46 results about "Metastatic lesion" patented technology

To gain a better understanding of tumor angiogenesis, new techniques for isolating endothelial cells (ECs) and evaluating gene expression patterns were developed. When transcripts from ECs derived from normal and malignant colorectal tissues were compared with transcripts from non-endothelial cells, over 170 genes predominantly expressed in the endothelium were identified. Comparison between normal- and tumor-derived endothelium revealed 79 differentially expressed genes, including 46 that were specifically elevated in tumor-associated endothelium. Experiments with representative genes from this group demonstrated that most were similarly expressed in the endothelium of primary lung, breast, brain, and pancreatic cancers as well as in metastatic lesions of the liver. These results demonstrate that neoplastic and normal endothelium in humans are distinct at the molecular level, and have significant implications for the development of anti-angiogenic therapies in the future.

To gain a better understanding of tumor angiogenesis, new techniques for isolating endothelial cells (ECs) and evaluating gene expression patterns were developed. When transcripts from ECs derived from normal and malignant colorectal tissues were compared with transcripts from non-endothelial cells, over 170 genes predominantly expressed in the endothelium were identified. Comparison between normal- and tumor-derived endothelium revealed many differentially expressed genes, including a large nujber of genes that were specifically elevated in tumor-associated endothelium. Experiments with representative genes from this group demonstrated that most were similarly expressed in the endothelium of primary lung, breast, brain, and pancreatic cancers as well as in metastatic lesions fo the liver. Theses results demonstrate that neoplastic and normal endothelium in humans are distinct at the molecular level, and have significant implications for the development of anti-angiogenic.

Tumor necrosis factor (TNF) is capable of inducing apoptosis by interacting with specific TNF receptors on the surface of cancer cells. Because multiple members of TNF ligand and receptor are present within each superfamily, over 300 different ligand-receptor combinations exist. Activated blood leukocytes produce TNF as part of the immune response to cancer, as well as producing chemokines to attract other leukocytes to the site. A method is disclosed of detecting significant induction of a variety of TNF superfamily subtype and chemokine mRNAs in blood leukocytes when whole blood is exposed to heat-aggregated IgG or anti-T cell receptor antibodies as a model of immune system interactions. Substantial individual-to-individual variation is observed in TNF subtypes and chemokines induced. Since peripheral blood leukocytes are the supply of anti-cancer immune cells, the quantitation of ex vivo inducibility of appropriate TNF ligands and chemokines in blood will be useful in individualized cancer immunotherapy. If the tumor mass is small, such as with early invisible metastatic lesions, appropriate TNF assaults may be sufficient to prevent relapse.

We achieved the present invention on the basis of the finding that an excellent therapeutic effect against pancreatic cancer can be obtained by administering an IL-6 inhibitor and an antimetabolite to pancreatic cancer patients. We also found that metastatic lesions from human pancreatic cancer can be reduced and ascites can be eliminated.

To gain a better understanding of tumor angiogenesis endothelial cells (ECs) were isolated and gene expression patterns were evaluated. When transcripts from ECs derived from normal and malignant colorectal tissues were compared with transcripts from non-endothelial cells, over 170 genes predominantly expressed in the endothelium were identified. Comparison between normal- and tumor-derived endothelium revealed differentially expressed genes, including many that were specifically elevated in tumor-associated endothelium. Experiments with representative genes from this group demonstrated that most were similarly expressed in the endothelium of primary lung, breast, brain, and pancreatic cancers as well as in metastatic lesions of the liver. These results demonstrate that neoplastic and normal endothelium in humans are distinct at the molecular level.

A brachytherapy applicator for treatment of metastic lesions in a load bearing region is provided. The applicator comprises an elongate tube body having a proximal and a distal end and defining an open internal area. A fixation element located on an outer portion of the tube allows the applicator to be fixed in position in relation to a target region while delivering a dose of therapeutic radiation. The fixation element can fix the applicator to tissue and / or a stabilization element implanted within a patient. A source of radiation positioned within the elongate body, before, during, or after implantation of the applicator, provides the therapeutic radiation.

The invention relates to a mouse model with lung metastasis of gastric cancer and an establishment method thereof, and belongs to the technical field of experimental animals. According to the mouse model and the establishment method thereof, BGC-823 and MKN-45 gastric cancer cells are cultured in vitro, and resuspended to a proper concentration with sterile PBS when the cell viability is strong. After the cells are cultured inside the body of immunodeficient NUDE and SCID mice inoculated in immunodeficience through the caudal vein, the mouse model with lung metastasis of gastric cancer is successfully obtained by the identifications including the statistics of surface lung nodules, HE staining and IHC staining. According to the mouse model establishment, needed experimental conditions and operation are simple and convenient, lung metastasis lesions after the experiment are obvious, metastasis efficiency is high, and mice with metastatic lesions have moderate survival cycles. In the evaluation and statistics of the metastasis results, the macroscopic counting of the lung nodules is improved into the microscopic counting of the IHC staining positive cells, thereby obtaining more objective and accurate results. The animal model of tumor metastasis may be widely used in scientific research and teaching.

Methods and compositions for modulating the FGF effect on the sensitivity of malignant and normal cells to anticancer agents are provided. In particular, methods and compositions for inhibiting FGF-induced resistance to a broad spectrum of anticancer agents in solid and soft-tissue tumors, metastatic lesions, leukemia and lymphoma are provided. Preferably, the compositions include at least one FGF inhibitor in combination with a cytotoxic agents, e.g., antimicrotubule agents, topoisomerase I inhibitors, topoisomerase II inhibitors, antimetabolites, mitotic inhibitors, alkylating agents, intercalating agents, agents capable of interfering with a signal transduction pathway (e.g., g., a protein kinase C inhibitor, e.g., an anti-hormone, e.g., an antibody against growth factor receptors), an agent that promotes apoptosis and / or necrosis, an interferon, an interleukin, a tumor necrosis factor, and radiation.In other embodiments, methods and composition for protecting a cell in a subject, from one or more of killing, inhibition of growth or division or other damage caused, e.g., by a cytotoxic agent, are provided. Preferably, the method includes: administering, to the subject, an effective amount of at least one FGF agonist, thereby treating the cell, e.g., protecting or reducing the damage to the dividing cell from said cytotoxic agent.

The present invention relates to methods for treating brain metastasis by inhibiting gap junction functionality. It is based, at least in part, on the discovery that cancer cells expressing Protocadherin 7 and Connexin 43 form gap junctions with astrocytes that promote the growth of brain metastases, and that inhibition of Protocadherin 7 and / or Connexin 43 expression in cancer cells reduce progression of brain metastases. It is further based on the discovery that treatment with gap junction inhibitors tonabersat and meclofenamate inhibited progression of brain metastatic lesions and enhanced the anti-cancer activity of the conventional chemotherapeutic agent, carboplatin.