Aurora A Kinase Inhibitor Response Prediction via Biomarker Profiling
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Solution Overview
Problem
Current cancer treatments face challenges in identifying which patients will respond effectively to therapies, leading to unnecessary trial-and-error approaches and potential harm.
Innovation Solution
The disclosure provides methods for determining the genetic profile of patients to identify specific markers associated with responsiveness to Aurora A Kinase inhibitors, such as alisertib, allowing for personalized treatment strategies.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If cancer treatments are administered without genetic profiling, then all patients receive the same therapy, but this leads to trial-and-error approaches and potential harm from ineffective treatments
Solution Approach 1:
The patent performs genetic profiling of patients before administering cancer therapy to identify biomarkers that predict response to Aurora A kinase inhibitors. This preliminary action of genetic testing and biomarker identification enables clinicians to select the most appropriate treatment upfront, avoiding trial-and-error approaches and reducing the time patients spend on ineffective therapies.
2Adaptability or versatility
If genetic profiling is performed to identify responders, then treatment can be personalized, but this increases diagnostic complexity and requires additional testing
Solution Approach 1:
The patent extracts and focuses on specific biomarkers and genetic mutations that are most predictive of response to Aurora A kinase inhibitors. By identifying and measuring only these key biomarkers rather than performing comprehensive genomic analysis, the diagnostic process is simplified while still enabling personalized treatment selection. This extraction of critical information reduces diagnostic complexity while maintaining adaptability.
Data Source
AI summary
Disclosed herein are WNT and Hippo pathway markers associated with sensitivity to treatment with Aurora A kinase inhibitors. Claimed genes include LEF1, MAP3K7, APC, FZD2, PRKCA, RORA, CAMK2G, JUN, XP01, ROR2, CCND1 & CTNNB1 (WNT pathway) and AMOT, DVL2, LATS1, LATS2, MOB1 B, NPHP4, TJP1, TJP2, WCC1, WWTR1 & YAP1 (Hippo pathway). Sensitivity to treatment with an Aurora A kinase inhibitor is observed when the aforementioned markers have mutations in tumor cells. Compositions and methods are provided to assess marker genes to predict response to Aurora Kinase A inhibition treatment and for patient selection.


