115 results about "Tumor progression" patented technology

A computer implemented method of distinguishing tumor progression from treatment-related necrosis in digital images of a subject implements a multimodal deep learning architecture from MRI data of a selected anatomical portion of the subject, such as a brain, and corresponding dPET data for the subject with a tracer applied to the anatomical portion of the subject. The computer stores co-registered MRI data frames with dPET data frames as three dimensional (3D) parametric PET maps to identify multi-modal image features of segmented tumor data. A convolutional neural network uses MRI data and selected multi-modal image features as inputs and the computer concatenates respective output latent feature vectors from the respective sections of the at least one CNN. Feeding concatenated feature vectors to fully connected layers of the multimodal architecture distinguishes tumor progression from treatment-related necrosis of the anatomical portion of the subject.

The invention belongs to the technical field of gene engineering, and relates to an esophageal squamous cell carcinoma diagnostic kit based on a peripheral blood mononuclear cell methylation marker and application. The kit comprises a primer pair which is used for detecting the methylation of a cg05914150 site, a cg06769875 site, a cg07475126 site, a cg08433285 site, a cg10038907 site, a cg17968322 site, a cg19572487 site, a cg20184330 site, a cg22741248 site and a cg22823192 site. According to the detection kit provided by the invention, the type of a detected sample is peripheral blood, the sample is relatively easy to obtain and non-invasive, and the patient compliance is relatively good. Abnormal methylation changes mostly exist in the early progression process of tumors, early diagnosis of ESCC can be achieved through the methylation detection method provided by the invention, and the five-year survival rate of ESCC patients is effectively increased.

The invention provides a compound for releasing a urine fluorescent biomarker under induction of mitochondrial DNA mutation as well as a preparation method and application of the compound, and belongs to the technical field of medicines. The compound disclosed by the invention is prepared by the following steps: complementarily pairing a hybrid nucleic acid nano-carrier containing single-stranded DNA (Deoxyribose Nucleic Acid), an annular fluorescent reporter molecule and a Cas12a / crRNA compound through bases of DNA or RNA, and then coating polyethyleneimine and hyaluronic acid. A CRISPR / Cas12a system is selected as a converter of tumor specific mitochondrial DNA mutation information and urine fluorescence signals, a nano delivery system which responds to mtDNA single base mutation and is used for tumor progress monitoring and early metastasis warning is designed and synthesized, and the nano delivery system has a good application prospect in tumor progress monitoring and early metastasis sensitive detection.

The invention discloses siRNA (small interfering Ribonucleic Acid) targeting TMEM86A and application thereof, and relates to the technical field of biology, the siRNA comprises the following positive-sense strands and antisense strands: siRNA-001: a positive-sense strand: 5 '-GAAGAGCGAAGGACCCAAATT-3'; according to the tumor-associated macrophage, TMEM86A has a positive-sense strand of 5 '-TTTGGGTCCTTCGCTTCT-3', an antisense strand of 5 '-TTTGGGTCCTGTCGCTTCT-3', siRNA-002 has a positive-sense strand of 5 '-GGCTCATGGTTCGGTTTT-3', and an antisense strand of 5 '-AAACCGAACCCATGAGCCT-3'. According to the tumor-associated macrophage, single cell sequencing analysis finds that TMEM86A is highly expressed in tumor-associated macrophages, and the development of tumors is inhibited by designing siRNA of TMEM86A to target the tumor-associated macrophages in a colon cancer tumor microenvironment.

This invention discloses the application of integrin αv inhibitors combined with γ-secretase inhibitors in the preparation of drugs for treating tumors. The study found that the combined use of integrin αv inhibitors and γ-secretase inhibitors in tumor treatment exhibits a synergistic effect, not only inhibiting in situ tumor growth but also significantly suppressing tumor invasion, distant metastasis, and other malignant progression, thus helping to slow tumor progression, improve treatment efficacy, and enhance patient prognosis. Furthermore, the study found that the combined use of integrin αv inhibitors and γ-secretase inhibitors can reduce the production of the intracellular free domain of integrin αv and inhibit the activation of the classical downstream pathway of integrin αv. The combined use of integrin αv inhibitors and γ-secretase inhibitors shows broad application prospects in tumor treatment.

The invention belongs to the technical field of biological medicine, and particularly relates to application of GLUT5 serving as a colorectal cancer biomarker in development of an in-vitro detection kit, a prognosis model and an inhibitor. The GLUT5 is highly expressed in colorectal cancer tumor-related fibroblasts (CAFs), the expression level of the GLUT5 is remarkably related to poor prognosis of a patient, and the GLUT5 can be used as a molecular basis for auxiliary diagnosis and an independent prognosis factor. In mechanism, the GLUT5 promotes tumor progression by mediating fructose metabolism reprogramming of the CAFs. A full-chain solution from early diagnosis and precise prognosis to targeted therapy is provided for colorectal cancer, and the clinical transformation value is remarkable.

Described herein are particle-driven radiogenomics systems and methods that can be used to identify imaging features for prediction of intratumoral and interstitial nanoparticle distributions in cancers (e.g., in low grade and / or high-grade brain cancers (e.g., gliomas, e.g., primary gliomas)). In certain embodiments, the systems and methods described herein extract and combine quantitative multi-dimensional data generated from structural, functional, and / or metabolic imaging. In certain embodiments, the combined multidimensional data is linked to intratumoral and interstitial nanoparticle distributions. For example, this linked data can be used to determine quantitative functional-metabolic multimodality particle-based imaging features and to predict treatment efficacy. These techniques provide an improved quantitative ability to measure treatment response and determine tumor progressions compared to traditional size-based imaging methods.

The invention discloses application of a lactic acid modified gene ENO1 inhibitor in preparation of a medicine for treating nasopharynx cancer, and relates to the technical field of biological medicines. A head and neck squamous cell carcinoma prognosis model containing seven lactylation related genes is constructed by analyzing a TCGA database, the model can effectively distinguish patient risks, the total lifetime of a high-risk group is remarkably shortened, and a risk score is an independent prognosis factor; the functions of the key gene ENO1 are deeply studied through in-vitro experiments, and experimental results show that silencing of the ENO1 gene in nasopharynx cancer 5-8F cells causes up-regulation of cell pan-lactylation level, up-regulation of MMP2 expression and down-regulation of E-cadherin expression, and migration and invasion ability of tumor cells is significantly enhanced. The prognosis model provided by the invention has an important clinical prediction value, inhibition of ENO1 can promote tumor progression through abnormal lactylation, and a new thought is provided for taking ENO1 as a treatment target.

The invention relates to application of a KRT7-AS inhibitor in preparation of a medicine for treating ovarian cancer or paclitaxel drug resistance of the ovarian cancer. The invention discloses a mechanism of KRT7-AS for promoting ovarian cancer progression by inhibiting ferroptosis for the first time. After KRT7-AS is knocked down by utilizing an shRNA (short hairpin ribonucleic acid) inhibition technology, biological behaviors of ovarian cancer cells and ovarian cancer paclitaxel drug-resistant cells are influenced: proliferation, migration and invasion capabilities are reduced to different degrees, and meanwhile, ferroptosis is activated to inhibit tumor growth. The invention provides a new thought and a potential target for precise treatment of ovarian cancer, and is expected to bring good news to ovarian cancer patients. Long-chain non-coding RNA KRT7-AS is novel carcinogenic lncRNA of ovarian cancer, and the effect of KRT7-AS knockout in the ovarian cancer cell process is researched. By targeting KRT7-AS, ferroptosis of ovarian cancer cells is regulated and controlled, so that tumor progression is influenced. The KRT7-AS inhibitor is used for targeting KRT7-AS, can be used as a treatment method for treating ovarian cancer, and is an innovative strategy for treating ovarian cancer.

The invention provides a pilot small-molecule compound and application thereof, the structural formula of the pilot small-molecule compound is shown in the specification, and application of the small-molecule compound in preparation of a preparation for inhibiting FGL2 activity. The pilot small molecule compound provided by the invention can be combined with FGL2 protein to play a role in inhibiting the FGL2 protein, so that the development process of tumors is slowed down.

The present invention relates to a pharmaceutical composition for use in the treatment of both low-grade and high-grade glioblastoma in a human subject. The composition comprises a synergistic combination of the following active agents: R-Ketorolac, Bumetanide, and Niflumic acid. This specific combination is designed to exert a synergistic therapeutic effect against glioblastoma by targeting multiple molecular pathways involved in tumor progression, inflammation, and ion transport. In a further aspect of the invention, there is provided a method for selecting a subpopulation of glioblastoma subjects who are responsive to the aforementioned treatment. This method comprises identifying genetic profiles predictive of a favorable therapeutic response to the combined administration of R-Ketorolac, Bumetanide, and Niflumic acid.

The invention relates to the technical field of biological medicines, and particularly discloses siRNA for inhibiting CD44v6 expression in tumors and application of the siRNA. The siRNA molecule can specifically target mRNA of CD44v6, and efficient knock-down is achieved on the gene level and the protein level (the interference efficiency reaches 70%-90%); in-vitro experiments prove that the siRNA can significantly inhibit the proliferation ability and clone formation ability of gastric cancer cells (such as AGS and HGC-27); in-vivo and in-vitro experiments further show that the siRNA can enhance the sensitivity of gastric cancer cells to a ferroptosis inducer RSL3 and generate a synergistic anti-tumor effect. The invention further provides a pharmaceutical composition containing the siRNA and application of the pharmaceutical composition in preparation of drugs for treating malignant tumors such as gastric cancer, and a new strategy and means are provided for overcoming the problem that tumor progression is fast.

Exemplary system and methods propagate a lesion to measure tumor progression and response. Plural images of a patient obtained during plural computed tomography scans are received which include a set of baseline images and a set of supplement images obtained at a different time points. Each received image is analyzed to detect an organ and perform organ segmentation on the image in which an organ is detected. A contour for at least one baseline image in the set of baseline images on which organ segmentation is performed is received from a user. The annotated baseline image is aligned onto a supplement image of the set of supplement images. The aligned images are registered based on the lesion of interest, and universal lesion segmentation is performed to predict new lesion contours. Biomarkers are extracted from the registered and aligned images based on new lesion contours associated with the lesion of interest.

Aspects of the disclosure provide a formulation for treating advanced pancreatic cancer, comprising a combination of a cannabinoid, a terpene, and a flavonoid. To enhance bioavailability and targeted delivery, the formulation is incorporated into a nanoplatform, such as a nanoemulsion, optimizing absorption and delivery to cancer cells. The nanoparticle-based composition specifically targets advanced stages of pancreatic cancer, aiming to inhibit tumor progression and improve clinical outcomes.

Provided are a recombinant adenovirus or adenoviral vector expressing GLP1 receptor agonist that shows expected anti-tumor effects and prolonged survival time in tumor-bearing subjects and the pharmaceutical composition comprising the same.

Provided are a recombinant adenovirus or adenoviral vector expressing GLP1 receptor agonist that shows expected anti-tumor effects and prolonged survival time in tumor-bearing subjects and the pharmaceutical composition comprising the same.

The invention discloses an application of a GABAA alpha 6 receptor knockout substance and a combined drug thereof in preparation of a bladder cancer treatment product. The invention provides an application of a substance for knocking out a GABAA alpha 6 receptor gene and a macrophage inhibition drug in preparation of a tumor treatment product. The invention also provides application of a substance for knocking out the GABAA alpha 6 receptor gene and a macrophage inhibition drug in preparation of a product for inhibiting tumor progression. By knocking out the GABAA alpha6 receptor gene, the regulation effect of the GABAA alpha6 receptor gene on CD8 + T cell functions is researched, the application value of the GABAA alpha6 receptor gene in bladder cancer treatment is verified, and a new strategy is provided for clinical treatment.

The application belongs to the technical field of biological medicine, and particularly relates to a cell penetration inhibitory peptide and application thereof in breast cancer. Specifically, aiming at the interaction between circHIF-1alpha (11, 12) and IGF2BP2, a novel compound named cell penetration IGF2BP2 inhibitory peptide (IIP) is designed to intervene, so as to inhibit the energy metabolism re-regulation and tumor progression of breast cancer. The application first discloses a new use of IIP as an inhibitor of circHIF-1alpha (11, 12). In-vitro experiments prove that IIP can significantly inhibit the energy metabolism reprogramming and tumor progression of breast cancer cells. In summary, the application provides an innovative breast cancer treatment method based on the interaction between circRNA and protein, and successfully intervenes the disease process of breast cancer through the design and application of IIP, which opens up a new direction and possibility for the development of breast cancer treatment.

The invention discloses an application of charantin IV in preparation of a tumor treatment medicine. The invention provides and verifies that the charantin IV can significantly inhibit the activity of cancer cells by inducing disulfiram death of cancer cells for the first time, can further promote gefitinib to overcome the drug resistance of cancer cells and inhibit the progress of drug-resistant tumors, and provides a new direction and theoretical basis for drug research, development and treatment of gefitinib drug-resistant non-small cell lung cancer.

The present invention provides the use of NAMPT inhibitors in the manufacture of medicaments for preventing and / or treating pigmented villonodular synovitis (PVNS), and belongs to the field of medicine. In the present invention, based on the PVNS-PDX mouse model, it is found that NAMPT inhibitor FK866 exhibits significant therapeutic effects on PVNS, such as improving clinical symptoms related to the disease and inhibiting the proliferation of PVNS grafts. It is discovered that FK866 can target the NAMPT-ITGA5-JUND signaling axis, alleviate endothelial cell damage and vascular permeability, reduce synovial inflammation, decrease the volume of synovial tumor grafts, mitigate hemorrhagic lesions of PVNS, and hinder tumor progression. Therefore, NAMPT inhibitors have broad application prospects in the manufacture of medicaments for preventing and / or treating PVNS.

The application belongs to the field of traditional Chinese medicines, and particularly relates to a traditional Chinese medicine composition for treating lung cancer bone metastasis and application thereof. The main active ingredients of the traditional Chinese medicine composition include, in mass parts, 20-40 parts of radix codonopsis, 20-40 parts of poria, 20-40 parts of astragalus, 10-30 parts of atractylodes, 10-20 parts of licorice, 10-30 parts of curcuma, 10-20 parts of pinellia, 5-10 parts of dried tangerine or orange peel, 20-40 parts of oldenlandia, 10-30 parts of psoralea, 10-30 parts of drynaria, 10-30 parts of epimedium, and 10-20 parts of jackinthepulp. Animal experiments show that the traditional Chinese medicine composition can not only inhibit primary tumor growth, but also slow down tumor progression of bone metastasis. When combined with a chemotherapy drug, the traditional Chinese medicine composition can not only significantly enhance the tumor inhibition effect of the chemotherapy drug, but also significantly prolong the survival time of mice, relieve weight loss and organ toxic side effects caused by the chemotherapy drug.

The invention provides application of pentenedioic acid (GC) in enhancing the anti-tumor effect of T cells through metabolic reprogramming, and belongs to the technical field of biological medicine. It is found that in the tumor development process, GC is supplemented in an exogenous mode, tumor growth can be rapidly inhibited, and the anti-tumor effect depends on a TME regulation and control mechanism. Through GC treatment, the TME immune landscape can be significantly remodeled; gC treatment not only can enhance the effector function of the CD8 + T cells, but also can delay the depletion process of the CD8 + T cells; and the infiltration CD8 + T cells in the tumor of the GC treatment group are obviously increased. Particularly, after the CD8-resistant antibody is used for removing mouse CD8 + T cells, the anti-tumor effect of GC completely disappears, and it is confirmed that the tumor inhibition effect depends on the CD8 + T cells. Therefore, the invention proves that the lysine catabolic metabolite GC, as an immunostimulatory metabolite, can shape the immune activated TME by reactivating the functions of tumor infiltrating CD8 + T cells.

The invention discloses application of amikacin in preparation of a medicine for treating melanoma, and relates to the technical field of biological medicine. The invention provides application of at least one of amikacin, pharmaceutically acceptable salts of amikacin, stereoisomers of amikacin, solvates of amikacin and polymorphic substances of amikacin in preparation of drugs for treating melanoma. In the invention, amikacin can inhibit proliferation, migration and invasion of melanoma cells; in a mouse transplantation tumor model, amikacin can also obviously delay tumor progression, and meanwhile obvious toxic reaction does not occur. Therefore, amikacin has the potential of serving as a new candidate drug for treating melanoma, can be used for treating melanoma, and provides a new research direction for reutilization of antibiotic drugs and treatment of melanoma.

The invention discloses application of FUT2 in improvement of cancer radiotherapy sensitivity, and belongs to the technical field of biological medicine. The invention provides an application of an FUT2 gene / protein as a target spot in any one of the following items: (1) an application in preparation of a product for improving cancer radiotherapy sensitivity; (2) application in preparation of a product for predicting the cancer radiotherapy effect; and (3) application in preparation of a product for predicting the prognosis effect of cancer radiotherapy. It is found for the first time that FUT2 reprograms a tumor immune microenvironment in vivo and promotes pancreatic ductal adenocarcinoma cell death in a mode independent of the metabolic activity of FUT2, FUT2 can enhance the effect of cancer radiotherapy, and the effect of FUT2 in enhancing anti-tumor immunity during radiotherapy depends on protein abundance of FUT2. The tumor immune microenvironment is reprogrammed by regulating and controlling tumor progression through an unconventional metabolic function, the action range of FUT2 in cancers is widened, effective support is provided for cancer radiotherapy sensitization, and good clinical value is achieved.

According to the invention, a novel immune checkpoint molecule SIDT1 is found. The SIDT1 is a powerful T cell inhibition factor mainly expressed on CD8 < + > T cells. A series of SIDT1 inhibitors are identified in the invention. The SIDT1 inhibitor can enhance the anti-tumor CD8T cell reaction and limit tumor progression, so that a new thought is provided for treatment and prevention of related tumor patients with PD-1 treatment resistance.

The invention provides an application of CLCA2 or a carrier for overexpressing the CLCA2 or a lentivirus for overexpressing the CLCA2 in preparation of a medicine for treating triple negative breast cancer. The invention firstly points out that the CLCA2 is a regulatory factor for promoting the apoptosis of triple negative breast cancer cells, and compared with a wild mouse, the mouse overexpressing the CLCA2 shows that the tumor progression of the triple negative breast cancer is obviously inhibited. It is proposed for the first time that the drug target CLCA2 can regulate and control cell apoptosis of the triple-negative breast cancer, the sensitivity of platinum chemotherapeutic drugs (carboplatin) of the triple-negative breast cancer is enhanced by inhibiting a PI3K-AKT signal channel, and a new regulatory factor is provided for improvement of a cell apoptosis signal channel.

The invention provides application of quercetin in preparation of a medicine for regulating intestinal microbiological disorder caused by bladder cancer, and belongs to the technical field of medical technology. It is found for the first time that quercetin regulates intestinal flora in the occurrence and development process of bladder cancer, effectively enriches tumor-related intestinal beneficial bacteria, can reverse disorder of in-vivo metabolic markers and reduces the level of L-serine, and therefore the effect of inhibiting the progress of bladder tumor is achieved.

The application provides application of a compound of a general formula I or a pharmaceutically acceptable salt, a hydrate, a solvate, a prodrug, a tautomer, a stereoisomer thereof as a MALT1 inhibitor, the MALT1 tumor inhibitor can inhibit the expression of a MALT1 gene or inactivate the function of a MALT1 protein, the compound of the general formula can play the role of inhibiting the expression of the MALT1 gene or inactivating the function of the MALT1 protein by affecting the expression of a MALT1 protein death domain. The screened small molecule compound can inhibit the RNA expression of a marker in tumor cells and delay tumor progression in a tumor model mouse; in addition, when the small molecule compound is combined with an immune checkpoint inhibitor, the small molecule compound can synergize with the immune checkpoint inhibitor, and the curative effect is significantly enhanced.

This application discloses the application of PLAC8 as a target in the preparation of tumor therapeutic drugs, involving the field of biomedical technology. This application clarifies that the "sympathetic nervous system-β2-AR-PLAC8-cholesterol metabolism-M2 polarization" pathway is the core driving pathway for stress-related tumor progression and chemotherapy resistance. It reveals the molecular mechanism by which PLAC8 inhibits cholesterol synthesis through phosphorylation at the S67 site, binding to the N-terminal domain of SREBP2, recruiting OGT to mediate SREBP2O-GlcNAc glycosylation. Through strategies such as gene silencing, β2-AR antagonist intervention, and targeted delivery of siPLAC8 via mannose-modified lipid nanoparticles (LNPs), the application achieved the effects of inhibiting M2 macrophage accumulation, inhibiting tumor growth, and reversing chemotherapy resistance in various tumor models, including gallbladder cancer, intrahepatic cholangiocarcinoma, and prostate cancer. Furthermore, the LNPs delivery system showed no significant toxicity. This research provides a novel therapeutic target centered on PLAC8 and a safe and effective targeted intervention strategy for stress-related tumors, highlighting its clinical translational value.