

The presence of the ancient anti-inflammatory peptide α-melanocyte stimulating hormone (α-MSH [1-13], SYSMEHFRWGKPV) in barrier organs such as gut and skin suggests a role in the nonspecific (innate) host defense system. α-MSH and other amino acid sequences derived from α-MSH were determined to have antimicrobial influences, including against two major and representative cutaneous and mucosal pathogens: Staphylococcus aureus and Candida albicans. C-MSH peptides had antimicrobial effects against S. aureus and significantly reversed the enhancing effect of urokinase on S. aureus colony formation. α-MSH and other amino acid sequences reduced C. albicans viability and germination. α-MSH peptides also enhanced C. albicans killing by human neutrophils. The antimicrobial agent is selected from the group consisting of one or more peptides including the amino acid sequence KPV, one or more peptides including the amino acid sequence MEHFRWG, or a biologically functional equivalent of any of the foregoing. The most effective of the peptides were those bearing the C-terminal amino acid sequence of α-MSH, i.e., α-MSH (1-13), (6-13), and (11-13). The α-MSH “core” sequence (4-10), important for melanotropic effects, was also effective but significantly less potent. Antimicrobial influences of α-MSH peptides could be mediated by their well-known capacity to increase cellular cAMP; this messenger was significantly augmented in peptide-treated yeast. α-MSH has potent anti-inflammatory effects and is expected to be useful for treatment of inflammation in human and veterinary disorders. Reduced killing of pathogens is a detrimental consequence of therapy with corticosteroids and nonsteroidal anti-inflammatory drugs during infection. Therefore, anti-inflammatory agents based on α-MSH peptides that do not reduce microbial killing, but rather enhance it, would be very useful. The antimicrobial effects of these α-MSH peptides occurred over a broad range of concentrations including the physiological (picomolar) range.

The present invention relates to methods and compositions designed for the treatment, management, or prevention of cancer, particularly, metastatic cancer. In one embodiment, the methods of the invention comprise the administration of an effective amount of an antibody that binds to EphA2 and agonizes EphA2, thereby increasing EphA2 phosphorylation and decreasing EphA2 levels. In other embodiments, the methods of the invention comprise the administration of an effective amount of an antibody that binds to EphA2 and inhibits cancer cell colony formation in soft agar, inhibits tubular network formation in three-dimensional basement membrane or extracellular matrix preparation, preferentially binds to an EphA2 epitope that is exposed on cancer cells but not non-cancer cells, and / or has a low Koff, thereby, inhibiting tumor cell growth and / or metastasis. The invention also provides pharmaceutical compositions comprising one or more EphA2 antibodies of the invention either alone or in combination with one or more other agents useful for cancer therapy.