78 results about "Tumor regression" patented technology

The present invention relates to ligands which bind to human tumor necrosis factor alpha (TNF) in a manner such that upon binding of these ligands to TNF the biological activity of TNF is modified. In preferred forms the ligand binds to TNF in a manner such that the induction of endothelial procoagulant activity of the TNF is inhibited; the binding of TNF to receptors on endothelial cells is inhibited; the induction of fibrin deposition in the tumor and tumor regression activities of the TNF are enhanced; and the cytotoxicity and receptor binding activities of the TNF are unaffected or enhanced on tumor cells. The ligand is preferably an antibody, F(ab) fragment, single domain antibody (dABs) single chain antibody or a serum binding protein. It is preferred, however, that the ligand is a monoclonal antibody or F(ab) fragment thereof.

Disclosed are antibodies that specifically inhibit VEGF binding to only one (VEGFR2) of the two VEGF receptors. The antibodies effectively inhibit angiogenesis and induce tumor regression, and yet have improved safety due to their specificity. The present invention thus provides new antibody-based compositions, methods and combined protocols for treating cancer and other angiogenic diseases. Advantageous immunoconjugate and prodrug compositions and methods using the new VEGF-specific antibodies are also provided.

A method is disclosed for disrupting capillary blood flow and trapping materials such as chemotherapeutic agents in undesirable tissue, including cells of a cancerous or non-cancerous tumor. The method involves the placement of electrodes into or near the vicinity of capillary vessels supplying blood to capillaries in the undesirable tissue, and application of electrical pulses causing capillary blood flow disruption. In some cases, the electric pulses irreversibly permeate the cell membranes, thereby invoking cell death. The irreversibly permeabilized cells are left in situ and are removed by the body's immune system. The process may further comprise monitoring blood flow and/or infusion of a material such as a chemotherapeutic agent or marker into the blood.

The present invention is a non-topical method of therapeutically treating human cancer patients which comprises an administration of an anti-cancer medicament comprising at least one simple organic or inorganic salt of zinc in at least a minimally effective concentration to suppress malignant tumor growth and induce tumor regression in-vivo. Administration can be performed by oral, parenteral, and/or body cavity routings; and the therapeutic treatment method is effective for the treatment of a diverse range of primary human cancers and metastatic diseases.

Methods of regressing or inhibiting a tumor in a subject by administering an agent capable of blocking, inhibiting, or ameliorating vascular endothelial growth factor (VEGF)-mediated activity to a subject in need thereof such that the tumor is regressed or inhibited. The method of the invention results in a reduction of tumor size and inhibition of tumor metastases. This method is particularly useful for patients suffering from bulky, metastatic cancers.

Current approaches for treating cancer are limited, in part, by the inability of drugs to affect the poorly vascularized regions of tumors. We have found that spores of anaerobic bacteria in combination with agents which interact with microtubules can cause the destruction of both the vascular and avascular compartments of tumors. Two classes of microtubule inhibitors were found to exert markedly different effects. Some agents that inhibited microtubule synthesis, such as vinorelbine, caused rapid, massive hemorrhagic necrosis when used in combination with spores. In contrast, agents that stabilized microtubules, such as the taxane docetaxel, resulted in slow tumor regressions that killed most neoplastic cells. Remaining cells in the poorly perfused regions of tumors could be eradicated by sponzlated bacteria. Mechanistic studies showed that the microtubule destabilizers, but not the microtubule stabilizers, radically reduced blood flow to tumors, thereby enlarging the hypoxic niche in which spores could germinate. A single intravenous injection of spores plus selected microtubule-interacting agents was able to cause regressions of several tumors in the absence of excessive toxicity.

A method of treating cancerous tumors is presented herein. The method includes injecting an effective dose of a plasmid encoded for IL-12, B7-1 or IL-15 into a cancerous tumor and subsequently administering at least one high voltage, short duration pulse to the tumor. The electroporation pulses may be administered at least 700V/cm for a duration of less than 1 millisecond. The intratumor treatments with electroporation may be administered in at least a two-treatment protocol with the time between treatments being about 7 days. The intratumor treatments with electroporation may be administered in a three-treatment protocol with a time of four days between the first and second treatments and a time of three days between the second and third treatments. It was found that the intratumor treatments using electroporation not only resulted in tumor regression but also induced an immune memory response which prevented the formation of new tumors.

Based on an anti-ICAM3 antibody obtained by immunizing a mouse with BaF3 cells having artificially over-expressed ICAM3, a chimeric antibody has been successfully prepared which exerts cytotoxic actions, including both a proliferation-suppressing activity and an ADCC activity, on a blood cancer cell line, and which exerts a tumor regression activity in vivo.

The present invention relates to methods and devices (100) for performing electroporation therapy in vivo. Using electroporation therapy (EPT) described in the present invention, electroporation performed using the device (100) of the present invention is combined with chemotherapeutic drugs to treat tumors and cause tumor regression in vivo. In one embodiment, the present invention provides an EPT method using low voltage long pulses to induce cell death. One embodiment of the invention includes a system for performing clinical electroporation comprising a needle array electrode (114) with a "keying" element that determines the given therapeutic voltage pulse. value, and/or select the switch mode for the array. There are a variety of electrode applicator designs to access and treat a variety of tissue sites. Another embodiment provides a laparoscopic needle applicator, preferably in combination with an endoscope for minimally invasive EPT.

The invention relates to use of interferon in treatment of a tumor, and related products and a method, particularly relates to the field of tumor treatment, and especially aims at overcoming the resistance of the tumor on an antibody therapy. Particularly, the invention relates to application, and related product and method for inhibiting growth and recurrence of the tumor and causing tumor regression by combined utilization of interferon, especially I-type interferon, and a compound for blocking up a programmed death 1 or programmed death ligand (PD-1/PDL) passage.

Disclosed is the surprising discovery that aminophospholipids, such as phosphatidylserine and phosphatidylethanolamine, are specific, accessible and stable markers of the luminal surface of tumor blood vessels. The present invention thus provides aminophospholipid-targeted diagnostic and therapeutic constructs for use in tumor intervention. Antibody-therapeutic agent conjugates and constructs that bind to aminophospholipids are particularly provided, as are methods of specifically delivering therapeutic agents, including toxins and coagulants, to the stably-expressed aminophospholipids of tumor blood vessels, thereby inducing thrombosis, necrosis and tumor regression.

The present invention relates to devices, systems and methods for treating tumors. In particular, the present invention relates to enclosures housing cell-coated supports for promoting regression of tumors, such as cancerous tumors, papillomas, and warts. In preferred embodiments, the present invention provides methods of promoting tumor regression employing enclosures secreting therapeutic proteins.

This invention relates to macromolecular prodrugs having antitumor activity when activated by GSH, and methods for synthesizing and administering these to patients. More particularly, this invention relates to, inter alia, the synthesis and use of polyacrylamide carriers to target anticancer prodrugs to tumors, and to release active antitumor agents selectively in tumor cells. These active antitumor agents target the active site of the methylglyoxal-detoxifying enzyme glyoxalase I to thereby cause tumor regression.

Specially designed non-mammalian GnRH analogs resistant to degradation by the tumor tissue enzymes, post-proline peptidases as well as endopeptidases, are disclosed. The GnRH analogs are further defined as analogs of chicken II GnRH, salmon GnRH, or herring GnRH, but can include any non-mammalian GnRH analog with similar amino acid structure. These non-mammalian analogs incorporate D-arginine, D-leucine, D-tBu-Serine or D-Trp or other similar amino acids at position 6 and ethylamide or aza-Gly-amide or similar amides at position 10. These analogs demonstrate preferential binding to tumor cell GnRH receptors that is greater relative to the binding of the mammalian analogs to the tumor cell GnRH receptor. These non-mammalian GnRH analogs may be used in pharmaceutical preparations, and it specifically in various treatments as an anti-tumor, anti-proliferation, anti-metastatic and/or an apoptotic agent. The non-mammalian GnRH analogs are also provided in pharmaceutical preparations that may be used clinically for tumor regression when used in very low doses and administered in pulsatile fashion.

The present invention is directed to methods for inhibiting tumor cell growth, causing tumor regression or eliminating tumor cells in a mammal afflicted with a tumor by administering to a TRAIL-sensitive cell a vector having a DNA expression cassette containing a promoter and a DNA sequence encoding TRAIL, wherein the expression of TRAIL results in tumor inhibition, regression or elimination.