Pharmacogenomics: PGX Oncology Panel


Pharmacogenomics: PGX Oncology Panel analyzes an individual’s genetic variations relevant to cancer treatment and the metabolism of oncology drugs.


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What is a PGX Oncology Panel?

Pharmacogenomics: PGX Oncology Panel is an analysis of an individual’s genetic variations or mutations in genes relevant to cancer treatment and the metabolism of oncology drugs. It aims to provide healthcare providers with genetic information to guide personalized cancer treatment plans, optimizing the effectiveness of chemotherapy or targeted therapy while minimizing adverse drug reactions and side effects.

This genetic test is particularly important in oncology because cancer treatments can be highly toxic, and tailoring them to an individual’s genetic profile can improve outcomes and reduce the risk of complications.

Why get a PGX Oncology Panel?

This panel analyzes 3 genes that play a significant role in maintaining the body’s metabolism. Variations in these genes can lead to differences in the way that individuals metabolize medication drugs. By understanding the genotype of patients, healthcare providers are able to make informed decisions in regards to patients healthcare.

What’s in the Panel:

  • CYP2D6,
  • G6PD &


CYP2D6 is a gene that codes for an enzyme called cytochrome P450 2D6. This enzyme plays a significant role in the metabolism of a wide range of drugs, particularly those used in healthcare, including many prescription medications.

Key points about CYP2D6:
  • CYP2D6 is primarily involved in the metabolism of drugs that contain basic nitrogen atoms in their chemical structure. These drugs are often used to treat various medical conditions, such as depression, anxiety, pain, and cardiovascular disorders.
  • Genetic variations in the CYP2D6 gene can lead to variations in enzyme activity. Individuals may have CYP2D6 enzymes that function at different rates, ranging from poor metabolizers (slow metabolism) to extensive metabolizers (normal metabolism) to ultrarapid metabolizers (fast metabolism). This genetic variability can significantly impact how individuals respond to drugs metabolized by CYP2D6.
  • CYP2D6 plays a crucial role in converting prodrugs (inactive drug forms) into their active metabolites. Therefore, the activity level of CYP2D6 can influence the effectiveness and safety of certain medications. For example, poor metabolizers may not convert prodrugs into their active forms effectively, leading to reduced drug efficacy, while ultrarapid metabolizers may experience rapid drug metabolism, potentially resulting in elevated drug concentrations and increased risk of side effects.
  • Healthcare providers may use genetic testing to guide medication selection, dosing, and adjustments, particularly for drugs known to be metabolized by CYP2D6. This personalized approach aims to optimize drug therapy and minimize the risk of adverse drug reactions or therapeutic failure.
  • CYP2D6 metabolizes medications such as antidepressants (e.g., fluoxetine, venlafaxine), antipsychotics (e.g., haloperidol), analgesics (e.g., codeine, tramadol), and antiarrhythmics (e.g., propafenone).


G6PD stands for Glucose-6-Phosphate Dehydrogenase, which is an enzyme found in the body. This enzyme plays a crucial role in protecting red blood cells from damage caused by certain chemicals, drugs, and infections.

Key points about G6PD:
  • G6PD is responsible for maintaining the balance of chemicals called glutathione in red blood cells. Glutathione helps protect red blood cells from oxidative stress, which can damage these cells and lead to conditions like hemolytic anemia.
  • G6PD deficiency is a genetic condition resulting from mutations in the G6PD gene, causing lower or abnormal enzyme levels. One or both parents can pass down this deficiency, and it impairs the enzyme’s proper functioning.
  • G6PD deficiency can cause hemolytic anemia, a condition where red blood cells are destroyed faster than they can be produced. This can result in symptoms such as fatigue, pale skin, jaundice (yellowing of the skin and eyes), and dark urine.
  • Certain factors can trigger hemolysis (the destruction of red blood cells) in individuals with G6PD deficiency. These triggers include infections, certain foods (e.g., fava beans), drugs (e.g., some antibiotics and antimalarials), and chemical substances (e.g., naphthalene, found in mothballs).
  • G6PD deficiency is common, especially in areas with historical or current malaria prevalence. This is because G6PD deficiency can provide some protection against malaria, and the genetic variation has persisted in these regions over time.
  • Healthcare providers can diagnose G6PD deficiency by conducting blood tests that measure the enzyme’s activity and identify specific genetic mutations. Healthcare providers often recommend this testing before prescribing certain medications to individuals at risk of G6PD deficiency.
  • There is no specific cure for G6PD deficiency, but individuals can manage the condition by avoiding triggers and taking precautions when necessary. This may involve avoiding certain foods, medications, and chemical exposures.
  • Severe hemolysis in G6PD-deficient individuals can be life-threatening, underscoring the need for awareness among patients and healthcare providers regarding triggers.


Methylene Tetrahydrofolate Reductase, often abbreviated as MTHFR, is an enzyme that plays a vital role in a metabolic pathway involving folate, a B-vitamin. This pathway is responsible for converting homocysteine, an amino acid, into methionine, another amino acid. Additionally, it plays a role in synthesizing DNA and repairing damaged DNA.

Key points about MTHFR:
  • MTHFR catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a form of folate that is essential for the synthesis of methionine and, subsequently, S-adenosylmethionine (SAMe). SAMe is a critical molecule involved in various biochemical reactions in the body, including DNA methylation, neurotransmitter synthesis, and more.
  • The MTHFR gene can have different genetic variants or mutations that affect its enzyme activity. Two of the most well-studied MTHFR variants are C677T and A1298C. MTHFR enzyme activity may vary in degree depending on the specific variants a person inherits.
  • Reduced MTHFR enzyme activity, often associated with certain genetic variants, can lead to elevated levels of homocysteine in the blood. High homocysteine levels pose risks, including cardiovascular disease and newborn neural tube defects.
  • MTHFR is a key enzyme in the folate metabolism pathway. Folate is essential for DNA synthesis and repair, making MTHFR critical for maintaining genetic integrity.
  • MTHFR genetic testing can identify specific variants in the MTHFR gene. Healthcare providers can use this information to assess an individual’s risk for elevated homocysteine levels and associated health conditions.
  • Dietary intake of folate, through sources like leafy green vegetables, beans, and fortified foods, can help support individuals with reduced MTHFR enzyme activity.
  • Healthcare providers use genetic information to recommend dietary changes or supplements for MTHFR-related health concerns.

Benefits of the PGX Oncology Panel

Some of the key benefits of the panel are:

  • Aids healthcare providers in selecting personalized medications based on genetic makeup, enhancing treatment effectiveness.
  • Tailoring medication to a patient’s genetics enhances treatment, leading to better symptom relief and improved health.
  • Identify genetic variations to reduce the risk of adverse drug reactions, helping providers choose safer medications.
  • Additionally, without PGX testing, healthcare providers resort to trial and error for medication and dosing. By comparison, PGX panels can expedite this process by providing insights into a patient’s likely responses to various medications.

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