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Cancer-Critical Genes I: Proto-oncogenes

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

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Published on: February 21, 2018

Leukemogenic transformation by HOXA cluster genes.

Christian Bach¹, Sebastian Buhl, Dorothée Mueller

¹Department of Genetics, University Erlangen, Erlangen, Germany.

|February 5, 2010

Summary

Anterior HOXA genes, excluding HOXA2 and HOXA5, promote hematopoietic malignancy by blocking differentiation and cooperating with Meis1. These genes can independently cause acute myeloid leukemia, challenging previous assumptions.

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Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells

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HOX Loci Focused CRISPR/sgRNA Library Screening Identifying Critical CTCF Boundaries

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Published on: March 31, 2019

Area of Science:

Hematopoiesis research
Cancer genetics
Molecular biology

Background:

HOX homeobox genes regulate normal and malignant hematopoiesis.
Abdominal-type HOXA genes, such as HOXA9, are known leukemogenic factors.
The oncogenic potential of anterior HOXA genes in hematopoiesis is largely unexplored.

Purpose of the Study:

To comprehensively assess the oncogenic potential of all HOXA genes in primary hematopoietic cells.
To investigate the role of anterior HOXA genes in cellular transformation and acute myeloid leukemia development.
To determine if anterior HOXA genes' transforming function is mediated by endogenous HOXA9.

Main Methods:

Assessed oncogenic potential of all HOXA genes in primary hematopoietic cells.
Utilized co-transplantation assays with Meis1.
Generated and transplanted permanent cell lines derived from HOXA gene-transformed cells.
Conducted kinetic studies with inducible HOX derivatives.

Main Results:

All HOXA genes, except HOXA2 and HOXA5, blocked or delayed hematopoietic differentiation and cooperated with Meis1.
HOXA13 promoted monocytoid development, while other active HOXA genes immortalized granulocytic/monocytic populations.
Anterior HOXA genes (HOXA1, HOXA4, HOXA6) transformed cells, inducing myeloproliferation and acute myeloid leukemia upon transplantation.
Anterior HOXA genes autonomously contributed to transformation, independent of endogenous HOXA9 expression.

Conclusions:

Anterior HOXA genes possess significant oncogenic potential in hematopoiesis.
HOXA5 does not exhibit tumor-suppressor functions as previously suggested.
These findings reveal a previously unrecognized role for anterior HOXA genes in hematopoietic malignancies, expanding our understanding of leukemogenesis.