42 results about "Precancerous Cells" patented technology

The invention relates to a CRISPR/Cas9 enrichment sequencing method applied in large-scale screening of cancer genes. Firstly, an sgRNA library is established; then the sgRNA library is packaged by lentiviruses, and viruses are collected; the sgRNA library is screened in a cancer cell line, the obtained cells are extracted and screened, and genome DNAs of precancerous cells are screened; finally, enrichment of sgRNAs in the genome DNAs is carried out. When the provided method is compared with the prior art, the screening process of CRISPR/Cas9 cells is improved, the virus infection efficiency is determined and the virus MOI value is determined through a simple method and by utilization of puromycin resistance of infected cells, importantly, the restriction enzyme cutting method and a high flux method are combined, correct chromatin fragments can be obtained effectively, false positive caused by non-specific PCR amplification can be lowered, a DNA template of sgRNAs can be amplified efficiently, and a library establishment efficiency is raised.

Therapeutic methods for inhibiting the growth of preneoplastic/neoplastic vertebrate cells that abnormally express MN protein are disclosed. Screening assays are provided for identifying compounds, preferably organic compounds, preferably aromatic and heterocylic sulfonamides, which inhibit the enzymatic activity of MN/CA IX and that are useful for treating patients with preneoplastic/neoplastic disease. Further, the CA IX-specific inhibitors when labeled or linked to an appropriate visualizing means can also be used diagnostically/prognostically for preneoplastic/neoplastic disease, and for imaging use, for example, to detect hypoxic precancerous cells, tumors and/or metastases, by selectively binding to activated CA IX, preferably CA IX activated under hypoxic conditions, and not to inactive CA IX. Such detection of hypoxic conditions can be helpful in determining effective treatment options, and in predicting treatment outcome and the prognosis of disease development. Still further, the CA IX-specific inhibitors can be used therapeutically to selectively target hypoxic cells expressing activated CA IX. The CA IX-specific inhibitors can be labelled or conjugated to radioisotopes for radiotherapy of hypoxic cells. Alternatively, the CA IX-specific inhibitors can be used for gene therapy coupled to vectors for targeted delivery to hypoxic preneoplastic/neoplastic cells expressing activated CA IX on their surfaces. In an alternative mode of the invention, CA IX-specific inhibitors may be used therapeutically to target acidic conditions of a tumor, e.g., to increase pHe in order to enhance the efficacy of weak base chemotherapeutic drugs.

The present invention provides compositions and methods for the treatment of cancer, and is predicated at least in part on the use of gene fusion regions as therapeutic targets. The fusion region target may be physically embodied at the level of DNA, RNA or protein. Typically the fusion region is specific to cancerous or precancerous cells, meaning that any therapy directed to the target may not significantly affect non-cancerous tissue. The fusion region may be targeted by protein or nucleic acid molecules capable of specifically binding to the region.

Conventional cancer immunotherapy falls short at efficiently expanding T cells that specifically target cancerous cells in numbers sufficient to significantly reduce the tumor size or cancerous cell number in vivo. To overcome this limitation, provided herein are nanoparticles coated with MHC class I and/or class II molecules presenting tumor-specific antigens and co-stimulatory molecules and their use to expand antigen-specific anti-tumorigenic T cellsto levels not achieved in current immunotherapeutic techniques. These antigen-specific anti-tumorigenic T cells include cytotoxic T cells, effector T cells, memory T cells, and helper T cells that are necessary to initiate and maintain a substantial immune response against metastatic or non- metastatic cancerous, pre-cancerous, or neoplastic cells in vivo.; The present invention describes a systemic approach to targeting cancerous or pre-cancerous cells that are circulating cells, as in lymphomas, migratory metastatic cells, and solid tumors.

A method for determining if a subject with cancer or precancerous lesions or a benign tumor, will respond to treatment with an inhibitor selected from the group comprising an inhibitor of one or more enzymes in the mevalonate pathway, an inhibitor of geranylgeranyl transferase, an inhibitor of farnesyl transferase or an inhibitor of squalene synthase, by (i) obtaining a sample of the cancer cells, precancerous cells or benign tumor cells from the subject, (ii) assaying the cells in the sample for the presence of a mutated p53 gene or a mutant form of p53 protein or a biologically active fragment thereof, and (iii) if the cells have the mutated p53 gene or mutant form of the p53 protein, then determining that the subject will respond to treatment with the inhibitor or combinations thereof. Some embodiments are directed to treatment with the inhibitors.

The present invention provides a pharmaceutical composition that includes a) one or both of i) a peptide ligand that binds a zeta receptor and ii) at least one cancer chemotherapeutic agent; and b) a sustained release formulation. The invention also provides a combination including at least a portion of a tissue comprising one or more cells harboring a zeta receptor, such as a cancer cell or a precancerous cell, in contact with a pharmaceutical composition of the invention. Additionally the invention provides a method of treating a pathology that responds to a peptide ligand that binds a zeta receptor that includes a step of contacting a tissue characteristic of the pathology and containing cells harboring a zeta receptor, with a pharmaceutical composition of the invention. The invention further provides methods of inhibiting proliferation or metastasis of a cancer in a subject, including a) surgically excising a tumor characterizing the cancer from the subject; b) ensuring maximal removal of a tumor margin from the tumor site; and c) disposing a pharmaceutical composition of the invention upon a tissue remaining at a tumor margin wherein the tissue contains one or more tumor cells (such as a cancer cell or a precancerous cell) harboring a zeta receptor. The peptide ligand of a zeta receptor may be an enkephalin, an endorphin, a dynorphin, or a derivative thereof. Additionally the pharmaceutical composition may include one or more cancer chemotherapeutic agents.

The present invention provides a method for predicting whether an individual (e.g., patient) will benefit from a (one or more) treatment for cancer comprising determining the amount of p66-Shc present in cancerous cells or precancerous cells (e.g., displasia) of the individual. If the amount of p66-Shc present in the cells of the individual is lower than the amount of p66-Shc in a control, then the individual will likely benefit from the treatment.

The present invention provides novel tricyclic spiro-oxathiine naphthoquinone derivatives, a synthetic method for making the derivatives, and the use of the derivatives to induce cell death and/or to inhibit proliferation of cancer or precancerous cells. The naphthoquinone derivatives of the present invention are related to the compound known as β-lapachone (3,4-dihydro-2,2-dimethyl-2H-naphtho(1,2-b)pyran-5,6-dione).

Supramolecular assemblies for delivering active agents to cancerous or precancerous tissues in a subject are provided. These supramolecular assemblies are also useful in assays for detecting and imaging of cancerous and precancerous cells. The assemblies are protease-sensitive and comprise a peptide linkage containing a protease consensus sequence. The assemblies can be selectively targeted to cancerous tissue where the protease enzymes degrade the peptide linkage thereby releasing the active agents which were physically or mechanically contained in or retained by the supramolecular assembly.

The present invention provides a universal system that detects cancer cells at all stages including early developmental stages as well as matured cancerous tumors. The system relates to monitoring the environment surrounding abnormally metabolizing cells, e.g., predominantly glycolytic cells, cancerous cells, precancerous cells, and/or cells with reduced mitochondrial Electron Transport Chain activity. Nanosensors detect chemical signatures of the organic compounds released by cancer cells into bodily fluids or to the air to detect cancerous or precancerous metabolisms in samples such as urine, saliva, sweat, blood or breath. Treatments provided in recognition of the signature metabolic changes occurring in cancer cells target the abnormal metabolism generally with special emphasis relating to changed mitochondrial metabolism and cell survivability. The treatments include, but are not limited to: therapeutic compositions and methods for treating, delaying, slowing or preventing one or more cancers.

The invention provides use of a CDK inhibitor in preparation of drugs for inducing aging of precancerous cells of an object, use of the CDK inhibitor in preparation of drugs for preventing or treating a precancerous lesion or cancer of the object, and use of the CDK inhibitor in preparation of drugs for inducing immune response of the object to aged cells.

A method for automated detection, monitoring and treatment of dysplasia by analyzing 3D reconstructed images of cells obtained from a specimen includes a biological specimen classifier that classifiescells from the sputum specimen as normal or abnormal. If abnormal cells are detected, then the abnormal cells are further classified as pre-cancerous or cancerous. Pre-cancerous cells are further sub-classified as being of glandular origin or squamous origin (dysplastic cells). This information would be used to define patient therapy so that if the cells are classified as dysplastic, then a cancer chemoprevention pharmaceutical like iloprost is administered to the subject over a predetermined time period to achieve a therapeutic dosage, and if only malignant cells were found or malignant andpre-cancerous cells were found, then next steps would involve patient triage to biopsy and surgery and possibly use of a cancer chemoprevention pharmaceutical.