117 results about "Metastatic breast cancer" patented technology

The present invention relate for a method for prognosis cancer, in particular metastatic breast cancer comprising doing a dosage of Nectin 4, in a soluble form or in transmembrane form, in a sample, the presence of Nectin 4 being indicative of a cancer.

A combination of a 4-anilino-3-cyanoquinoline compound (e.g. HKI-272, SKI-606, EKB-569) and a capecitabine compound in the treatment of a neoplasm is provided. Regimens, kits, and methods for treatment of neoplasm, including breast cancer including metastatic breast cancer, and lung cancer, using this combination, optionally in combination with other anti-neoplastic agents, or immune modulators are also described.

A combination of HKI-272 compound and a vinorelbine compound in the treatment of a neoplasm is provided. Regimens, kits, and methods for treatment of neoplasm, including breast cancer including metastatic breast cancer, and lung cancer, using this combination, optionally in combination with other anti-neoplastic agents, or immune modulators are also described.

A combination of temsirolimus and trastuzumab in the treatment of cancer is provided. A combination of temsirolimus and HKI-272 is provided. A combination of a trastuzumab and a HKI-272 is also provided. Regimens and kits for treatment of metastatic breast cancer, containing trastuzumab, temsirolimus and / or HKI-272, optionally in combination with other anti-neoplastic agents, or immune modulators are described.

A combination of temsirolimus and trastuzumab in the treatment of cancer is provided. A combination of temsirolimus and HKI-272 is provided. A combination of a trastuzumab and a HKI-272 is also provided. Regimens and kits for treatment of metastatic breast cancer, containing trastuzumab, temsirolimus and / or HKI-272, optionally in combination with other anti-neoplastic agents, or immune modulators are described.

Neutropenia is the dose-limiting toxicity of the tri-weekly docetaxel (Taxotere®) schedule. Here, we evaluate in Metastatic Breast Cancer (MBC) patients (N=38) a computerized method for predicting docetaxel-induced neutropenia, and use the model to identify improved docetaxel and Granulocyte Colony Stimulating Factor (G-CSF) regimens. Pharmacokinetics / pharmacodynamics (PK / PD) models were created and simulated concomitantly with a mathematical granulopoiesis model. Individual baseline neutrophil counts and docetaxel schedules served as inputs. Our trial validated the model accuracy in predicting nadir timings (r=0.99), grade 3 / 4 neutropenia (86% success) and neutrophil profiles (r=0.62). Model was robust to CYP3A-induced variability, except for slightly less accurate grade 3 / 4 neutropenia predictions. Simulations confirm smaller toxicity of the weekly docetaxel regimen than the tri-weekly one, and suggest an optimal G-CSF support for alleviating neutropenia, 60 μg / day QD×3, 6-7 days post-docetaxel, administered tri- and bi-weekly, and 4 days post weekly docetaxel>33 mg / m2.

A novel inhibitor of Rac activity based on the structure of the established Rac / Rac-GEF inhibitor NSC23766 is discloses. The compound EHop-016, with an IC50 of 1.1 μM, is a 100-fold more efficient inhibitor of Rac activity than NSC23766. EHop-016 is specific for Rac1 and Rac3 at concentrations ≦5 mM. At higher concentrations, EHop-016 inhibits the close homolog Cdc42. In MDA-MB-435 cells, EHop-016 (≦5 mM) inhibits the association of the Rac-GEF Vav2 with a nucleotide-free Rac1(G15A), which has a high affinity for activated GEFs. EHop-016 does not affect the association of the Rac-GEF Tiam-1 with Rac1(G15A) at similar concentrations. EHop-016 also inhibits the Rac activity of MDA-MB-231 metastatic breast cancer cells and reduces Rac-directed lamellipodia formation in both cell lines. EHop-016 decreases Rac-downstream effects of p21-activated kinase (PAK)1 activity and directed migration of metastatic cancer cells. At low concentrations (<5 μM), EHop-016 does not affect cell viability.

Provided in the present invention are a compound for treating tumours and a use thereof, and also provided are a compound as shown in formula I or a pharmaceutically acceptable salt thereof. The compound provided in the present invention has a high medicine peak concentration, a high medicine absorption and a long elimination half life, and can improve the efficacy of the medicine in clinical use and reduce the frequency of the dosages. The compound or the pharmaceutically acceptable salt thereof prepared by the present invention can act as a PARP inhibitor medicine, have a certain anti-tumour activity, and especially have a good therapeutic activity on triple negative, primary or metastatic breast cancer, colon cancer, uterine cancer, pancreatic cancer, lung cancer, stomach cancer, leukemia, melanoma, solid tumors or intracranial tumors, and provide a new choice for clinical medication.

The present invention is drawn to methods of repairing lytic bone lesions and tumor growth in an individual. In this regard, the present invention discloses use of a Wnt ligand either alone or in combination with anti-Wnt signaling antagonist therapy. The individuals who might benefit from such method may include but are not limited to the ones with multiple myeloma, osteoporosis, post-menopausal osteoporosis, fractures, metastatic breast cancer or metastatic prostate cancer.

The present invention relates to a method of treating patients with solid tumors, leukemias, and other malignancies using a combination of zosuquidar and a calicheamicin-antibody conjugate, such as Mylotarg. The invention is also directed to pharmaceutical formulations comprising zosuquidar and calicheamicin-antibody conjugates. The formulations are particularly effective in treating relapsed Acute Myelogenous Leukemia (AML) and metastatic breast cancer.

Embodiments of the present invention concern methods related to treating, prognosticating and / or diagnosing at least brain metastatic breast cancer. Embodiments of the methods include characterizing circulating tumor cells for the presence or absence of EpCAM and, upon identification of EpCAM negative cells and identification of the status of other markers (such as heparanase and / or Notch1, for example), treating the individual based on the determination of the characterization.

Described herein are methods for the treatment of breast cancer in a subject. In particular, methods are provided for the treatment of resistant, metastatic breast cancer with a combination of entinostat and an aromatase inhibitor.

A novel inhibitor of Rac activity based on the structure of the established Rac / Rac-GEF inhibitor NSC23766 is discloses. The compound EHop-016, with an IC50 of 1.1 μM, is a 100-fold more efficient inhibitor of Rac activity than NSC23766. EHop-016 is specific for Rac1 and Rac3 at concentrations ≦5 mM. At higher concentrations, EHop-016 inhibits the close homolog Cdc42. In MDA-MB-435 cells, EHop-016 (≦5 mM) inhibits the association of the Rac-GEF Vav2 with a nucleotide-free Rac1(G15A), which has a high affinity for activated GEFs. EHop-016 does not affect the association of the Rac-GEF Tiam-1 with Rac1(G15A) at similar concentrations. EHop-016 also inhibits the Rac activity of MDA-MB-231 metastatic breast cancer cells and reduces Rac-directed lamellipodia formation in both cell lines. EHop-016 decreases Rac-downstream effects of p21-activated kinase (PAK)1 activity and directed migration of metastatic cancer cells. At low concentrations (<5 μM), EHop-016 does not affect cell viability.

The inventors of the present invention have surprisingly discovered that EGFR expression in nonmetastatic breast cancer patients with CK-negative CTCs could induce EMT process. A simultaneous detection of both EGFR and EMT markers (VIM and Slug) in CTCs might improve prognostic or predictive information in patients with operable breast cancer.

A composition comprising at least one AAV vector formulated for central nervous system delivery is described. The composition comprises at least one expression cassette which contains sequences encoding an anti-neoplastic immunoglobulin construct for delivery to the brain operably linked to expression control sequences therefor and a pharmaceutically acceptable carrier. The anti-neoplastic immunoglobulin construct may be an immunoglobulin modified to have decreased or no measurable affinity for neonatal Fc receptor (FcRn). Also provided are methods of using these constructs in preparing pharmaceutical compositions and uses thereof in anti-neoplastic regimens, particularly for primary and / or metastatic cancers of the brain.

The invention discloses an anticancer drug complex. The anticancer drug complex has a core-shell structure, wherein a core of the core-shell structure is an anticancer active component, and a shell ofthe core-shell structure is formed by combining at least one of neuropeptide Y or a subtype thereof with a zeolite imidazate skeleton structure material. The invention also discloses a preparation method of the anticancer drug complex, wherein the method comprises the following steps: 1) dissolving a zinc source, 2-imidazolaldehyde and the anticancer active component in a solvent respectively, toobtain three solutions; 2) mixing the three solutions in the step 1 evenly, carrying out centrifugal separation and drying; and 3) dispersing the dried product in the step 2) in a solvent, adding atleast one of neuropeptide Y or the subtype thereof, and carrying out a stirring reaction for 12-72 h. The invention also discloses an application of the anticancer drug complex in preparation of drugsfor cancer treatment, preferably, cancer includes breast cancer with high expression of neuropeptide Y1 receptors and high metastatic breast cancer.

This patent describes a method and materials to treat cancer diagnosed at an early stage, particularly breast cancer. It considers that metastatic breast cancer growth includes periods of dormancy, that surgery to remove a primary tumor can induce metastatic growth, and that women with Down Syndrome rarely get breast cancer. It elevates the level of an antiangiogenic drug produced by chromosome 21 preferably Endostatin in plasma preferably at least one day prior to surgery and kept at that high level preferably indefinitely. The therapy specifically excludes drugs that significantly inhibit the VEGF pathway since that is important for wound healing. This method will prevent results of surgery from stimulating tumor growth and angiogenesis of micrometastatic disease that is much easier to prevent than control after the fact. This can be done indefinitely since there is no acquired resistance that develops, as happens in most cancer therapies.