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Targeted Cancer Therapies

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...

Targeted Cancer Therapies

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Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...

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Related Experiment Video

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Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

KRAS testing in clinical laboratory: optimizing targeted therapy.

Leticia Miravalle¹, Joel A Lefferts, Mohammad Al-Haddad

¹Department of Pathology, Indiana University School of Medicine, IN 46202, U.S.A.

Cancer Genomics & Proteomics

|September 20, 2012

Summary

Shift termination assay effectively detects KRAS mutations in various samples, crucial for colorectal cancer treatment response. This simple, robust method shows high agreement across different testing techniques.

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Area of Science:

Oncology
Molecular Diagnostics
Genetics

Background:

Activating KRAS mutations occur in over 30% of colorectal tumors.
KRAS mutations are linked to poor response to anti-EGFR therapies.
Accurate KRAS mutation testing is critical for treatment selection.

Purpose of the Study:

Evaluate a new commercial KRAS mutation detection kit using shift termination assay technology.
Assess the performance of the assay on the ABI-3130XL genetic analyzer.
Compare results with alternative methodologies across various sample types.

Main Methods:

Utilized a commercial shift termination assay kit for KRAS mutation detection.
Employed the ABI-3130XL genetic analyzer for analysis.
Compared results with parallel testing in reference laboratories using diverse methodologies.
Tested formalin-fixed paraffin-embedded tissue, fine-needle aspirates, and cyst fluid specimens.

Main Results:

Achieved 100% correlation for formalin-fixed paraffin-embedded tissue and fine-needle aspirate samples.
Demonstrated 93% correlation for cyst fluid specimens.
Showcased high agreement between the shift termination assay and alternative methods.

Conclusions:

Shift termination assay is a simple, robust, and sensitive method for KRAS mutation identification.
The assay is effective across a wide variety of specimen types.
This method provides reliable KRAS mutation detection for clinical applications.