65 results about "Small-cell carcinoma" patented technology

A targeted osmotic lysis (TOL) of tumor cells that over-express voltage-gated sodium channels (VGSCs) has been developed that uses a combined therapy of a drug that blocks sodium, potassium-adenosine triphosphatase (Na+, K+-ATPase) that is then followed by an activation of VGSCs, for example, by electrical or pharmacological stimulation. Activation of VGSCs conducts sodium into the cancer cells in much greater amounts than non-cancer cells. Water follows this sodium gradient into the cancer cells, causing swelling and lysis. Because non-cancerous cells do not over-express VGSCs, less sodium and less water will enter the cells, and the non-cancerous cells will not lyse. This method is applicable to all cells that over-express VGSCs, including, but not limited to, highly invasive breast cancer, prostate cancer, small cell lung cancer, non-small cell lung carcinoma, lymphoma, mesothelioma, neuroblastoma, and cervical cancer.

The present invention provides fusion proteins for the detection and treatment of neuroectodermal tumors. Previous work demonstrated that chlorotoxin is specific for glial-derived or meningioma-derived tumor cells. The current invention has extended the use of chlorotoxin-cytotoxin fusion proteins to treat the whole class neuroectodermal tumors such as gliomas, meningiomas, ependymonas, medulloblastomas, neuroblastomas, gangliomas, pheochromocytomas, melanomas, PPNET's, small cell carcinoma of the lung, Ewing's sarcoma, and metastatic tumors in the brain. Also, diagnostic methods are provided for screening neoplastic neuroectodermal tumors.

An object of the present invention is to provide a method for detecting the oral squamous-cell carcinoma including the vicious degree through the change of the genome structure in the oral squamous-cell carcinoma as the index. The invention uses the genome structure in the oral squamous-cell carcinoma as the index, for detecting the oral squamous-cell carcinoma including the vicious degree. In addition, in the oral squamous-cell carcinoma, through recovering the deactivated gene, the multiplication of the oral squamous-cell carcinoma can be restrained.

The present invention relates to monoclonal antibody 1A7. This is an anti-idiotype produced by immunizing with an antibody specific for ganglioside GD2, and identifying a hybridoma secreting antibody with immunogenic potential in a multi-step screening process. Also disclosed are polynucleotide and polypeptide derivatives based on 1A7, including single chain variable region molecules and fusion proteins, and various pharmaceutical compositions. When administered to an individual, the 1A7 antibody overcomes immune tolerance and induces an immune response against GD2, which comprises a combination of anti-GD2 antibody and GD2-specific T cells. The invention further provides methods for treating a disease associated with altered GD2 expression, particularly melanoma, neuroblastoma, glioma, soft tissue sarcoma, and small cell carcinoma. Patients who are in remission as a result of traditional modes of cancer therapy may be treat with a composition of this invention in hopes of reducing the risk of recurrence.

In accordance with the invention, a novel gene translocation, (4p15, 6q22), in human non-small cell lung carcinoma (NSCLC) that results in a fusion proteins combining part of Sodium-dependent Phosphate Transporter Isoform NaPi-3b protein (SLC34A2) with Proto-oncogene Tyrosine Protein Kinase ROS Precursor (ROS) kinase has now been identified. The SLC34A2-ROS fusion protein is anticipated to drive the proliferation and survival of a subgroup of NSCLC tumors. The invention therefore provides, in part, isolated polynucleotides and vectors encoding the disclosed mutant ROS kinase polypeptides, probes for detecting it, isolated mutant polypeptides, recombinant polypeptides, and reagents for detecting the fusion and truncated polypeptides. The disclosed identification of the new fusion protein enables new methods for determining the presence of these mutant ROS kinase polypeptides in a biological sample, methods for screening for compounds that inhibit the proteins, and methods for inhibiting the progression of a cancer characterized by the mutant polynucleotides or polypeptides, which are also provided by the invention.

Methods are disclosed herein for treating a subject with a lung cancer. The lung cancer can be small cell carcinoma of the lung or non-small cell carcinoma of the lung.The methods include locally administering to the subject a therapeutically effective amount of the polyketal particle comprising a CpG oligodexoynucleotide. Optionally, the polyketal particle can include an imidazoquinoline compound.

It is an object to be achieved by the present invention to provide a method for detecting cancer and a cell growth inhibiting agent by the identification of genes exhibiting characteristic behavior in cancers such as oral squamous-cell carcinoma. The present invention provides a method for detecting cancer, which comprises detecting at least one gene alteration existing in chromosomal region 4q35 in a specimen.

The invention provides an in vitro method for predicting clinical outcome of a patient affected with a non-small cell lung carcinoma (NSCLC), which method comprises determining the expression level of at least 8 genes in a biological sample of said patient.

The invention discloses an application of chlorogenic acid or coumaroyl guinic acid in preparation of medicines for treatment of squamous-cell carcinoma and provides a chlorogenic acid composition andan application thereof for treatment of the squamous-cell carcinoma. The chlorogenic acid and coumaroyl guinic acid can effectively treat the squamous-cell carcinoma; by combining the two components,a composition can effectively treat the squamous-cell carcinoma with synergistic effect, so that the products have excellent application prospect.