Exon-Targeted Viral Vector Editing for Cancer Cell Proliferation
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Solution Overview
Problem
Existing cancer treatments, particularly those using genome editing technologies, are limited in efficacy due to random gene introduction and side effects, and there is a lack of effective therapies targeting cancer cells with various genetic mutations.
Innovation Solution
A non-pathogenic viral vector, such as the adeno-associated viral vector (AAV), is used to directly edit the genome of cancer cells by transducing full-length cDNA with stop codons into specific exons of genes like Kras, TP53, and APC, combined with a DNA nuclease to restore normal gene function and inhibit cancer cell proliferation.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If conventional viral vector transduction is used to introduce exogenous genes into cancer cell genomes, then gene therapy can be applied, but treatment efficiency drops and side effects occur due to random introduction
Solution Approach 1:
The patent applies local quality by targeting specific exon locations in cancer cell genomes rather than random integration. The viral vector is designed to introduce exogenous genes at predetermined sites within specific genes (e.g., Kras, TP53, APC), achieving both high efficiency and reliability through location-specific transduction.
Solution Approach 2:
The patent uses an intermediary mechanism involving viral vectors combined with DNA nucleases to achieve precise gene introduction. The viral vector serves as the intermediary carrier that delivers genetic material to specific locations in the genome, enabling controlled integration rather than random transduction.
2Adaptability or versatility
If random gene introduction is used in viral vector transduction, then treatment can be applied to various cancers, but side effects on non-targeted genes increase
Solution Approach 1:
The patent implements local quality by designing location-specific transduction for particular genes and exons relevant to cancer types. Instead of random genome-wide introduction, the system targets specific loci (e.g., exon 1 of Kras, exon 1 of TP53), thereby maintaining versatility across cancer types while minimizing harmful effects on non-targeted genes.
Solution Approach 2:
The patent applies segmentation by focusing on specific exon regions within genes rather than treating the entire genome uniformly. By segmenting the gene structure and targeting specific exons for transduction, the system achieves precise modification without affecting other genomic regions, thus reducing side effects.
3Reliability
If genome editing tools like CRISPR-Cas9 are used to repair mutant genes, then cancer cell proliferation can be inhibited, but the technology is still limited to hereditary diseases
Solution Approach 1:
The patent applies universality by adapting genome editing technology originally developed for hereditary diseases to treat cancers caused by somatic mutations. The viral vector system combined with DNA nucleases can target various cancer-related genes (Kras, TP53, APC) across different cancer types, making the therapy universally applicable to both hereditary and acquired mutations.
Solution Approach 2:
The patent uses parameter changes by modifying the application context of genome editing from hereditary to somatic mutations. By changing the target gene population and mutation type parameters, the system extends its applicability from hereditary diseases to cancers, achieving reliable proliferation inhibition across different disease categories.
Applied Scientific Principles
This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.
Function Achieved in This Case
The method effectively inhibits cancer cell proliferation with minimal impact on normal cells, offering a safer and more enduring gene therapy by restoring mutant gene functions and reducing side effects.
Implementation Method 1
a full-length cDNA with a stop codon of Kras is transduced into the first exon of Kras of a human cell genome DNA
Implementation Method 2
combined with a DNA nuclease to restore normal gene function
Data Source
AI summary
The invention relates to a viral vector formed or prepared such that a full-length cDNA having a stop codon of Kras is transduced into the first exon of Kras of a human cell genome DNA so that the viral vector can inhibit progression of cancer cells by directly editing a genome of cancer cells to repair a gene function.