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MIR17HG gene
Reviewed by Medicinsk Expert•Last updated: 2026-10-22•Gene

MIR17HG gene

The MIR17HG gene acts as a host for the miR-17~92 microRNA cluster, which regulates critical cellular processes including growth, development, and apoptosis.

Normal Function

The MIR17HG gene provides instructions for making the miR-17~92 microRNA cluster, which consists of six miRNAs: miR-17, miR-18a, miR-19a, miR-19b-1, miR-20a, and miR-92a-1. These molecules control gene expression and regulate signaling pathways involved in:

  • Cell growth and division (proliferation)
  • Cell maturation (differentiation)
  • Self-destruction of cells (apoptosis)

The cluster is necessary for the normal development of the skeleton, heart, kidneys, lungs, and nervous system. The MIR17HG gene is classified as an oncogene, meaning it has the potential to cause normal cells to become cancerous when mutated.

Health Conditions Related to Genetic Changes

Feingold syndrome

Genetic changes that reduce the amount of the MIR17HG gene cause Feingold syndrome type 2. This disorder is characterized by:

  • Abnormalities of the fingers and toes (brachymesophalangy)
  • Unusually small head size (microcephaly)
  • Learning disabilities

This condition is caused by 13q31.3 microdeletions, which remove the MIR17HG gene and potentially other nearby genes, disrupting signaling pathways during development.

Other disorders

Microduplications resulting in an extra copy of the MIR17HG gene have been associated with developmental issues, including skeletal overgrowth (polydactyly and macrocephaly) or impaired growth (brachydactyly and short stature). Some affected individuals also exhibit features of autism spectrum disorder.

Cancers

Gene amplification, which results in extra copies of the MIR17HG gene, has been found in diffuse large B-cell lymphoma. These somatic changes increase the amount of miR-17~92 miRNAs, leading to uncontrolled cell proliferation or reduced apoptosis, which allows cells to grow and divide uncontrollably.

Other Names for This Gene

  • C13orf25
  • FGLDS2
  • FLJ14178
  • LINC00048
  • MIHG1
  • miR-17-92
  • MIRH1
  • MIRHG1
  • NCRNA00048

Frequently Asked Questions

MIR17HG gene amplification is not detected in routine general cancer screenings like mammograms or colonoscopies. It is a somatic genetic change, meaning it occurs in non-germline cells and is not inherited. It has been specifically identified in diffuse large B-cell lymphoma (DLBCL) and some other solid tumors. Detection requires specialized molecular testing, such as fluorescence in situ hybridization (FISH) or next-generation sequencing, which is typically performed on tumor tissue after a cancer diagnosis has been made. It is not a predictive marker for the general population but rather a diagnostic and prognostic tool for specific cancer subtypes.
Children with a 13q31.3 microdeletion involving MIR17HG often face challenges with motor and cognitive development. Common outcomes include delayed speech and language milestones, learning disabilities, and potential intellectual disability ranging from mild to moderate. Physical management focuses on orthopedic care for hand and foot abnormalities to ensure functional use and prevent secondary complications. Early intervention services, including speech therapy, occupational therapy, and special education support, are critical for maximizing developmental potential. Regular follow-up with a geneticist and developmental pediatrician is recommended to monitor for evolving symptoms and adjust care plans accordingly.
Feingold syndrome type 2 is specifically caused by a microdeletion on chromosome 13q31.3 that removes the MIR17HG gene, which hosts the miR-17~92 microRNA cluster. This is distinct from Feingold syndrome type 1, which is caused by mutations in the MYCN gene. While both types present with similar physical features like short middle phalanges (brachymesophalangy) and microcephaly, the underlying genetic mechanism and prognosis can differ. Type 2 is often associated with a broader range of developmental issues due to the potential loss of other nearby genes in the deleted region, making precise genetic mapping crucial for accurate diagnosis and counseling.
Microduplications that result in an extra copy of the MIR17HG gene can lead to a spectrum of developmental issues. Some individuals may exhibit skeletal overgrowth features such as polydactyly (extra fingers or toes) and macrocephaly (unusually large head), while others may have impaired growth, brachydactyly (short fingers), and short stature. There is a documented association between these duplications and neurodevelopmental disorders, including autism spectrum disorder (ASD). The exact mechanism is thought to involve dysregulation of the miR-17~92 cluster, which affects brain development and cell signaling pathways during critical growth periods.
Source: MedlinePlus, National Library of Medicine

MedlinePlus brings together authoritative health information from the National Library of Medicine (NLM), the National Institutes of Health (NIH), and other government agencies and health-related organizations.

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