CRF Biomarker Gene Expression Analysis and Targeted Therapy

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Solution Overview

Problem

There is a lack of effective characterization and management of cancer-related fatigue (CRF), a distressing and debilitating symptom for cancer patients, due to insufficient understanding of its mechanisms and limited therapeutic targets.

Innovation Solution

Identification of specific genes such as SNCA, SLC25A37, and BCL2L1 that are up- or down-regulated in patients with CRF, allowing for diagnostic methods and therapeutic interventions by altering their expression or activity.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Duration of action of stationary object

If cancer treatments are advanced to increase cure and survival rates, then patient survival is improved, but cancer-related fatigue persists and impairs occupational and interpersonal performance

Engineering Contradiction:
Improvepatient survivalVSAvoidoccupational and interpersonal performance
Core Design Contradiction:
Duration of action of stationary objectVSReliability

Solution Approach 1:

The patent introduces inflammatory cytokines (IL-1, IL-6, TNF-α) as intermediary molecules that mediate the effect of cancer treatment on fatigue. These cytokines act as messengers between the tumor microenvironment and the central nervous system, explaining the mechanism by which treatment-induced inflammation leads to fatigue symptoms, thereby enabling targeted intervention strategies

Inventive Principle:
Principle #24Intermediary (Mediator)

2Reliability

If inflammatory cytokines are produced during cancer treatment to combat cancer, then cancer treatment effectiveness is improved, but fatigue symptoms worsen due to CNS alteration

Engineering Contradiction:
Improvecancer treatment effectivenessVSAvoidfatigue symptoms
Core Design Contradiction:
ReliabilityVSObject-affected harmful factors

Solution Approach 1:

The patent identifies inflammatory cytokines as the harmful factor causing fatigue, but also recognizes them as necessary components of the cancer treatment response. The approach converts this harmful effect into a diagnostic target by measuring cytokine levels and gene expression patterns, enabling monitoring of treatment response and fatigue severity without changing the fundamental treatment paradigm

Inventive Principle:
Principle #22Blessing in disguise (Convert harm into benefit)

3Ease of manufacture

If there is insufficient characterization of CRF mechanisms, then treatment management is poor, but identifying genetic markers enables accurate diagnosis and treatment

Engineering Contradiction:
Improvetreatment managementVSAvoidCRF mechanism characterization
Core Design Contradiction:
Ease of manufactureVSLoss of information

Solution Approach 1:

The patent replaces complex physiological and biochemical characterization of CRF with molecular genetic markers. Instead of measuring multiple physiological parameters and cytokine levels, the invention uses specific gene expression patterns (SNCA, SLC25A37, BCL2L1) as proxies that directly indicate CRF status, simplifying diagnosis and enabling routine clinical application

Inventive Principle:
Principle #28Mechanics substitution (Replace mechanical system)

Data Source

PatentUS8597883B2Biomarkers for cancer-related fatigue and use thereof
Publication Date: 2013.12.03 THE GOVERNMENT OF THE UNITED STATES OF AMERICA AS REPRESENTED BY THE SECRETARY DEPARTMENT OF HEALTH & HUMAN SERVICES
  • US8597883B2 patent drawing
  • US8597883B2 patent drawing
  • US8597883B2 patent drawing

AI summary

Described herein is the identification of genes that are significantly up- or down-regulated in patients suffering from cancer-related fatigue (CRF), providing a means for the diagnosis and treatment of CRF. In particular, provided herein is a method of diagnosing a subject with CRF by detecting expression of at least one gene associated with CRF in a sample obtained from the subject; and comparing expression of the at least one gene to a control. Also described herein is a method of treating a patient with CRF by administering to the subject an agent that alters expression or activity of a gene associated with CRF. Further provided is array that includes a plurality of genes associated with CRF, such as TNFRSF25, SLC6A8, OGT, SNCA, APBA2, CASK, OR2W3, MYL4, IL7R, ARHGEF10 and ITGA6.