965 results about "Cell cycle" patented technology

Methods and compositions for identifying high-grade cervical disease in a patient sample are provided. The methods of the invention comprise detecting overexpression of at least one biomarker in a body sample, wherein the biomarker is selectively overexpressed in high-grade cervical disease. In particular claims, the body sample is a cervical smear or monolayer of cervical cells. The biomarkers of the invention include genes and proteins that are involved in cell cycle regulation, signal transduction, and DNA replication and transcription. In particular claims, the biomarker is an S-phase gene. In some aspects of the invention, overexpression of a biomarker of interest is detected at the protein level using biomarker-specific antibodies or at the nucleic acid level using nucleic acid hybridization techniques. Kits for practicing the methods of the invention are further provided.

Antisense oligomers directed to bacterial cell division and cell cycle-encoding nucleic acids are capable of selectively modulating the biological activity thereof, and are useful in treatment and prevention of bacterial infection. The antisense oligomers are substantially uncharged, and contain from 8 to 40 nucleotide subunits, including a targeting nucleic acid sequence at least 10 nucleotides in length which is effective to hybridize to (i) a bacterial tRNA or (ii) a target sequence, containing a translational start codon, within a bacterial nucleic acid which encodes a protein associated with cell division or the cell cycle. Such proteins include zipA, sulA, secA, dicA, dicB, dicC, dicF, ftsA, ftsI, ftsN, ftsK, ftsL, ftsQ, ftsW, ftsZ, murC, murD, murE, murF, murG, minC, minD, minE, mraY, mraW, mraZ, seqA, ddlB, carbamate kinase, D-ala D-ala ligase, topoisomerase, alkyl hydroperoxide reductase, thioredoxin reductase, dihydrofolate reductase, and cell wall enzyme.

This invention relates to single session image guided all field simultaneous radiation therapy combined with hyperthermia. Hyperthermia renders the radiation resistant cells as more radiation sensitive cells. The high and super-high dose rate radiation greatly improves the RBE of the photon radiation. It also minimizes photon radiation therapy's OER and cell cycle dependent tumor cell kill by minimizing the repair capacity of cell after photon radiation. Single session hyperthermia and radiation therapy overcomes the thermotolerance-associated inefficiency of hyperthermia treatment as it is when hyperthermia is combined with fractionated, lower dose rate radiation. The synergetic effects of sublethal damage repair inhibiting single session hyperthermia-combined with high dose and dose rate single session radiation therapy, and combined chemotherapy brings the photon radiation therapy's tumor cure and control capabilities closer to high LET radiation therapy.

Novel substituted azole diones are provided that kill cells, suppress cell proliferation, suppress cell growth, abrogate the cell cycle G2 checkpoint and / or cause adaptation to G2 cell cycle arrest. Methods of making and using the invention compounds are provided. The invention provides substituted azole diones to treat cell proliferation disorders. The invention includes the use of substituted azole diones to selectively kill or suppress cancer cells without additional anti-cancer treatment. The invention includes the use of cell cycle G2-checkpoint-abrogating substituted azole diones to selectively sensitize cancer cells to DNA damaging reagents, treatments and / or other types of anti-cancer reagents.

The invention relates to small molecules which function as inhibitors of the interaction between p53 and MDM2. The invention also relates to the use of these compounds for inhibiting cell growth, inducing cell death, inducing cell cycle arrest and / or sensitizing cells to additional agent(s).

Methods and compositions for evaluating the prognosis of a breast cancer patient, particularly an early-stage breast cancer patient, are provided. The methods of the invention comprise detecting expression of at least one, more particularly at least two, biomarker(s) in a body sample, wherein overexpression of the biomarker or a combination of biomarkers is indicative of breast cancer prognosis. In some embodiments, the body sample is a breast tissue sample, particularly a primary breast tumor sample. The biomarkers of the invention are proteins and / or genes whose overexpression is indicative of either a good or bad cancer prognosis. Biomarkers of interest include proteins and genes involved in cell cycle regulation, DNA replication, transcription, signal transduction, cell proliferation, invasion, proteolysis, or metastasis. In some aspects of the invention, overexpression of a biomarker of interest is detected at the protein level using biomarker-specific antibodies or at the nucleic acid level using nucleic acid hybridization techniques.

Methods and systems for recording and mapping lineage information and molecular events in individual cells are provided. Molecular changes, which may result from random or specific molecular events, are introduced to defined regions in cells over multiple cell cycle generations. Techniques such as fluorescent imaging are applied to track and identify the molecular changes before such information is used for lineage analysis or for identifying key processes and key players in cellular pathways.

The present invention concerns methods for treating cell proliferative diseases, tumors associated with viral infections, and certain viral infections. The disclosed methods use compounds which inhibit heat shock protein 90 proteins. Such methods block Rb negative or deficient cells in the G2 / M phase of the cell cycle and rapidly causes their destruction.

A novel gene 65B13 expressed specifically and transiently in dopaminergic neuron precursor cells immediately after cell cycle exit was obtained by the present invention. The cellular expression of 65B13 can be used as an index to select cells that are suitable in terms of their safety, survival rate, and network formation ability, for transplant therapy of neurodegenerative diseases such as Parkinson's disease.

The present invention relates to chemical compounds having a general formula Iwherein A1, A2, C1, C2, D, L1, L2, Z and R1-8 are defined herein, and synthetic intermediates, which are capable of modulating various protein kinase receptor enzymes and, thereby, influencing various disease states and conditions related to the activities of such kinases. For example, the compounds are capable of modulating Aurora kinase thereby influencing the process of cell cycle and cell proliferation to treat cancer and cancer-related diseases. The invention also includes pharmaceutical compositions, including the compounds, and methods of treating disease states related to the activity of Aurora kinase.

The present invention discloses novel mechanisms in the aging process and describes novel methods for high-throughput screening to identify, detect, and purify agents to be used for improving mitochondrial function, maintaining the cell cycle-arrested state in senescent and post mitotic cells, and thus preventing or treating age-related diseases or disorders associated with accelerated mitochondrial function loss, telomere dysfunction, and / or deterioration of the growth-arrested state. The present invention also discloses a number of compounds or compositions identified from this method. The present invention further provides the use of low doses of rapamycin or its analogs as a mimic of caloric restriction in preventing age-related diseases or disorders.

Disclosed herein are methods and uses for preventing melanoma, reducing progression of atypical nevi, and inducing cell cycle arrest and / or apoptosis in a melanoma cell through oral and enteral administration of sulforaphane to subjects indicated to be at risk due to factor(s) such as medical history of atypical nevi, melanoma, or UV exposure. Sulforaphane can be administered orally as a safe and well-tolerated natural agent as a chemopreventive strategy in individuals with atypical melanocytic nevi.

The invention relates to small molecules which function as inhibitors of the interaction between p53 and MDM2. The invention also relates to the use of these compounds for inhibiting cell growth, inducing cell death, inducing cell cycle arrest and / or sensitizing cells to additional agent(s).

The invention discloses a micro-fluidic chip detection system based on single-cell multi-parameter representation. The micro-fluidic chip detection system mainly comprises a micro-fluidic chip, an optical detection module, an impedance detection module and a processor, wherein the micro-fluidic chip is formed by sequentially aligning and bonding three layers of substrates, two symmetrical transport focusing runners and two symmetric outlet runners are arranged on the runner layer, a cross-shaped structure is formed by a junction of the two transport focusing runners and the outlet runners, electrodes of the upper layer of substrate and the lower layer of substrate are oppositely arranged to form a counter electrode structure, and each of the two outlet runners is provided with the counter electrode structure. According to the micro-fluidic chip detection system disclosed by the invention, a plurality of parameter of a single cell can be simultaneously represented, the accuracy and the sensitivity of cell detection are improved, a sheath liquid is not needed, and complex immunolabelling pretreatment is not needed. The micro-fluidic chip detection system has the advantages of low cost, simplicity in operation, high flux, high integration and automation degree and the like. The micro-fluidic chip detection system disclosed by the invention can be widely applied to the fields of cell cycle, cell differentiation, drug screening, early diagnosis and treatment of illnesses, and the like.

Pharmaceutical compositions and compounds are provided. The compounds of the invention demonstrate anti-proliferative activity, and may promote apoptosis in cells lacking normal regulation of cell cycle and death. In one embodiment of the invention, pharmaceutical compositions of the compounds in combination with a physiologically acceptable carrier are provided. The pharmaceutical compositions are useful in the treatment of hyperproliferative disorders, which disorders include tumor growth, lymphoproliferative diseases, angiogenesis. The compounds of the invention are substituted pyrazoles and pyrazolines.

The present invention relates to chemical compounds having a general formula I wherein A1, A2, C1, C2, D, L1, L2, Z and R1- are defined herein, and synthetic intermediates, which are capable of modulating various protein kinase receptor enzymes and, thereby, influencing various disease states and conditions related to the activities of such kinases. For example, the compounds are capable of modulating Aurora kinase thereby influencing the process of cell cycle and cell proliferation to treat cancer and cancer-related diseases. The invention also includes pharmaceutical compositions, including the compounds, and methods of treating disease states related to the activity of Aurora kinase.

This application discloses plant polynucleotide sequences encoding polypeptide regulators of plant growth and reproduction, and their methods of use.

The present invention relates to chemical compounds having a general formula Iwherein A, B, C1, C2, D, L1, L2 and R3-4 are defined herein, and synthetic intermediates, which are capable of modulating various protein kinase receptor enzymes and, thereby, influencing various disease states and conditions related to the activities of such kinases. For example, the compounds are capable of modulating Tie-2 and Aurora kinase enzymes thereby influencing angiogenesis and the process of cell cycle and cell proliferation, respectively, to treat cancer and cancer-related diseases. The invention also includes pharmaceutical compositions, including the compounds, and methods of treating disease states related to the activity of various protein kinases.

The present invention includes compositions, methods and kits for non-nuclear transfer reprogramming an adult differentiated cell obtained from an adult tissue into an ES-like cell. The reprogrammed cell can be converted into an ES-like cell which can be re- or trans-differentiated into various differentiated cell types. The present invention further relates to identification of a novel signaling pathway, and components thereof, which effect reprogramming of a cell. The present invention further comprises compositions, methods and kits for regulating the mammalian cell cycle and cellular proliferation, as well as for treating diseases and for identifying components that affect the cell cycle, and reprogram cells, among other things.

The invention relates to the field of biotechnology and mainly relates to a use of an early-generation human umbilical cord mesenchymal stem cell exosome in promotion of human bone mesenchymal stem cell growth. The use method is a method for promoting bone mesenchymal stem cell growth. The invention also relates to an extraction method of a human umbilical cord mesenchymal stem cell exosome. The early-generation human umbilical cord mesenchymal stem cell exosome and human bone mesenchymal stem cells are co-cultured so that human bone mesenchymal stem cell growth is obviously promoted, cell doubling time is shortened and a ratio of an S period in a cell period is increased.

This invention discloses the use of an E-selectin antagonist and a mobilizer of hematopoietic stem cells or progenitor cells in methods and compositions for treating or preventing immunocompromised conditions resulting from medical treatment. The present invention is particular relevant for prophylaxis and / or treatment of hematopoeitic disorders including neutropenia, agranulocytosis, anemia and thrombocytopenia in individuals receiving or proposed to receive treatments that target rapidly dividing cells or that disrupt the cell cycle or cell division.

The invention relates to small molecules which function as inhibitors of the interaction between p53 and MDM2. The invention also relates to the use of these compounds for inhibiting cell growth, inducing cell death, inducing cell cycle arrest and / or sensitizing cells to additional agent(s).

A method of cellular evaluation based on the electronic nature of cells is reveled though cellular reproductions use of a magnetic force. The dynamic process of nuclear response is shown to be electronic in nature relative to DNA mediating electrons hydrogen bonding in bases pairing of DNA though out the a cell cycle and finally during metaphase one see the magnetic component of interaction. The electrostatic understanding of magnetic force is not well defined in physics in the process of electrodynamic. Cells use electrodynamic interaction within the cell are being studied as the basis and using the cell to measure and define electrodynamic interaction with the system that is biological a call. Specifically DNA thought the electronic interaction interactions. It appears infrared spectrum holds promises to help in revel these mechanisms. The promise of understanding or merely evaluation of electrodynamic interaction holds great promise to science with the greatest medical implication to understand genomic responses in cells. Understanding how the DNA interacts within a cell dynamic transition are known to take place and these are regulated thought electrodynamic interaction.

An improved method of nuclear transfer involving the transplantation of differentiated donor cell nuclei into enucleated oocytes of a species different from the donor cell is provided. The resultant nuclear transfer units are useful for the production of isogenic embryonic stem cells, in particular human isogenic embryonic or stem cells. These embryonic or stem-like cells are useful for producing desired differentiated cells and for introduction, removal or modification, of desired genes, e.g., at specific sites of the genome of such cells by homologous recombination. These cells, which may contain a heterologous gene, are especially useful in cell transplantation therapies and for in vitro study of cell differentiation. Also, methods for improving nuclear transfer efficiency by genetically altering donor cells to inhibit apoptosis, select for a specific cell cycle and / or enhance embryonic growth and development are provided.

The present invention provides methods and pharmaceutical compositions for inhibiting expressions of HIF and HIF regulated genes, inhibiting angiogenesis, inducing cell cycle arrest in tumor cells, and treating cell proliferating diseases or conditions.

Pituitary adenylate cyclase-activating polypeptide (PACAP) and its receptor system can be manipulated positively or negatively to regulate mitosis in neuronal precursor cells. The ligand / receptor system involves PACAP, PACAP receptor, PAC1, and related antagonists. The methods of regulation of the present invention may model be used to define cell cycle regulation in the developing neurons. The present invention may also be used to control or cure diseases related to or caused by damage to or destruction of neuronal cells.

The invention provides, in a general sense, a new labeling strategy employing compounds that are are N2S2 chelates conjugated to a targeting ligand, wherein the targeting ligand is a disease cell cycle targeting compound, a tumor angiogenesis targeting ligand, a tumor apoptosis targeting ligand, a disease receptor targeting ligand, amifostine, angiostatin, monoclonal antibody C225, monoclonal antibody CD31, monoclonal antibody CD40, capecitabine, a COX-2 inhibitor, deoxycytidine, fullerene, herceptin, human serum albumin, lactose, leuteinizing hormone, pyridoxal, quinazoline, thalidomide, transferrin, or trimethyl lysine. The present invention also pertains to kits employing the compounds of interest, and methods of assessing the pharmacology of an agent of interest using the present compounds.

The invention relates to small molecules which function as inhibitors of the interaction between p53 and MDM2. The invention also relates to the use of these compounds for inhibiting cell growth, inducing cell death, inducing cell cycle arrest and / or sensitizing cells to additional agent(s).