86 results about "Cell cycle progression" patented technology

The invention involves methods of inhibiting the cancer cell cycle to make cancer cells more susceptible to chemotherapeutic agents. In particular, inhibition of CDK4 and/or CDK6 inhibits cell cycle progression in cancer cells. When combined with chemotherapy such cell cycle inhibition can effectively treat even aggressive cancer types that are drug-resistant and intractable to most chemotherapies.

The p21 gene encodes a cyclin dependent kinase inhibitor which affects cell cycle progression, but the role of this gene product in altering tumor growth has not been established. The present inventors have now discovered that the growth of malignant cells in vivo is inhibited by expression of p21. Expression of p21 resulted in an accumulation of cells in G0/G1, alteration in morphology, and cell differentiation.

The present invention relates to a method of determining the presence of a retinoblastoma protein (Rb)-mediated cancerous or pre-cancerous condition in a sample of fixed cells that involves exposing the sample to an antibody that recognizes phosphorylation of serine on the retinoblastoma protein (pS-Rb), and identifying cells in the sample that are recognized by the anti-O body to pS-Rb, where the recognition of pS-Rb in the sample determines the presence of an Rb-mediated cancerous or pre-cancerous condition. The method also involves identifying the presence of specific cell cycle markers and positive and negative cell cycle regulators to assess the stage of disease progression in a cancer patient having an (Rb)-mediated cancer. The present invention also relates to methods of assessing the efficacy of cancer therapy for an Rb-mediated cancer, determining the mechanism of cell cycle progression in an Rb-mediated cancer, and identifying cells predisposed to developing an Rb-mediated cancerous condition.

Inositol hexaphosphate (IP-6) is a polyphosphorylated carbohydrate with potent antioxidant activity to prevent active oxygen species-mediated mutagenesis, cell injury and carcinogenesis. IP-6 also activates DNA repair mechanisms. Sublethal radiation causes DNA damage through the formation of free radicals, reactive oxygen species, and pyrimidine crosslinks leading to cellular proliferation, cell cycle arrest and apoptosis. In the skin it results in the induction of skin cancer, premature skin aging, immuno-suppression, inflammation, and cell death. Likewise sublethal exposure to ionizing radiation as in nuclear blasts (war-time, accidental, terrorist-induced etc), cosmic radiation, etc. also causes the same spectrum of damage to the cells and the organisms with acute symptoms and eventual high risk of many cancers. IP-6 and/or inositol and their pharmaceutically acceptable salts and derivatives, including pyrophosphates and citrate derivatives, significantly counteract the harmful effects of radiation, affecting cell cycle progression in a protective manner (more cells in the protective GI phase) as well as decreasing apoptosis and caspase-3 activation. Various salts of IP-6 are used with comparable efficacy and the combination of IP-6+inositol affords the best protection against radiation-induced cell injury. Thus IP-6 and inositol are effective agents for protection against nuclear, solar and other radiation injuries.

The present invention provides a cell imaging technique for automatically tracking the progression of a cell through the cell cycle over time through segmentation of a volume of two-dimensional time-lapse images. The technique allows long-term tracking of the cell cycle progression of an individual cell or multiple cells. Further, the invention provides a unique display of cell cycle progression, allowing an end user to easily determine changes to cell cycle progression for a cell of interest.

In one aspect, a method is provided of inhibiting proliferation of a mammalian cell comprising introducing into said cell an effective amount of at least one microRNA-specific inhibitor of at least one miR-106b family member. In another aspect a method is provided for accelerating proliferation of a mammalian cell comprising introducing into said cell an effective amount of at least one miR-106b family member.

The invention discloses the specificity marker protein TS/MEDP antibody preparation and the purpose. The molecular biology technology is utilized, and a new gene is cloned in a stomach cancer cell and is named as TS/MDEP. A polyclonal antibody for preventing the TS/MDEP is prepared, and a high specificity antibody is acquired through the antibody purification technology. The expression characteristics of the TS/MDEP gene in a tumor cell line and a tumor cell tissue are verified from the mRNA and protein level, the expression in 14 tumor cell lines including the tumor cell line is determined, the dependance of cell cycle is assumed, the excess expression exists in stomach cancer, breast cancer and cervical cancer tissues, no expression is in the corresponding normal tissues, and the expression exists in an embryo tissue. The high expression of the TS/MDEP in the embryo tissue with exuberant cell proliferation is validated, after growing up, the gene is closed, and the high expression exists in the tumor cells. The TS/MDEP has the seasonal specificity expression to clew the occurrence and the development of the cell cycle control abnormity caused by the high expression of the TS/MDEP. The obtained antibody for preventing the TS/MDEP can be used to monitor the cell cycle advancement and the clinical biological behavior of the gastroenteric tumor.

The present invention relates to immortalized avian cell lines suitable for production of biologicals or viruses for vaccination. In particular, the cell lines are derived from primary cells which are transformed with at least two viral or cellular genes, one of which causes cell cycle progression whereas the other interferes with innate protective mechanisms of the cell induced by dysregulated replication. The invention moreover relates to the production of said immortalized cell lines and their use for producing biologicals or viruses for vaccination.

The present invention discloses certain diterpenes that can be used to inhibit androgen receptor activity, induce apoptosis and block cell cycle progression of androgen receptor-dependent cells. Androgen receptor has been associated with various diseases such as prostate cancer, androgeneic alopecia, breast cancer, acne etc. Accordingly, the present invention further discloses methods of treating androgen receptor-associated diseases by administering the disclosed diterpenes.

A product and process for extending the replicative capacity of metazoan somatic cells using targeted genetic amendments to abrogate inhibition of cell-cycle progression during replicative senescence and derive clonal cell lines for scalable applications and industrial production of metazoan cell biomass. An insertion or deletion mutation using guide RNAs targeting the first exon of the transcript encoding each protein is created using CRISPR/Cas9. Targeted amendments result in inactivation of p15 and p16 proteins which increases the proliferative capacity of the modified cell populations relative to their unaltered parental populations. Combining these amendments with ancillary telomerase activity from a genetic construct directing expression of a telomerase protein homolog from a TERT gene, increases the replicative capacity of the modified cell populations indefinitely. One application is to manufacture skeletal muscle for dietary consumption using cells from the poultry species Gallus gallus; another is from the livestock species Bos taurus.

The invention describes human genes involved in cell cycle progression, including mitosis and meiosis. The invention also relates to the use of these “cell cycle progression” genes and proteins in the modulation of cell cycle progression in cells and methods for identifying modulators of these genes or proteins and hence modulators of mitosis and meiosis.

It is an object of the present invention to provide methods and compositions for protection of subjects from acute kidney injury by treating the subject with compounds that modulate the cell cycle. Modulating the cell cycle can comprise inducing G₀/G₁ cell cycle arrest, and/or inducing cell cycle progression. As demonstrated below, even a single administration of a compound which induces G₀/G₁ cell cycle arrest can protect subjects from AKI, and may be used prophylactically in advance of, or as a treatment following, various treatments or conditions that are known to be injurious to the kidney, followed optionally by release of the arrest. Once AKI is established, cell cycle progression can be induced to increase replacement of lost and damaged cells

The invention pertains to novel cyclin dependent kinase inhibitors (cdks) and specifically, but not exclusively, as inhibitors of cdk/cyclin complexes. As described herein, the inhibitors of this invention are capable of inhibiting the cell-cycle machinery and consequently may be useful in modulating cell-cycle progression, ultimately controlling cell growth and differentiation. Such compounds would be useful for treating subjects having disorders associated with excessive cell proliferation.

The invention discloses application of rabdocetsin in preparing a product for inhibiting proliferation of esophageal squamous carcinoma cells. Proofed by experiment, the application has the advantages that the rabdocetsin can effectively inhibit the proliferation of the esophageal squamous carcinoma cells, the cloning formation of the esophageal squamous carcinoma cells, affecting the cycle progress of the esophageal squamous carcinoma cells, inducing the retardation of the cycle of the esophageal squamous carcinoma cells, inhibiting the DNA (deoxyribonucleic acid) restoration of the esophageal squamous carcinoma cells, inducing the withering of the esophageal squamous carcinoma cells, regulating up the expression amount of cleaved-caspase-9, regulating up the expression amount of cleaved-caspase-3, regulating up the expression amount of cleaved-PARP, inhibiting Akt signal pathways, inhibiting NF-kappa B signal pathways, and inhibiting the growth of tumors caused by the esophageal squamous carcinoma cells; the important application value is realized.

A method of tracking a cell through a plurality of images includes selecting the cell in at least one image obtained at a first time, generating a track of the cell through a plurality of images, including the at least one image, obtained at different times using a backward tracking, and generating a cell tree lineage of the cell using the track.

Described herein are novel polyglycerol-amine polymeric nanocarriers in complex with microRNAs and their uses in the treatment of cancer, in particular glioblastoma. Delivery of the polymeric nanocarriers in complex with microRNAs in cell lines and in vivo inhibited cell proliferation, cell cycle progression, cell migration and tumor growth.

The invention provides application of Nifeviroc in preparing an antitumor drug, and provides an antitumor drug containing Nifeviroc. As is proved by cell experiments, after Nifeviroc acts on tumor cells, the cell cycle progress can be interfered, and the cell growth is inhibited, so that the cell cycle is stagnant at the G0-G1 stage; meanwhile, cell apoptosis can also be induced by increasing theactive oxygen content in the cells and lowering the mitochondrial membrane potential; meanwhile, Nifeviroc has an obvious effect of inhibiting invasion and metastasis of the tumor cells, by inhibitingadhesive power of the tumor cells to an extracellular matrix, the directed migration capability, the non-targeted migration capability and the in-vitro invasion capability of the cells are lowered, and the increase in size of the tumors in vivo can also be inhibited. As can be seen, Nifeviroc has a good effect of resisting the activity of the tumor, can be used for preparing the antitumor drug, does not have an obvious side effect, and has a good application prospect.

The present disclosure is directed to compositions and methods which utilize the tetracycline scaffold, preferably the scaffold of tetracycline or minocycline, and which significantly lack antibiotic activity. The compounds have neuroprotective attributes without interfering with the drugs capacity to pass through the blood brain barrier. These compounds have neuroprotective activity because of their inhibition of neuronal cell cycle progression. The compounds are characterized in part by a fifth ring joining positions 9 and 10.

The invention belongs to the fields of biotechnology and medicine, and relates to an inhibitor capable of inhibiting the excessive proliferation of keratinocytes, an inhibitor composition, and applications of the inhibitor. The inhibitor taking triptolide, triptonide or tripterine as the representative can inhibit the excessive proliferation of the keratinocytes, specifically, the expression levels of STAT1 and p-STAT1 can be inhibited, then the expression level of miR-17-92mRNA is down-regulated, then, miR-17-92 target gene CDKN2B is regulated, the secretion levels of inflammatory factors CXCL1, CXCL10, CXCL16 and IL-6 in cells are inhibited, and finally, the cell cycle progression and immune function abnormity are inhibited; triptolide, tripterine and triptonide can effectively inhibit the proliferation of the keratinocytes, and the effective doses respectively achieve 60nM, 100nM and 80nM.