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Related Experiment Video

Updated: May 26, 2026

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells

Published on: September 1, 2019

CREB and leukemogenesis.

Er-Chieh Cho¹, Bryan Mitton, Kathleen M Sakamoto

¹Division of Hematology/Oncology, Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California 90095-1752, USA.

Critical Reviews in Oncogenesis

|December 14, 2011

Summary

The cAMP response element binding protein (CREB) is overexpressed in acute myeloid leukemia (AML) and linked to poor patient outcomes. Understanding CREB

Area of Science:

Hematology
Molecular Biology
Cancer Research

Background:

Acute myeloid leukemia (AML) has poor survival rates despite intensive treatments.
Limited progress in reducing AML incidence and mortality necessitates understanding molecular drivers.
Transcription factors are critical in leukemogenesis, with cAMP response element binding protein (CREB) emerging as a key player.

Purpose of the Study:

To review the role of cAMP response element binding protein (CREB) in acute myeloid leukemia (AML) development.
To highlight CREB's function in regulating cellular processes vital to leukemogenesis.
To discuss the association between CREB overexpression and patient prognosis in AML.

Main Methods:

Literature review of studies investigating CREB in acute leukemia.

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Analysis of CREB's regulatory functions in cell proliferation, survival, and differentiation.

Examination of clinical data linking CREB expression levels to AML outcomes.

Main Results:

CREB is a transcription factor regulating key cellular functions.
Overexpression of CREB is frequently observed in bone marrow samples from AML patients.
Elevated CREB levels correlate with a poorer prognosis in AML.

Conclusions:

CREB plays a significant role in the development of acute myeloid leukemia.
CREB overexpression represents a potential biomarker for poor outcomes in AML.
Further research into CREB's mechanisms may offer new therapeutic strategies for AML.