34 results about "Tumor regression" patented technology

The invention relates to the technical field of medical decision and artificial intelligence, and discloses an artificial intelligence-driven new adjuvant therapy scheme optimization method and system for antral sinus cancer, and the method comprises the steps: S1, obtaining clinical data of a antral sinus cancer patient, and carrying out the preprocessing; s2, screening core features by adopting an iterative ReliefF algorithm, and constructing composite features; s3, constructing a prediction model based on a Bayesian optimization K-nearest neighbor algorithm, taking the composite features as input of the prediction model to predict treatment response, and outputting individual tumor recession grade probability distribution of the patient; s4, taking the tumor recession grade probability distribution as a core component of a state space, inputting the tumor recession grade probability distribution into a double-layer reinforcement learning framework based on a penalty mechanism to optimize a treatment decision, and outputting a personalized treatment strategy parameter set; and S5, performing real-time scanning and verification on the drug dosage parameters in the strategy parameter set, and outputting a final approved personalized treatment scheme. The precision and intelligent level of gastric antrum cancer treatment is improved.

The present disclosure relates to the field of radiotherapy, in particular, methods of and apparatus for treating cancer using ultra-high dose rate radiotherapy (FLASH). The apparatus may comprise a device configured to administer to the subject no more than five fractions of proton ultra-high dose rate radiotherapy (FLASH), said fractions having a range of radiation from 1.5 Gy to 60 Gy, collectively. The device may be configured such that the treatment is sufficient to prevent further growth of the tumor for at least 10% longer than standard of care radiotherapy, induce at least 10% more tumor regression than standard of care radiotherapy and / or delay tumor regrowth by at least about 2 months longer than standard of care radiotherapy.

Provided is use of a KIF18A inhibitor in preparing a medicament for treating ovarian cancer disease. Pharmacological studies have demonstrated that compounds 1-3 can inhibit the growth of ovarian cancer heterogeneous tumors, and a high dose of the compounds can cause tumor regression in mice. Compared with AMG650, a lower drug exposure of compounds 1-3 reduces the potential drug accumulation toxicity and possesses a significant therapeutic effect on ovarian cancer with good safety.

Provided are an anti-DLL3 antibody or an antigen-binding fragment thereof, a chimeric antigen receptor and a mutant thereof, and an enhanced chimeric antigen receptor comprising a PDL1 antagonist and an mIL7 element. Further provided are a nucleic acid encoding same, an expression cassette, vector and cell comprising the nucleic acid, a preparation method, and a use for preventing, treating, detecting, or diagnosing diseases related to DLL3. In the enhanced DLL3 chimeric antigen receptor, the PDL1 antagonist and the cell membrane IL7 cytokine element play a critical role in a long-term anti-tumor process. Animal efficacy experiments have shown complete tumor regression in all mice, indicating broad application prospects in the pharmaceutical field.

The present invention relates to artificial antigen presenting cell (aAPC) scaffolds to provide cells with specific functional stimulation to obtain phenotypic and functional properties ideal to mediate tumor regression or viral clearance. In particular, the scaffolds of the present invention comprise stabilized MHC class I molecules free of antigenic peptide. The scaffolds can be loaded with antigenic peptide on demand, providing an agile platform for effective expansion and functional stimulation of specific T cells in a peptide-MHC-directed fashion.

The present disclosure provides an anti-cancer lipid-based composition that kills very aggressive colorectal cancer cells. This composition is a concoction of an anti- cancer agent, 5-Fluorouracil and a glucocorticoid receptor (GR)-targeting cationic lipid delivery system, D1X. The uptake studies of these formulations have showed that formulations with dexamethasone enter into nucleus, bind GRE region and upregulate CYP3a5 gene. The intensity of upregulation is better than liposome without dexamethasone. Same results found in in vivo studies, the D1X5-FU shows better tumor regression and survivability than FOLFOX and FOLFIRI. The biodistribution studies showed that D1X5-FU targets only tumor tissues, not other organs. The pilot studies of tumor regression by other liposomal formulations- D1XLeucovorin, D1XOxaliplatin has showed better tumor regression than FOLFOX and FOLFIRI.

Targeting immune checkpoints, such as Programmed cell Death 1 (PD1), has improved survival in cancer patients by unleashing exhausted CD8+ T-cell thereby restoring anti-tumor immune responses. Most patients, however, relapse or are refractory to immune checkpoint blocking therapies. Here, the inventors show that NRP1 is recruited in the cytolytic synapse of PD1+CD8+ T-cells, interacts and enhances PD-1 activity. In mice, CD8+ T-cell specific deletion of Nrp1 improves spontaneous and anti PD1 antibody anti-tumor immune responses. Likewise, in human metastatic melanoma, the expression of NRP1 in tumor infiltrating CD8+ T-cells predicts poor outcome of patients treated with anti-PD1 (e.g. pembrolizumab). Finally, the combination of anti-NRP1 and anti-PD1 antibodies is synergistic in human, specifically in CD8+ T-cells anti-tumor response. Thus the therapeutic inhibition of NRP1 alone or combined with an immune checkpoint inhibitor (e.g. anti-PD1 antibody) could efficiently repress tumor growth in human cancer. The present invention also relates to multispecific antibodies comprising at least one binding site that specifically binds to an immune checkpoint molecule (e.g. PD-1), and at least one binding site that specifically binds to NRP-1. The present invention also relates to a population of cells engineered to express a chimeric antigen receptor (CAR) and wherein the expression of NRP-1 in said cells is repressed.

Methods for treating cancer and / or inducing tumor regression in mammals (e.g., humans) by increasing the metabolism of the mammal, administering a BA dye to the mammal, and thereafter exposing the tumor to actinic light for activation of the BA dye.

Methods for treating cancer and / or inducing tumor regression in mammals (e.g., humans) by increasing the metabolism of the mammal, administering a BA dye to the mammal, and thereafter exposing the tumor to actinic light for activation of the BA dye.

The present invention relates to a non-invasive magneto-acoustic apparatus for healthy tissue healing and cancer regression comprising at least one pulsed ultrasound unit (LIPUS), at least one permanent magnet, at least one module housing, at least one permanent magnets, at least one control system for controlling pulsed ultrasound unit to energize the unit with desired pulse duration, intensity and active / ON time. The invention is to synchronously use the low intensity pulsed ultrasound (LIPUS) and static magnetic field (SMF) to selectively activate cellular activities specific to cartilage, bone, skin leading to accelerated tissue healing, regeneration. The invention apparatus is to inhibit cancer cellular activities specific to cancers of breast, skin, bone leading to enhanced cancer regression, while leaving the healthy cells unaffected using magneto-acoustic apparatus appropriately. The apparatus exhibit no toxicity to healthy cells and can reduce overall treatment time and costs due to accelerated tissue repair and tumor regression.

The present invention pertains to the use of small molecules in the treatment of cancer. These compounds, which are small-molecule Furin inhibitors, show an ability to enhance sensitivity to immunotherapy and radiotherapy treatments, leading to tumor regression in mice and improved overall survival. Treatment of cancer cells with these compounds resulted in the elimination of the capacity for tumor cells and organoids to grow and invade. These results demonstrate the interest of using these small-molecule Furin inhibitors as therapeutic interventions for cancer patients.

The present invention relates to artificial antigen presenting cell (aAPC) scaffolds to provide cells with specific functional stimulation to obtain phenotypic and functional properties ideal to mediate tumor regression or viral clearance. In particular, the scaffolds of the present invention comprise stabilized MHC class I molecules comprising a heavy chain comprising an alpha-1 domain and an alpha-2 domain connected by a disulfide bridge, wherein said MHC class I molecules are free of antigenic peptide. The scaffolds can be loaded with antigenic peptide on demand, providing an agile platform for effective expansion and functional stimulation of specific T cells in a peptide-MHC-directed fashion.

The invention discloses application of 19-hydroxybufalin in preparation of a medicine for treating prostatic cancer, and belongs to the technical field of pharmaceutical preparations. The 19-hydroxybufalin is found to be targeted in vivo and in vitro for the first time, and the growth of prostate tumors is remarkably inhibited, so that the survival basis of tumor cells is fundamentally weakened, programmed death of the tumor cells is triggered, and tumor regression is effectively induced; a brand-new treatment approach is provided, namely, a non-classical drug target, namely HELLS, is degraded in a targeted manner, so that a new treatment choice is expected to be provided for a patient lacking existing target mutation; the provided 19-hydroxybufalin can be used for treating advanced prostate cancer, especially castration-resistant prostate cancer, and a new candidate treatment drug with great potential and a brand new treatment strategy are provided for effectively solving the problem that chemotherapy drug resistance and targeted therapy selection are limited in the castration-resistant prostate cancer at present.

Disclosed herein are methods of inhibiting tumor growth or producing tumor regression in a subject having a drug-resistant estrogen receptor alpha positive cancer or a mutant estrogen receptor alpha positive cancer. The methods entail administering to the subject a therapeutically effective amount of RAD1901 having the structure:or a salt or solvate thereof.

The present invention relates to a FLT3L–flagellin hybrid adjuvant with enhanced antigen cross-presentation efficacy and a vaccine composition comprising same. The hybrid adjuvant of the present invention demonstrated significant therapeutic efficacy as an adjuvant for a therapeutic cancer vaccine in a preclinical mouse model of cervical cancer, resulting in complete tumor regression and sustained protection. In addition, the hybrid adjuvant of the present invention induced tumor-specific antigen CD8+ T cell responses and progenitor-exhausted CD8+ T cells (Tpex) due to an increase in cross-presentation by conventional type 1 dendritic cells (cDC1) in tumor-draining lymph nodes and the tumor microenvironment, and the combination of TCV having the hybrid adjuvant applied thereto and anti-PD-1 therapy significantly improves survival outcomes in anti-PD-1–resistant tumors, and thus can be advantageously applied in anticancer immunotherapy using therapeutic cancer vaccines.

This invention relates to an antitumor agent based on respiratory tract symbiotic bacteria, its preparation method, and its application. Addressing the current clinical issue of the unclear role of respiratory flora in lung cancer patients' progression, we provide the first evidence that the respiratory tract symbiotic *Streptococcus osticulata* possesses antitumor activity. When *Streptococcus osticulata* is delivered back into the respiratory tract, it can stimulate an antitumor immune response, and its efficacy can be further enhanced by adenosylcobalamin. Currently, there is a lack of non-invasive, non-invasive inhaled treatments for lung cancer. The antitumor agent of this invention can be combined with novel non-invasive inhaled bacterial-metabolite immunotherapy to achieve a long-term chronic disease management model, representing a safe and transferable treatment approach. In addition to achieving effective lung tumor control when used alone, this therapy can synergistically enhance the efficacy of immunotherapy, inducing complete tumor regression in 50% of tumor-bearing mice.

The invention discloses a head and neck cancer chemotherapy recurrence animal model and a construction method and application thereof, and relates to the technical field of animal model construction. Comprising the following steps: S1, culturing head and neck cancer tumor cells with fluorescence labels under an in-vitro condition; s2, subcutaneously planting the head and neck cancer tumor fluorescent cells in a groin part of a model animal; s3, 5 days after planting, imaging and observing subcutaneous tumor formation of the model animal, and performing periodic chemotherapy; s4, monitoring through a living body imaging system until a tumor fluorescence signal basically disappears, and determining tumor regression; s5, stopping chemotherapy, continuing feeding for 5-6 weeks, and observing the tumor recurrence condition of the model animal to obtain the head and neck cancer chemotherapy recurrence animal model. The method is easy and convenient to operate, short in experimental period and low in consumption, non-invasive dynamic monitoring can be achieved through the living body imaging technology, the variability of the result is small, the success rate is high, and an ideal platform is provided for head and neck cancer recurrence research and drug screening.

The application relates to the fields of biological medicine and gene therapy, and discloses an IL1RN mRNA lipid nanoparticle drug and application thereof. The drug comprises a lipid nanoparticle and IL1RN mRNA encapsulated in the lipid nanoparticle; the IL1RN mRNA encodes a human IL1RN protein; and the lipid nanoparticle comprises ionizable lipids, phospholipids, cholesterol and pegylated lipids. The application encapsulates IL1RN-201 / 203 mRNA in conventional LNP for the first time, completes preparation characterization and in-vivo expression verification, and proves significant antitumor effect in a high-pressure tail vein transposon-induced in-situ KRAS mutant iCCA mouse model, and partial animals achieve complete tumor regression, thereby filling the blank in the field of IL-1 related inflammatory disease gene therapy and having outstanding originality and broad clinical conversion prospect.

The invention belongs to the field of chemical medicines, and particularly relates to a combined medicine of a medicine for intervening E3 ubiquitin ligase and an anti-tumor medicine for targeting HER2. The medicine for intervening the E3 ubiquitin ligase can block HER2 protein degradation or promote HER2 gene transcription, can enhance HER2 expression on the surfaces of tumor cells, and can enhance the sensitivity of HER2 negative tumors to HER2-targeted antitumor medicines. According to the present invention, the E3 ubiquitin ligase intervening drug and the HER2 targeting antitumor drug are combined so as to target the tumor tissue, induce the tumor regression and improve the complete remission rate of the tumor, such that the good anti-HER2 negative tumor effect is provided, no significant side effect exists, and the new strategy is provided for the treatment of the HER2 negative tumor.

The present invention relates to the discovery and characterization of novel, potent, and efficient STAT3 inhibitors which are two benzothiophene analogs named SIMMPYRA1 (SIM1) and SIMMPYRA2 (SIM2), and the method of their production by an in silico high throughput screening study. The presently disclosed STAT3 inhibitors specifically target STAT3 unregulated or irregular activation as in various STAT3-related diseases such as Triple-negative breast cancer (TNBC), a devastating form of breast cancer with poor life expectancy. The present invention discloses these inhibitors as potential prevention and treatment options for TNBC demonstrated by marked downregulation of several STAT3-dependent targets primarily IL6 and RANTES in TNBC cells, inducing apoptosis and / or downregulating cell growth suppression in multiple TNBC cells, and stimulating cytotoxicity and promoting tumor regression in vivo in a patient-derived xenograft (PDX) mouse model, without causing off-target side effects and preventing STAT3 activation-driven pathogenesis.

The invention relates to the field of medical image processing and artificial intelligence, in particular to a radiosensitivity prediction transfer learning system, which comprises a data preprocessing module for extracting and normalizing genome and PET image features of a patient; the topology maintaining feature decoupling network module constructs a feature space topological structure, and feature decoupling is achieved through manifold homeomorphic mapping; the multi-source-domain adaptive migration module guides adversarial learning based on geodesic distance, and constructs homotopy equivariant mapping to realize cross-domain feature migration; the prediction evaluation module is used for respectively constructing a parotid gland radioactive damage probability prediction network and a tumor recession rate prediction network; the clinical application interface module outputs a prediction result and provides radiotherapy scheme optimization suggestions, the problem of data heterogeneity between different platforms is effectively solved through a topology maintenance feature decoupling network, and the stability and accuracy of the model in cross-platform application are improved.

The invention relates to an anti-tumor preparation based on respiratory tract symbiotic bacteria as well as a preparation method and application thereof, and provides evidence for the first time aiming at the problem that the respiratory tract flora of a lung cancer patient is not exact in lung cancer progression clinically at present, and the evidence shows that the respiratory tract symbiotic bacteria oral streptococcus has an anti-tumor effect; when the oral streptococcus is delivered back to the respiratory tract, the anti-tumor immune response can be stimulated, and the curative effect of the oral streptococcus can be further enhanced through cobamamide. At present, a non-invasive and non-invasive inhalation type treatment mode for treating lung cancer is lacked clinically, and the anti-tumor preparation can be combined with a novel non-invasive inhalation type bacterium-metabolite immunotherapy to realize a long-term chronic disease management mode, and is a safe and convertible treatment means. On the basis that effective lung tumor control can be realized through independent use, the therapy can synergistically enhance the curative effect of immunotherapy, and tumors are induced to completely subside on 50% of tumor-bearing mice.

A computer-implemented method for predicting a clinical outcome of a patient, the method comprising: obtaining a pathology image associated with the patient; processing the pathology image including: determining a salient region of the pathology image; and segmenting the pathology image into a plurality of tiles; providing the processed pathology image as an input to a machine learning model configured to annotate the pathology image; obtaining, as an output of the machine learning model, the annotated pathology image associated with the patient, wherein the annotated pathology image includes annotations for different classes of tissues including a tumor regression; and determining, based on the annotated pathology image, a score indicative of the clinical outcome of the patient.

The application discloses a CD19-targeting bifunctional bridging molecule and application thereof in improving CAR-T cell targeting and curative effect. In view of the bottleneck of solid tumor target deficiency and antigen heterogeneity, the bifunctional "bridging molecule" DBCO-CD19 is covalently anchored on metabolic marker tumor cells with azido groups (-N3) on the surface by metabolic sugar engineering and copper-free click chemistry, so that the tumor cell surface presents CD19 antigens. The strategy converts the heterogeneous tumor atlas into a single standard CD19 target, and breaks away from the dependence on natural antigen expression. With the aid of the bridging molecule, CD19 CAR-T cells can establish precise immune recognition with target cells, and induce the formation of stable immune synapses. Research proves that the strategy can drive CAR-T cells to efficiently remove various tumors, significantly enhance deep infiltration of three-dimensional tumor spheres, and exhibit significant and continuous tumor regression.

The present invention pertains to the use of small molecules in the treatment of cancer. These compounds, which are small-molecule Furin inhibitors, show an ability to enhance sensitivity to immunotherapy and radiotherapy treatments, leading to tumor regression in mice and improved overall survival. Treatment of cancer cells with these compounds resulted in the elimination of the capacity for tumor cells and organoids to grow and invade. These results demonstrate the interest of using these small-molecule Furin inhibitors as therapeutic interventions for cancer patients.

Compositions, systems, and methods are described herein for the modulation, and in particular the reduction or inhibition, of expression or activity of MYC in a cell, animal or human subject. Such compositions, systems, and methods are useful to prevent, ameliorate, or treat diseases, including cell proliferation diseases and disorders such as cancer, particularly MYC-driven cancer. Compositions are described comprising a compound of formula (I), as well as pharmaceutical compositions or medicaments thereof. Also described are methods of use of such compositions to treat, prevent, or ameliorate diseases, including cell proliferation diseases and disorders such as cancer, in particular MYC-driven cancer. Compositions comprising conjugates and complexes of a compound of formula (I) are also described, which are also useful in the methods described herein. Methods are described comprising the use of a compound of formula (I), or pharmaceutical compositions thereof, for the reduction or inhibition of MYC expression or activity, and / or for achieving one or more desirable phenotypic outcomes such as, for example, decrease in cancer cell growth or proliferation, decrease in cancer cell viability, decrease in tumor volume (i.e., tumor regression), decrease in cancer metastasis, increase in animal or human survival, or other desired outcome with respect to particular phenotypes (e.g., body weight, metabolism, etc.). Related medicaments, kits, and methods of delivery of such compositions are described. Methods are also described for the development, manufacture, and / or synthesis of a compound of formula (I), as well as pharmaceutical compositions thereof. Furthermore, methods for diagnostics and testing comprising detecting MYC expression or activity levels, as well as compositions comprising kits for diagnostics and testing, are described.

The invention discloses a tumor vaccine as well as a preparation method and application thereof, and belongs to the technical field of tumor immunity. Aiming at the defects of long research and development period, high cost, non-obvious single-drug treatment effect and the like of the tumor vaccine at present, the invention provides a brand-new method for generating the tumor vaccine in a mouse body, a mode of pretreating the mouse by using an immune checkpoint inhibitor is utilized, and then tumor cells are inoculated subcutaneously; and after the tumor fades, the mouse can obtain strong immunocompetence to specific tumor cells, and an effect similar to that of a tumor vaccine is generated. Through verification, the mouse tumor vaccine prepared by the method provided by the invention can achieve very good tumor prevention and treatment effects. Meanwhile, the method is easy and convenient to operate, high in stability and low in cost, a brand new scheme for preparing the tumor vaccine is provided, and the possibility is provided for expanding to clinical tumor vaccines in the future.

Disclosed herein are methods of inhibiting tumor growth or producing tumor regression in a subject by administering to the subject a therapeutically effective amount of a combination of palbociclib and RAD1901.

The invention provides an application of CHCHD4 in preparation of a medicine for treating cancers. Specifically, the preparation for promoting CHCHD4 expression can be applied to preparation of drugs for treating cancers. The invention provides a treatment strategy for inhibiting tumor metastasis of triple negative breast cancer cells and promoting tumor regression through transcriptional activation of CHCHD4 genes. According to the treatment strategy, expression of CHCHD4 is activated and enhanced through gene transcription, metabolism and immune microenvironment of tumor cells are regulated and controlled, a new targeting strategy is provided for treatment of triple negative breast cancer, and important clinical application prospects are achieved.