336 results about "Cancer therapy" patented technology

Provided herein are chimeric antigen receptors (CARs) for cancer therapy, and more particularly, CARs containing a scFv from an anti-ROR-1 monoclonal antibody. Provided are immune effector cells containing such CARs, and methods of treating proliferative disorders.

The present invention provides a computer-implemented method for predicting the treatment response of a subject having a lung cancer to an immune checkpoint inhibitor (CPI) therapy, the method comprising: providing a mutation profile of the subject, said profile comprising the presence or absence of cancer-specific mutations at one or more locations in at least five genes selected from the group consisting of: NF1, STK11, TSC2, BRCA2, BRAF, STAG2, U2AF1, BRIP1, PDGFRA, CTNNA1, PDK1, FGF10, and FLT1; analysing the mutation profile to classify the profile as matching the mutation profile of a response signature or a resistance signature, wherein the subject is predicted to be likely to respond to the CPI therapy if the mutation profile for the subject is classified as matching the mutation profile of the response signature and is predicted to be likely not to respond to the CPI therapy if the mutation profile for the subject is classified as matching the mutation profile of the resistance signature. Also provided are related methods and systems for predicting the treatment response of a subject having a lung cancer to an immune checkpoint inhibitor (CPI) therapy.

Provided herein are chimeric antigen receptors (CARs) for cancer therapy, and more particularly, CARs containing a scFv from a CD33 monoclonal antibody. Provided are immune effector cells containing such CARs, and methods of treating proliferative disorders such as acute myeloid leukemia (AML), and relapsed or refractory AML.

The present invention provides a combination therapy for effectively treating and / or preventing diseases associated with cells expressing CA19-9, including cancer diseases such as pancreatic cancer and metastases thereof.

Embodiments of the present invention include methods of targeting acidosis (low pH) within the tumor microenvironment (TME) through the use of cathodic electrochemical reactions (CER). Low pH is oncogenic by supporting immunosuppression. Electrochemical reactions create local pH effects when a current passes through an electrolytic substrate such as biological tissue. Electrolysis has been used with electroporation (destabilization of the lipid bilayer via an applied electric potential) to increase cell death areas. However, the regulated increase of pH through only the cathode electrode has been ignored as a possible method to alleviate TME acidosis, which could provide substantial immunotherapeutic benefits. Here, ex vivo modeling shows that CERs can intentionally elevate pH to an anti-tumor level and that increased alkalinity promotes activation of naïve macrophages. Embodiments of the invention include pairing CER treatment protocols with existing electric field-based cancer therapies or use as a stand-alone therapy.

Provided herein are methods for determining a subtype of a small cell lung cancer in a patient based on the express status of ASCL1, NEUROD1, and POU2F3, which are expressed in a mutually exclusive fashion. The subtype of the cancer can be used to determine the sensitivity of the cancer to certain anti-cancer therapies. As such, also provided are methods of treating patients having small cell lung cancer based on the subtyping results.

The present invention is directed to (phthalazin-3-yl)amine derivatives of formula (I) as BFL-1 inhibitors for use in methods of treatment of leukemias, lymphomas and other cancers.

To provide a pharmaceutical composition for treating a subject affected with cancer.SOLUTION: A pharmaceutical composition containing an effective dose of FABP5 inhibitor to be used in combination with anti-cancer therapy or additionally used to anti-cancer therapy in treatment of a subject affected with cancer, where the FABP5 inhibitor has the following structure or an enantiomer or a racemate thereof, or a pharmaceutically acceptable salt thereof.SELECTED DRAWING: None

Described herein are compositions and methods for treating lung damage associated with cancer therapy, for example radiation-induced lung damage or chemotherapy-induced lung damage. Lung damage may be treated by administering heparin, optionally formulated with or administered concurrently with N-acetylcysteine. The compositions may be nebulized and administered via inhalation to treat lung damage.

Provided herein are methods and compositions for treating cancer in an individual comprising administering to the individual an effective amount of at least one CD122 / CD132 agonist, at least one immune checkpoint inhibitor and a viral composition comprising one or more viruses engineered to overexpress a tumor suppressor gene and / or an adenoviral death protein. Also provided herein are methods and compositions for treating cancer in an individual comprising administering to the individual an effective amount of at least one oncolytic viral composition and at least one CD122 / CD132 agonist and at least one immune checkpoint inhibitor. Also provided herein are methods of enhancing anti-tumor efficacy by administering the agents described above in combination with other cancer therapies. In highly aggressive forms of cancer, known to be generally resistant to immune therapies, these treatments unexpectedly resulted in complete tumor remissions and curative outcomes.

The present invention relates to application of 64Cu in radionuclide-based cancer therapy in humans. More specifically, the invention relates to 64Cu labeled conjugates for use in the treatment of cancer patients including 64Cu labelled Integrin αVβ3 binding conjugates, such as [64Cu]NODAGA-E[c(RGDyK)]2.

The present invention relates to a monoclonal antibody or an antigen-binding fragment thereof, which specifically binds to human CCR8 and is an antagonist, particularly an insurmountable antagonist, of the CCL1-CCR8 signaling pathway. The invention also relates to the antibody or antigen-binding fragment for use in therapy, particularly in the treatment of cancer.

Systems and methods for destroying or inhibiting cancer cells and other rapidly-dividing cells including an alternating polarity (AP) magnetic field generator and one or more AP electromagnetic coil adapted to be coupled to at least a portion of a patient's body, and a controller to control the AP magnetic field generator and at least one AP electromagnetic coil and cause the field generator and coil to apply AP magnetic field having a frequency of 0.5-500 KHz and a field strength of 0.5-5 mT to the at least a portion of the patient's body area to achieve a desired inhibiting effect on cancer cells or other rapidly-dividing cells. Treatments provided by the system may be co-administered with an anti-cancer therapy such as a chemotherapy drug, a hormone therapy drug, targeted therapy drugs, immunotherapy drugs, an angiogenesis inhibitor drug, or tumor treatment field therapy.

The present invention relates to methods, uses, and compositions for the treatment of cancer (e.g., a breast cancer or a pancreatic cancer). More specifically, the invention concerns the treatment of patients having cancer for the therapeutic inhibition of cancer cell growth and metastasis with an anti-Cadherin 11 monoclonal antibody with specific monoclonal antibody clones 23C6 or 3H10.

The ability to improve the adjusting of technical parameters in therapy plans found by Pareto navigation constitutes a technical problem, along with facilitating the decision-making of the planner (also called user) and simplifying the mathematical calculation of the solution. Proposed is a way to find and establish a therapy plan among a plurality of plan proposals for cancer therapy, each plan proposal representing as a solution one point in a navigation space (N) containing a plurality of setting parameters and establishing in a machine space (M) a setting for radiation doses to be administered by a radiation therapy machine for cancer therapy. The navigation space (N) contains at least one Pareto front (200) behind or on which available treatment plans are located as possible solutions and among which a user navigates, whereby a first plurality of available solutions calculated in advance as plan proposals is provided in a memory and retrieved or read out from the memory for display. The retrieved or read-out plan proposals are shown on a display and used by the user for navigation, whereby a large number of Pareto-optimal solutions with physical values or evaluations of dose values can be found among the points. Moreover, such solutions are also shown that are almost Pareto-optimal, within a tolerance range of at most ±5% from the Pareto optimum. In this way, a large first set of points with the physical values or evaluations of dose values is created and then stored in the memory. From this, a second set of points is calculated, which defines clinical targets. A decision space (D) is provided and shown in which at least the clinical targets are plotted on target axes (76, 876, 776). This is without the possibility of navigating in the decision space (D) on the target axes of the clinical targets, whereas binary selections in the decision space are made in the manner of restrictors to specify which plan proposals are not used as therapy plans. This enables a desired therapy plan to be found and determined from the large number of plan proposals.

Metastasis is a major cause of fatality and expense in cancer. Many metastatic patients express calcified, fibrotic, or deep-seated (lymph / Jung / brain) lesions that are not easily profiled. For such patients, decision-making regarding treatment selection is population-based and heavily reliant on standards of care and are not tailored to the individual's tumor. The present disclosure provides methods of identifying treatment protocols for cancer patients using released tumor cells (RTCs). Method described herein include isolating / enriching RTCs, profiling RTCs and comparing RTCs to reference RTC profile libraries.

Aspects of this invention are related to the use of N-desmethyl ruboxistaurin and pharmaceutically acceptable formulations thereof to modulate RSK signaling. Some aspects of the invention relate to the use of N-desmethyl ruboxistaurin to inhibit RSK. Some aspects of the invention provide methods of using N-desmethyl ruboxistaurin in the treatment of subjects with cancer, including breast cancer, ovarian cancer, prostate cancer, lung cancer, hepatocellular carcinoma, colorectal cancer, melanoma, osteosarcoma, myeloproliferative neoplasms, leukemia, and bladder cancer. The disclosed methods extend beyond disease treatment, including supportive care during radiation chemotherapy and prevention of cancer relapse. N-desmethyl ruboxistaurin administration, alone or in combination with other cancer therapies, inhibits RSK and shows a safety profile that supports its long-term use.

The invention provides methods to modulate hypoxia-mediated tumor immunity by administration of an O2 carrier polypeptide (eg., an H-NOX protein). The methods of the invention target both hypoxia inducible factor 1 alpha (HIF-1α) pathways and non-HIF-1α pathways of tumor immunity. Such methods are useful in the treatment of a wide variety of cancers and may be used alone or in combination with other anti-cancer therapies.

Provided herein are novel αPD-L1 antibodies and methods of using such antibodies for the treatment of cancers. In some embodiments, the antibodies are αPD-L1×αCD28 bispecific antibodies. Such antibodies enhance anti-tumor activity by providing a costimulatory signal for T-cell activation against tumor cells while advantageously also blocking inhibitory PD-L1:PD-1 pathway interactions.

The present invention relates to a method of determining the responsiveness of a cancer patient to treatment with a compound that inhibits a KRAS protein or a KRAS protein mutant or treatment with a compound that inhibits the interaction between MDM2 and p53, the method comprising measuring the survivin level in a first sample obtained from the patient prior to treatment with the compound, measuring the level of survivin in a second sample obtained from the patient during or after treatment with the compound, comparing the level of survivin in the second sample to the level of survivin in the first sample, and determining the level of survivin in the second sample when compared to the level of survivin in the first sample. When the survivin level in the second sample decreases, it is determined that the patient is responsive to treatment with the compound. The invention further relates to the use of survivin in compounds for determining the inhibition of KRAS protein or KRAS protein mutants, or in compounds for inhibiting the interaction between MDM2 and p53, or a pharmaceutical formulation comprising said compound that inhibits a KRAS protein or a KRAS protein mutant or said compound that inhibits an interaction between MDM2 and p53 in a method of treating cancer.

Provided are methods relating to SIRPgamma as a biomarker for cancer cells, and in particular of cancer stem cells and lung adenocarcinoma. Disclosed are also methods of treatment, which involve administering a SIRPgamma targeted agent to a subject with cancer, alone or with another cancer therapy. Methods for diagnosing cancer, identifying subjects with high SIRPgamma levels for treatment, and monitoring SIRPgamma expressing tumors are also provided.

The present disclosure provides methods and compositions for predicting response to an immunotherapy and treating cancer comprising determining a copy number or genomic alteration status of the cancer at a genomic region within or genetically linked to human chromosome 6q23.2-25.1 or within or genetically linked to a gene comprised within the genomic region. The present disclosure further provides methods and compositions for treating cancer using the identification of the copy number or genomic alteration status to administer a treatment regimen.

The present invention relates to a multispecific antibody comprising at least a FAP [alpha] binding region comprising a first heavy chain variable region and a first light chain variable region and a DR4 binding region comprising a second heavy chain variable region and a second light chain variable region. The invention further provides pharmaceutical compositions comprising the antibodies and the use of the antibodies for therapeutic and diagnostic procedures, particularly in cancer therapy.

A pro-inflammatory and vasoconstrictor and endothelin-1 (ET-1) are pathogenic molecules related to a series of cardiovascular diseases. Unlike ET-1 signaling for vasoconstriction of the main artery, we have proven herein that coronary microvessels exhibit a unique signaling mechanism for constriction (independent of PKC, CPI-17, and intracellular calcium storage). The pathophysiological level of ET-1 acts preferentially on the microvessels to exert persistent vasoconstriction by activating Rho kinase upon binding to ETAR of the ET-1 receptor. The ETAR antagonist BQ123 only blocks but cannot reverse vasoconstriction against ET-1. In contrast, ROCK inhibitors (e.g., H-1152) are effective to reverse arteriolar systole against ET-1. Thus, ROCK inhibition is a potent and specific choice for the treatment of coronary ischemic disease (abnormal vasoconstriction) associated with microvascular dysfunction due to excessive production of ET-1. The ROCK inhibitors may also be used to treat microvascular diseases associated with diabetic retinopathy as well as microvascular dysfunction caused by cancer therapy or immunosuppressive drugs. Since H-1152 can also reduce the basal tension of microvessels, a ROCK inhibitor is also a good diagnostic agent when used during angiography or by a non-invasive method.

The invention relates to cancer biology, more specifically to the treatment of KRAS mutant cancers. A potent cancer therapy is provided by the combination of a farnesyl transferase inhibitor compound and a KRAS inhibitor compound.

The present disclosure relates to agents, such as binding proteins, that bind to vascular CD93 wherein binding of the agents to CD93 results in one or more of i) inhibition of perivascular tumor cell migration, ii) inhibition of tumor cell invasion, and iii) inhibition of tumor cell proliferation. The agent or binding protein, nucleic acid molecule or pharmaceutical composition thereof can be used in medical treatment, such as cancer therapy. The binding proteins may also be used to engineer cells to express chimeric antigen receptors having binding proteins of the disclosure as antigen binding domains.

The present invention relates to the field of medicine. It more particularly relates to new anti-soluble CD146 (sCD146) protein antibodies, in particular multispecific antibodies comprising antigen binding regions that specifically bind sCD146 and VEGF proteins, to nucleic acids and vectors encoding and / or expressing such antibodies, and to cells and compositions comprising such product(s), as well as to uses thereof, typically in the treatment of cancer, preferably cancer resistant to treatments involving an anti-VEGF antibody. The invention also relates to uses of anti-sCD146 antibodies for predicting or monitoring the response of a subject to a treatment of cancer involving an anti-VEGF agent, and to related methods.

Disclosed herein are methods and systems for treating cancer including glioblastoma, recurrent glioblastoma, or newly diagnosed glioblastoma, using the administration of ultra-low radio frequency energy (u / RFE®), either alone or in combination with one or more conventional cancer therapies. In some embodiments, the one or more conventional cancer therapies include chemotherapy or an anti-angiogenic therapy or other therapies.

The invention relates to the field of biological medicine, in particular to combination of antibody-drug conjugates and cancer therapy (especially kinase inhibitors or chemotherapy) and application thereof.

Multimodal cancer immunotherapy is a combination of cancer immunotherapies used to treat cancer in patients. T cell receptor diversity is used as a component of a method to treat cancer involving cancer therapy, including multimodal cancer immunotherapy.