Related Experiment Video

Updated: Jun 19, 2026

Analyzing Tumor Gene Expression Factors with the CorExplorer Web Portal
08:00

Analyzing Tumor Gene Expression Factors with the CorExplorer Web Portal

Published on: October 11, 2019

The EGFR pathway as an example for genotype: phenotype correlation in tumor genes

Ulrike Mogck1, Eray Goekkurt, Jan Stoehlmacher

  • 1Department of Internal Medicine I, University Hospital Carl Gustav Carus, University Dresden, Dresden, Germany.

Methods in Molecular Biology (Clifton, N.J.)
|November 3, 2009
PubMed

Insights

Tumor DNA variations impact cancer growth and treatment resistance. Epidermal growth factor receptor (EGFR) genotype and Kirsten-Ras (KRAS) mutations influence response to anti-EGFR therapies in colorectal cancer.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Tumor-specific and germ-line DNA variations are key drivers of tumor growth and treatment resistance.
  • Epidermal growth factor receptor (EGFR) genotype plays a critical role in cancer treatment resistance.
  • EGFR signaling pathways regulate cancer cell proliferation and survival.

Purpose of the Study:

  • To investigate the correlation between EGFR genotype and KRAS mutation status.
  • To determine the impact of these genetic factors on anti-EGFR therapy response in colorectal cancer.

Main Methods:

  • Analysis of EGFR polymorphic DNA sequences.
  • Assessment of Kirsten-Ras (KRAS) gene mutational status.
  • Correlation of genetic findings with anti-EGFR therapy outcomes in colorectal cancer patients.

Main Results:

  • Specific EGFR genotypes and KRAS mutations are identified as determinants of response to EGFR inhibitors.
  • The study establishes a link between genetic profiles and therapeutic efficacy.
  • Genomic status significantly influences treatment outcomes in colorectal cancer.

Conclusions:

  • EGFR genotype and KRAS mutational status are crucial predictive biomarkers for anti-EGFR therapy in colorectal cancer.
  • Understanding these genetic determinants can guide personalized treatment strategies.
  • Targeted therapies based on EGFR and KRAS status can optimize patient outcomes.

More Related Videos

A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds13:34

A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds

Published on: April 6, 2016

Related Concept Videos

Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

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

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...
Epistasis Analysis01:09

Epistasis Analysis

Although Mendel chose seven unrelated traits in peas to study gene segregation, most traits involve multiple gene interactions that create a spectrum of phenotypes. When the interaction of various genes or alleles at different locations influences a phenotype, this is called epistasis. Epistasis often involves one gene masking or interfering with the expression of another (antagonistic epistasis). Epistasis often occurs when different genes are part of the same biochemical pathway. The...