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8 results about "Chemotherapy resistant" patented technology

Chemotherapy drug resistance can be intrinsic or acquired: Intrinsic resistance means a cancer cell is resistant from the start. If chemotherapy kills all the nonresistant cells in a tumor, the resistant cells will survive and reproduce. Then the tumor will grow back fully resistant.

Method for preparing nk cell-derived nanovesicles and uses thereof

The application provides a preparation method of NK cell-derived nanovesicles and application thereof. Specifically, the application provides NK cell-derived nanovesicles (NK-NVs) which are similar to the characteristics and functions of NK cell-derived extracellular vesicles by an extrusion method / stress gradient membrane remodeling technology, and also provides a drug composition, a drug delivery system and corresponding use of the NK-NVs as a delivery carrier for delivering an antitumor drug. The preparation method of the application can mass-produce NK-NVs and kill various types of tumor cells. The NK-NVs have multiple advantages in drug delivery, so that they are expected to be a new choice for tumor immunotherapy, especially for tumor cells with drug resistance, and can significantly improve the sensitivity to chemotherapeutic drugs, and have a wide application prospect.
Owner:GUIZHOU XINGBOYUAN BIOMEDICAL TECHNOLOGY CO LTD

Role of uck1 in promoting treatment sensitization of colorectal cancer

PendingCN122440821ATherapy resistantEfficacy
The present application relates to the role of UCK1 in promoting the sensitization of colorectal cancer treatment. The present application discloses the key role of UCK1 in the treatment of colorectal cancer. Clinical samples show that the expression of UCK1 in tumor tissues is reduced, and its low expression is related to chemotherapy resistance and poor prognosis. Studies have shown that UCK1 enhances the efficacy of oxaliplatin (OXA) by regulating metabolic pathways, and promotes B cell activation, thereby recruiting CD8 + T cells, and strengthens anti-tumor immunity. UCK1 overexpression can significantly improve OXA sensitivity and produce a synergistic effect with anti-PD-1 therapy. The present application proposes a new strategy centered on activating UCK1, providing a theoretical basis and application prospect for improving the response of colorectal cancer chemotherapy and immunotherapy.
Owner:THE FIRST AFFILIATED HOSPITAL OF SUN YAT SEN UNIV +1

tRF5-22-sectca-1, tRF5-22-sectca-1 detection reagents, kits and uses thereof

PendingCN122357548AOncologyChemo therapy
This invention belongs to the field of molecular biology technology, specifically involving tRF5-22-SeCTCA-1, tRF5-22-SeCTCA-1 detection reagents, kits, and their applications. This invention discovers and verifies that tRF5-22-SeCTCA-1 plays a key regulatory role in the process of 5-fluorouracil (5-FU) chemotherapy resistance in colorectal cancer, filling a gap in the research of tRNA-derived fragments (tRFs) in colorectal cancer chemotherapy resistance. It is the first tRF molecule reported to be associated with 5-FU chemotherapy resistance in colorectal cancer, providing a novel molecular target and research direction for predicting chemotherapy resistance in colorectal cancer. This invention also provides a therapeutic strategy targeting tRF5-22-SeCTCA-1 and establishes α-ketoglutarate as an independent reversal agent, providing multi-dimensional technical solutions for the precision diagnosis and treatment of colorectal cancer and the reversal of chemotherapy resistance.
Owner:SUN YAT SEN MEMORIAL HOSPITAL SUN YAT SEN UNIV

Use of plac8 as a target in preparation of tumor treatment drugs

PendingCN122075516AOrganic active ingredientsDigestive systemPhosphorylationTargeted interventions
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.
Owner:XIN HUA HOSPITAL AFFILIATED TO SHANGHAI JIAO TONG UNIV SCHOOL OF MEDICINE

A method, system, and apparatus for computer-aided screening of drugs based on temozolomide and ADAMTS1

PendingCN122369571ACell-Extracellular MatrixM2 phenotype
This invention discloses a method, system, and apparatus for computer-aided drug screening based on temozolomide and ADAMTS1. This application is the first to discover that ADAMTS1 is significantly enriched in recurrent gliomas following temozolomide exposure; temozolomide strongly induces a stable senescence program, leading to excessive secretion of ADAMTS1. This senescence-induced protease coordinates significant changes in extracellular matrix composition. The remodeled microenvironment acts as a mechanobiochemical signaling agent, recruiting and polarizing host-derived myeloid cells to transform into the immunosuppressive M2 phenotype, thereby conferring chemotherapy resistance to residual glioma cells through paracrine signaling. This application reveals that the "senescence-ADAMTS1-ECM-M2" axis is a key non-cellular autonomous mechanism of temozolomide resistance. Targeting ADAMTS1-mediated matrix reprogramming can eliminate the immunosuppressive niche in gliomas and overcome chemotherapy resistance, showing broad application prospects.
Owner:INST OF LAB ANIMAL SCI CHINESE ACAD OF MEDICAL SCI

Methods and compositions for non-myeloablative bone marrow reconstitution

The disclosure relates generally to methods and compositions for performing bone marrow transplants using a non-myeloablative chemotherapeutic agent and chemotherapeutic-resistant cells. Using the methods and compositions described herein, a patient's bone marrow may be reconstituted and the patient avoids adverse side effects, including myeloablation and / or an impaired immune system.
Owner:WEIRD SCIENCE LLC

A bone-targeting, metabolic drive-relieving, chemotherapy-resistant polymer, dual-drug inhibitor nano-delivery particle, and preparation method and application thereof

PendingCN122444983ABone targetingCisplatin sensitivity
The present application relates to the technical field of targeted nanoparticles, in particular to a bone-targeting metabolic-driven chemotherapy resistance relieving polymer, a dual-drug inhibitor nano delivery particle and a preparation method and application thereof. The nano delivery particle comprises the bone-targeting metabolic-driven chemotherapy resistance relieving polymer MALss ALN , the polymer MALss Gi , and an MCT1 inhibitor. The present application discloses a metabolic reprogramming nano therapeutic system targeting osteosarcoma and a preparation and application method thereof, aiming to solve the problem of poor sensitivity of cisplatin, cope with the complex immune microenvironment of osteosarcoma, and propose a new nano therapeutic strategy for overcoming chemotherapy resistance and immune inactivation by precisely regulating the metabolic-immune axis.
Owner:THE THIRD XIANGYA HOSPITAL OF CENT SOUTH UNIV