34 results about "P53 expression" patented technology

A method of stimulating an immune response to a tumor in an immunocompetent subject by administering a p53 expression construct to a tumor. The construct expresses p53 in tumor cells in an amount sufficient to stimulate an immune response against the tumor. Both viral and non-viral delivery systems are contemplated. The method can be combined with chemotherapy agents as well as with other cancer therapies.

It has been demanded to improve the poor solubility of curcumin to develop an anti-tumor compound capable of inhibiting the growth of various cancer cells at a low concentration. Thus, disclosed is a novel synthetic compound, a bis(arylmethylidene)acetone, which has both of an excellent anti-tumor activity and a chemo-preventive activity. A bis(arylmethylidene)acetone (i.e., a derivative having a curcumin skeleton) which is an anti-tumor compound and has a chemo-preventive activity is synthesized and screened. A derivative having enhanced anti-tumor activity and chemo-preventive activity can be synthesized.

During lung injury, p53 expression increases, inducing plasminogen activator inhibitor-1 (PAI-1) while inhibiting expression of urokinase-type plasminogen activator (uPA) and its receptor (uPAR), resulting in apoptosis of lung epithelial cells (LECs). In the bleomycin lung injury model, p53 and PAI-1 are induced while uPA and uPAR are inhibited. A 20 residue peptide DGIWKASFTTFTVTKYWFYR termed PP-1 (the Cav-1 scaffolding domain) or peptide NYHYLESSMTALYTLGH, termed PP-2, protected LECs from bleomycin-induced apoptosis in vitro and in vivo and prevented subsequent pulmonary fibrosis by attenuating lung epitheilial damage. Pharmaceutical compositions, peptide multimers and deliverable polypeptides comprising the above peptides are dislcosed. The peptides and functional variants, peptide multimers, cell-targeted polyepeptides and pharmaceutical compositions are used in methods for inhibiting apoptosis of injured or damaged lung epithelial cells and for treating acute lung injury and consequent pulmonary fibrosis.

The present invention provides a method for preventing or treating cancer or tumorgenesis disorder comprising administering a prevention or treatment effective amount of a p53 mediated secretome component, such as Gal-3, to a patient in need thereof, thereby preventing or treating cancer or tumorgenesis disorders. Compositions and methods useful for modulating the secretome, including Gal-3, of a cell, comprising increasing extracellular levels of Gal-3, p53 expression, or expression of a downstream effector of p53, in the cell are also provided. Furthermore, methods for identifying tumor targets, diagnostic or prognostic indicators, and therapeutic strategies comprising determining extracellular levels of secreted proteins or secretomes, including Gal-3 are also provided. The present invention provides a novel tumor suppressive mechanism of p53 involving paracrine induction of apoptosis through extracellular Gal-3 levels. The invention also provides evidence that cancer cells are more susceptible to the treatment than normal cells, suggesting augmented expression of the receptor component to Gal3.

A method for the cultivation of human tumor suppressor gene green fluorescent protein carrier, design primers on GENBANK with reference to human anti-cancer gene sequence, collect peripheral blood of early lung cancer patients to extract total RNA, and use reverse transcription polymerase chain reaction (RT-PCR) Amplify the P53 fragment, clone the gene fragment directionally onto the pMD18-T vector, construct the pMD18-P53 recombinant plasmid, identify the recombinant plasmid by PCR amplification, enzyme digestion and sequencing, and digest the pMD18-P53 Identify and extract the directional clone of the P53 target gene into the pEGFP-N1 eukaryotic expression vector to construct the pEGFP-N1-P53 expression vector. The beneficial effects of the present invention are: using the eukaryotic expression vector pEGFP-N1, which is safe, stable, strong in replication, high in expression rate, and easy to detect, as the transport carrier of human anti-cancer genes, thereby constructing a safe, stable, easy-to-detect, safe and reliable The eukaryotic expression vector pEGFP-N1-P53 is used for the prevention and treatment of cancer.

In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.

The present invention relates to the use of p53 gene therapy to treat recurrent cancers in combination with a radio- or chemotherapy. Patients with recurring cancers are treated with a p53 expression construct followed by subsequent radio- or chemotherapy treatment. Viral and non-viral delivery systems, as well as various radio- and chemotherapy regimens are disclosed.

The present invention relates to a new use of Hades as a tumor suppressor target, more particularly to a composition for suppressing tumor comprising an expression or action inhibitor of Hades protein having an amino acid sequence of SEQ ID NO: 2 as an effective ingredient. The present inventors have found that the overexpressed Hades protein interacts with p53 to inhibit the exonuclear mechanism of p53 and the knowdown of Hades induces increase in the expression of p53, demonstrating that Hades is a negative regulator to p53. Therefore, it would be understood that the inhibition of Hades overexpressed in tumor cells contributes to tumor-supressive effects of p53. The drug candidates capable of modulating the expression of the Hades protein, inhibiting the actions of the Hades protein or inhibiting interecation between Hades and p53 are considered a promising anticancer drug.

The invention is based on a finding that silencing CIP2A (KI-AA1524) gene sensitizes cancer cells for apoptosis-inducing activity of certain small molecule chemotherapeutic agents. Thus, the invention is directed to a respective combination therapy, sensitization method and pharmaceutical compositions. The invention further relates to a method of selecting cancer therapy for a subject on the basis of CIP2A and p53 expression and/or protein activity in a sample obtained from said subject.

Methods for the prevention, suppression, and inhibition of growth of a papilloma-virus transformed cell in a hyperplastic lesion using a topically applied p53 expression cassette are disclosed. In addition, there are provided pharmaceutical preparations of a p53 expression cassette suitable for topical delivery to a papillomavirus-transformed cell in a hyperplastic lesion.

The invention relates to the field of biological medicine, in particular to a cell strain capable of inducing and realizing dual-stabilization of P53 expression and a construction method and application thereof. As for the cell strain capable of inducing and realizing the dual-stabilization of the P53 expression, the cell strain U-2OSE6tet6 was collected in China Center for Type Culture Collection on August 12, 2010, and the collection number is CCTCC No: C201075. Experiments prove that the cell strain U-2OSE6tet6 capable of inducing and realizing the dual-stabilization of the P53 expression can indirectly change the P53 content in U-2OSE6tet6 cells by regulating the expression of an E6 gene through doxycycline, and provide an experimental platform for studying relevant action mechanism of the P53 of screening medicaments for treating osteosarcoma.

The invention belongs to the biomedical field and relates to the application of p53 in preparing for a drug preparation for remedying the tumor. A p53 gene coding product is a transcription regulator which can induce the apoptosis or the block of the cell cycle by regulating lower target gene. An over-expression of the p53 can very effectively induce the apoptosis of tumor cells. Attenuated salmonella typhimurium can be used as a carrier to introduce the p53 to express inside the tumor cells and kill the tumor cells. The development of a novel treatment drug which considers the salmonella with the p53 as orally taken gene not only solves the problem of non-injection path of a protein polypeptide drug but also more importantly provides the tumor treatment with a safe, effective, peculiar and economical method.

The invention provides diagnostic, prognostic, and therapeutic uses for detecting COP1 overexpression in a variety of cancers. The methods and uses can further include detecting p53 expression. The invention also provides reagents and kits for use in screening for test compounds that interfere with COP1 and p53 binding.