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Simplified Intrafemoral Injections Using Live Mice Allow for Continuous Bone Marrow Analysis

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Bone marrow failure as a risk factor for clonal evolution: prospects for leukemia prevention.

Grover C Bagby¹, Gabrielle Meyers

¹OHSU Cancer Institute, Oregon Health & Sciences University, 3181 SW Sam Jackson Park Road, CR-145, Portland, OR 97239, USA. grover@ohsu.edu

Hematology. American Society of Hematology. Education Program

|November 21, 2007

Summary

Patients with bone marrow failure syndromes face a higher risk of developing clonal neoplasms like leukemia. Evidence suggests resistant cells are selected from the stem cell pool, paving the way for new leukemia prevention strategies.

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Modeling Chemotherapy Resistant Leukemia In Vitro

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Published on: February 9, 2016

Area of Science:

Hematology
Oncology
Stem Cell Biology

Background:

Bone marrow failure syndromes (BMFS) increase the risk of clonal neoplasms, including paroxysmal nocturnal hemoglobinuria (PNH), myelodysplasia (MDS), and acute myelogenous leukemia (AML).
Acquired aplastic anemia survivors have a 10-20% risk of developing clonal disease within 10 years.
Inherited BMFS significantly elevate the relative risk of clonal neoplasms in both children and adults.

Purpose of the Study:

To elucidate the mechanisms underlying clonal evolution in bone marrow failure syndromes.
To validate a model of clonal evolution involving extracellular apoptotic cue resistance.
To inform new therapeutic strategies for aplastic states and leukemia prevention.

Main Methods:

Review and synthesis of accumulated evidence on clonal evolution in BMFS.
Validation of a proposed model using preclinical models.
Analysis of mechanisms involving stem cell pool selection and apoptotic resistance.

Main Results:

A model supporting the selection of extracellular apoptotic cue-resistant cells from the stem cell pool has been validated.
Preclinical models confirm the paradigm of clonal evolution in BMFS.
The findings provide a basis for reconsidering therapeutic objectives in aplastic states.

Conclusions:

Understanding clonal evolution mechanisms is crucial for managing BMFS.
The validated model offers a rational basis for developing leukemia prevention trials.
Targeting apoptotic resistance may represent a novel therapeutic avenue.