611 results about "Cancer therapy" patented technology

The present invention relates to magnetic, catalytically active, and radiosensitizing nanoparticles (NanoXcats) and the method for their production. A method is disclosed for the production of functionalized greigite nanoparticles with a narrowband size distribution (10-30 nm) for use in multimodal cancer therapy. NanoXcats are superparamagnetic Fe3S4 nanoparticles whose surfaces are equipped with polar functional groups. The surface structures of NanoXcats are suitable for conjugation with, or for covalent or electrostatic binding of, active substances, which may be cancer drugs, cell growth inhibitors, or NO donors. Due to the EPR effect, NanoXcats are preferentially internalized by tumor cells. The targeted accumulation of NanoXcats in tumor tissue is achieved by an external inhomogeneous magnetic field. NanoXcats exhibit enhanced catalytic activity in tumor cells.The catalytic activity of intracellular NanoXcats can be triggered, controlled, and enhanced by low-dose X-rays. Surface-bound drugs are additionally activated in tumor cells by the catalytic activity of NanoXcats. NanoXcats act as superoxide dismutase, nitric oxide synthase, and Fenton catalyst. They catalyze, for example, reactions of the superoxide anion radical to hydrogen peroxide, of L-arginine to NO, and of hydrogen peroxide to the hydroxyl radical.

The discovery and application of immune checkpoint inhibitors (ICI) have significantly promoted cancer treatment. However, the response rate is still low in gastrointestinal (GI) cancers. To explore novel adjuvant treatment options, we performed fecal microbiota transplantation (FMT) of healthy donors on 10 GI cancer patients with resistance to anti-PD-(L) 1 treatment. The combination of FMT and anti-PD1 treatment was well tolerated and no serious adverse reaction was observed. Two out of 10 patients restored clinical responsiveness to anti-PD1 after FMT. Clinical benefits were shown to be associated with better colonization of co-occurred immunogenic microbes from donors, alongside activated immune status reflected by the peripheral immune cell population. Moreover, we identified microbial signatures of ICI responsiveness and validated in an independent cohort. Our study demonstrates the feasibility of FMT as a potential adjuvant therapy for ICI irresponsive GI cancer patients and laid a foundation for LBP / consortia development to enhance ICI efficacy.

Provided herein are kinase fusion nucleic acid molecules and polypeptides, methods related to detecting kinase fusion nucleic acid molecules and polypeptides in cancer, as well as methods of treatment and uses related thereto. Detection of a kinase fusion nucleic acid molecule or the fusion polypeptide encoded by the fusion nucleic acid molecule can be used to identify individuals that may benefit from treatment with an anti-cancer therapy.

Drug delivery nanoparticle compositions and methods for the treatment of a cancer are provided that can be used individually or in combination. These compositions and methods include: (1) exogenous vaccination using neoantigens or tumor-associated antigens to potentiate an anti-tumor immune response; (2) nanoparticle-based drug delivery targeting the liver, aimed at reprogramming the hepatic immune environment to reduce or eliminate tumor antigen tolerance, thereby enhancing the immune system's ability to combat metastatic cancer; and (3) expansion of the liver metastasis treatment platform to target tumor-associated lymphoid structures, supporting the immune response at the primary tumor site. Any of these methods may be optionally combined with chemo-immunotherapy for enhanced efficacy.

The invention relates to the technical field of cancer treatment, and provides application of a lactyltransferase inhibitor in pancreatic cancer and immunotherapy thereof. According to the present invention, the histone lactosyltransferase inhibitor and the anti-programmed death receptor-1 antibody are combined to form the composition for pancreatic cancer and immunotherapy thereof, such that the recognition and the removal of the immune system on the cancer cells can be enhanced, the growth of the pancreatic cancer tumor can be effectively inhibited, and the survival time of the pancreatic cancer patient can be prolonged. The histone lactosyltransferase inhibitor reduces the infiltration level of tumor-associated neutrophil, increases the infiltration level of CD8 positive T cells, reverses the composition of a pancreatic cancer inhibitory immune microenvironment, and generates a synergistic anti-tumor effect with an anti-programmed death receptor-1 antibody. The traditional Chinese medicine composition is suitable for early-stage, middle-stage and late-stage treatment of pancreatic cancer, improves the survival rate and the treatment effect of pancreatic cancer patients, remarkably reduces the side effects of treatment and improves the living quality of the pancreatic cancer patients.

Provided herein are methods for treating cancer comprising intranasal administration of an oncolytic virus or an oncolytic virus-based vector, comprised in a mesenchymal stem cell (MSC), an MSC-derived EV, or in an MSC-derived bioxome. Further, the MSCs, MSC-derived EVs, or MSC-derived bioxomes disclosed herein may be used for treating a central nervous system (CNS) related disorder.

The present invention relates to a treatment of cancer combining enzymatic with metabolic means of selective attack on cancer cells.

The present invention pertains to the field of predictive medicine in which diagnostic assays, prognostic assays, and monitoring therapy can be used for prognostic (predictive) purposes to thereby treat an individual having cancer. Accordingly, one aspect of the present invention relates to methods of treating a subject having cancer by determining the amount and / or activity level of ZNFX1 in the context of a biological sample (e.g., blood, serum, cells, or tissue) to thereby determine whether an individual afflicted with a cancer is likely to respond to anti-cancer therapy, whether in an original or recurrent cancer.

The present invention relates to polypeptides which are covalently bound to molecular scaffolds such that two or more peptide loops are subtended between attachment points to the scaffold. In particular, the invention describes peptides which are high affinity binders of membrane type 1 metalloprotease (MT1-MMP). The invention also describes drug conjugates comprising said peptides, conjugated to one or more effector and / or functional groups which have utility in imaging and targeted cancer therapy.

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 relates to combined therapy of cancer using an epithelial cell adhesion molecule (EpCAM) inhibitor and a Wnt signaling inhibitor. Specifically, the EpCAM inhibitor is an antibody which is directed to an extracellular domain (EpEX) of EpCAM. The combined therapy is effective in inducing apoptosis of cancer cells, inhibiting cancer sternness properties, tumor progression and / or metastasis, and / or prolonging survival of a cancer patient.

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.

The present disclosure provides a method of identifying a tumor for immunotherapy. The method comprises culturing tumor cells obtained from a subject; exposing the tumor cells to nanoparticles comprising a positively-charged surface and an interior comprising (i) a core and (ii) at least two nucleic acid layers, wherein each nucleic acid layer is positioned between a cationic lipid bilayer; and measuring interferon-alpha and interleukin 6 (and optionally Chemokine (C-C motif) ligands 4) produced by the tumor cells. A method of treating a subject with cancer also is provided. The method comprises culturing tumor cells from the subject; exposing the tumor cells to the nanoparticles; measuring interferon-alpha and interleukin 6 (and optionally Chemokine (C-C motif) ligands 4) produced by the tumor cells; and administering an immune checkpoint inhibitor to the subject. Any of the methods may also comprise measuring CXCL 10.

Provided herein are anaplastic lymphoma kinase (ALK) fusion nucleic acid molecules and polypeptides, methods related to detecting ALK fusion nucleic acid molecules and polypeptides in cancer, as well as methods of treatment and uses related thereto. Detection of an ALK fusion nucleic acid molecule or polypeptide can be used to identify individuals that may benefit from treatment with an anti-cancer therapy.

Provided is the use of histone H1 levels as a biomarker for ELANE pathway-related cancer therapies.

A method for cancer diagnosis and treatment. In particular, in identifying associations between biomedical markers which is indicative of having a diagnostic, prognostic or predictive value for a medical condition, in particular nasopharyngeal cancer (NPC) metastasis after radiation therapy. The biomedical marker or group of biomedical markers associated with a high likelihood of responsiveness of a subject to a cancer therapy, preferably radiation therapy, wherein said biomedical marker or group of biomedical markers comprises at least 1, 2, 3, 4, or all markers selected from CXCR6, ASPHD2, DDX39B and AGAP9. Furthermore, an assay for detecting, diagnosing, graduating, monitoring or prognosticating a medical condition, or for detecting, diagnosing, monitoring or prognosticating the responsiveness of a subject to a therapy against said medical condition, in particular nasopharyngeal cancer, is provided, as well as a corresponding method for classifying a subject and a medical decision support system.

Disclosed herein is Differential Subclone Eradication and Resistance Analysis (DSER), a method developed to identify molecular targets for improved therapy by direct comparison of genomic features of eradicated and resistant subclones in pre-and post-treatment samples from a patient with BRCA2-deficient metastatic prostate cancer. FANCI and EYA4 were identified as candidate DNA repair-related targets for converting subclones from resistant to eradicable, and RNAi-mediated depletion of FANCI confirmed it as a potential target. The EYA4 alteration was associated with adjacent L1 transposon insertion during cancer evolution upon treatment. L1 activation was inhibited by the antiretroviral drug azidothymidine. In conclusion DSER provides an informative intermediate step toward effective precision cancer medicine, especially in cases with dramatic but temporary metastatic tumor regression. L1 transposon activation may be a modifiable source of cancer genomic heterogeneity, suggesting the potential of leveraging newly discovered triggers and blockers of L1 activity to overcome therapy resistance.

Methods for prognosticating if an individual afflicted with a malignant tumor is likely to respond favorably to immunotherapy comprising testing for the presence or absence of DARC expression in the tumor, and if no DARC expression is detected, identifying the individual as not being suitable for immunotherapy, and optionally administering an anti-cancer therapy other than immunotherapy to the individual, or if DARC expression is detected, then identifying the individual as being suitable for immunotherapy, and optionally administering immunotherapy or any other anti-cancer therapy to the individual.

Systems, compositions, and methods are described that utilize three dimensional tumor models incorporating tissue barrier (such as a stromal barrier) around tumor cells in culture, which permit replication in vivo immune cell response to tumor cells. Such tumor models are used to accurately assess appropriate therapeutic modes and protocols that are likely to be effective against the individual's tumor. Such tumor models can be used to selectively expand immune cells that are responsive to tumor cells utilized in the model. Such an expanded population of immune cells can subsequently be utilized therapeutically.

The invention relates to inhibitors of JAK proteins for use in the treatment of cancer. In vitro methods for screening of candidate agents as JAK inhibitors, and methods for the selection of a subject suffering from cancer as candidate for a cancer therapy comprising in particular JAK inhibitors are also disclosed.

The present invention relates to a treatment of cancer combining enzymatic with metabolic means of selective attack on cancer cells.

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.

The present disclosure provides methods of identifying a disease-specific immunogenic peptide through a series of selection steps. Immunogenic epitopes identified by methods of the present disclosure are applicable for use in peptide-based immunotherapy, preferably cancer therapy. Furthermore, the methods of the present disclosure may be performed in a high-throughput manner and serve as a means of personalized vaccine development and therapy. Also provided are compositions of immunogenic peptides as well as methods of treatment comprising said compositions.

Methods of predicting development of an anticancer therapy-related adverse event (AE) in a subject to be treated with an anticancer therapy, comprising calculating an AE probability score for factors expressed by the subject, and combining the AE probability score to produce a total AE probability score, wherein a total AE probability score is proportional to the subject's probability of developing an AE in response to the anticancer therapy, are provided.

Disclosed herein are methods, compositions, and devices for use in diagnosis and treatment of disease, including cardiovascular disease, and such disease and dysfunction as related to cancer therapy administration. The methods include sequencing a panel of regions in cell-free nucleic acid molecules and detecting one or more biomarkers that are indicative of a cardiovascular disease and dysfunction.

Some embodiments of the invention include inventive compounds (e.g., compounds of Formula (I), (II), or (III)) and compositions (e.g., pharmaceutical compositions) which inhibit IRAK and / or FLT3 and which can be used for treating, for example, certain diseases. Some embodiments include methods of using the inventive compound (e.g., in compositions or in pharmaceutical compositions) for administering and treating (e.g., diseases such as hematopoietic cancers, myelodysplastic syndromes (MDS), acute myeloid leukemia (AML), etc.). Additional embodiments provide disease treatment using combinations of the inventive IRAK and / or FLT3 inhibiting compounds with other therapies, such as cancer therapies.

Methods for treating a cancer patient with a neutrophil-to-lymphocyte ratio (NLR) greater than 3 are disclosed, comprising administering a nonsteroidal glucocorticoid receptor antagonist (GRA) to such a cancer patient, effective to reduce the patient's NLR. The methods include administering a nonsteroidal GRA and a cancer treatment to such a cancer patient, effective to reduce the patient's NLR and enhance the treatment of the cancer patient. The GRA may be orally administered. The nonsteroidal GRA may be a nonsteroidal compound comprising a heteroaryl ketone fused azadecalin structure (e.g., relacorilant) or an octahydro fused azadecalin structure (e.g., exicorilant). The cancer treatment may include chemotherapy, immunotherapy, radiation therapy, administration of an anti-angiogenic agent, administration of a growth factor inhibitor, and surgery. The methods may enhance the cancer treatment, improve the prognosis of the cancer patient, improve the survival of the cancer patient, and provide beneficial clinical effects and advantages to the patient.

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.

The invention provides methods to modulate hypoxia-mediated tumor immunity by administration of an O2 carrier polypeptide (e.g., 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.