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Related Experiment Video

Updated: Jan 10, 2026

Performing Data Mining And Integrative Analysis Of Biomarker in Breast Cancer Using Multiple Publicly Accessible Databases
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An InDel Genomic Variant within a Bifunctional Super-Enhancer for LINC00636 and CD47 Regulation in Breast Cancer.

Carolina Di Benedetto1, Amelia Tsark1, Daniza Diane Acenas1

  • 1Department of Radiation Oncology, University of California, San Francisco, San Francisco, CA, USA.

Biorxiv : the Preprint Server for Biology
|November 24, 2025
PubMed
Summary

A common genetic variant in breast cancer super-enhancers influences gene expression. This insertion-deletion variant impacts chromatin accessibility, affecting tumor-promoting genes and cell death.

Keywords:
CD47LINC00636Super-enhancerbreast cancergenomic variation

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Area of Science:

  • Genomics
  • Cancer Biology
  • Epigenetics

Background:

  • Super-enhancers are key regulatory elements driving cancer-promoting genes.
  • The impact of genomic variations within super-enhancers on cancer remains largely unknown.
  • Understanding these variations is crucial for identifying novel therapeutic targets.

Purpose of the Study:

  • To investigate the role of genomic variation in a breast cancer super-enhancer.
  • To determine how a specific insertion-deletion variant affects gene regulation and cancer progression.
  • To explore the function of LINC00636 in senescence and breast cancer.

Main Methods:

  • Identification of a bifunctional super-enhancer regulating LINC00636 and CD47 in breast cancer.
  • Analysis of a common germline insertion-deletion variant within the super-enhancer.
  • Assessment of chromatin accessibility, gene expression, apoptosis resistance, senescence, and immune cell infiltration following variant manipulation.

Main Results:

  • A common germline insertion variant is associated with reduced super-enhancer accessibility.
  • Deletion of the insertion increases accessibility, upregulating LINC00636 and CD47.
  • Upregulated genes promote tumor-associated features: apoptosis resistance, senescence, and altered macrophage infiltration.

Conclusions:

  • A common insertion-deletion variant fine-tunes super-enhancer activity, influencing breast cancer progression.
  • The insertion allele may confer a protective role against tumor-promoting effects.
  • LINC00636 plays a novel role in senescence and breast cancer development.