Growth Factor Receptor Agonist Association for Neoplastic Cell Conversion
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Solution Overview
Problem
Existing treatments for neoplastic diseases, such as cancer, are invasive, costly, and often ineffective in converting neoplastic cells into non-neoplastic cells, leading to temporary suppression of proliferation or adaptation and resistance, and fail to address metastatic cells and cancer stem cells.
Innovation Solution
Pharmaceutical associations and compositions that activate growth factor receptors (GFR) to convert neoplastic cells into non-neoplastic cells through extracellular means, promoting self-healing and self-recovery without genome modification, using GFR-binding compounds and bioactive carriers.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If conventional chemotherapy or radiotherapy is used to treat neoplastic cells, then proliferation is suppressed or cells are destroyed, but healthy cells are damaged and resistance develops
Solution Approach 1:
Instead of using inhibitors to block growth factor receptors as in conventional therapy, this patent uses agonists to activate them. The inverted approach converts neoplastic cells into non-neoplastic cells by inducing differentiation and self-healing, rather than simply suppressing proliferation or destroying cells.
Solution Approach 2:
The treatment enables neoplastic cells to self-heal and convert into non-neoplastic cells through activation of endogenous growth factor receptors. The cells' own repair mechanisms are harnessed to correct the neoplastic phenotype, eliminating the need for continuous external intervention and reducing resistance development.
2Quantity of substance
If surgery is used to remove localized neoplastic cells, then tumor mass is reduced, but invasive procedures are required and dormant tumors may be unblocked
Solution Approach 1:
The mechanical approach of surgical removal is replaced with a biochemical mechanism. Growth factor receptor agonists are administered to induce cellular conversion, substituting physical intervention with molecular signaling to achieve tumor regression without invasive procedures.
Solution Approach 2:
The treatment leverages the body's own cellular mechanisms to convert neoplastic cells into non-neoplastic cells. This self-service approach allows the organism to treat itself, avoiding the need for external surgical intervention and reducing the risk of unblocking dormant tumors.
3Reliability
If gene therapy is used to replace defective genes, then genetic function is restored, but immune responses and integration issues arise
Solution Approach 1:
Instead of replacing defective genes with foreign DNA as in conventional gene therapy, this patent activates endogenous growth factor receptors to induce cellular conversion. The inverted strategy uses the cell's own existing machinery rather than introducing external genetic material, thereby avoiding immune responses and integration problems.
Solution Approach 2:
The treatment utilizes the cell's inherent growth factor receptor signaling pathways to drive conversion from neoplastic to non-neoplastic state. By relying on endogenous mechanisms rather than exogenous gene delivery, the approach eliminates immune rejection and genomic integration risks associated with traditional gene therapy.
Data Source
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AI summary
The present disclosure provides a pharmaceutical association for use in the treatment, prevention and/or diagnostic of a neoplastic disease, said association comprising at least one growth factor receptor-binding compound, which activates at least one growth factor receptor of a neoplastic cell, and at least one bioactive carrier forming at least one covalent or non-covalent interaction with said at least one growth factor receptor-binding compound, and wherein said association reduces or suppresses, in the neoplastic cell, the gene expression of at least one cyclin D and/or reduces or suppresses the formation of at least one complex formed between said at least one cyclin D and at least one of cyclin dependent-kinase 4 or 6.