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Related Concept Videos

Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
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Related Experiment Video

Updated: Jul 14, 2026

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells
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CREB--a real culprit in oncogenesis.

Yeung-Tung Siu1, Dong-Yan Jin

  • 1Department of Biochemistry, The University of Hong Kong, Hong Kong, China.

The FEBS Journal
|June 15, 2007
PubMed
Summary

Constitutive activation of cAMP response element-binding protein (CREB) drives tumor cell proliferation. Cancer cells exploit CREB pathways through genetic alterations and coactivator activation, promoting oncogenesis.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cellular Biology

Background:

  • cAMP response element-binding protein (CREB) is a transcription factor activated by stimuli.
  • CREB regulates critical cellular processes like growth, proliferation, and survival.

Purpose of the Study:

  • To review evidence supporting CREB's role in cancer development (oncogenesis).
  • To explore mechanisms by which tumor cells achieve constitutive CREB activation.

Main Methods:

  • Literature review of existing research on CREB and oncogenesis.
  • Analysis of genetic and molecular alterations leading to CREB dysregulation.

Main Results:

  • Tumor cells constitutively activate CREB via gene amplification, translocations, viral proteins, or tumor suppressor inactivation.

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  • These alterations converge on CREB phosphorylation and/or transducer of regulated CREB activity (TORC) coactivator activation.

    • Conclusions:

    • CREB plays a direct role in driving uncontrolled cell proliferation in cancer.
    • Targeting CREB activation pathways may offer therapeutic strategies for oncogenesis.