Hematopoietic stem cells (HSCs) remain quiescence or undergo self-renewal toward differentiation to replenish mature blood cells throughout adult life. Under hematopoietic homeostasis, HSCs returns to steady state to minimize exhaustion. However, under condition of stress, including aging, DNA damage, chronic inflammation, radiation, metabolic and oxidative stress, etc., HSCs experience abnormal differentiation and dysregulations in repair mechanisms. Stress-response pathways could offer fitness of HSC and contribute to rapid growth of malignant cells.
Studies have shown that: loss of function of genes (e.g., DDX41, SF3B1, etc.) could result in DNA replication stress and lead to genetic instability and impair cell proliferation; Mutation in transcriptional repressor ETV6 impacts hematopoiesis and promotes leukemogenesis; HSC exhaustion via redox stress could contribute to initial leukemia stem cell transformation. Pharmacological targeting of the hematopoietic stress is highly needed to limit malignant transformation.
The purpose of this research topic is to stimulate research in understanding molecular processes in response of stress in hematopoietic cells, also identifying new therapeutic targets for blood disorders and blood cancer.
Quiescence in pre-leukemic HSCs is crucial for the progression and maintenance of the leukemia clone. However, the underlying molecular mechanisms are not entirely clear. Genetic screening has been done in recent studies, and quiescence-associated genes are indispensable for proliferation and survival of leukemia cells. Studies in markers of inflammation and other stress will help attenuation of disease progression.
In response to stress, cell signaling pathways (e.g., AMPK) are involved in gene transcriptional/epigenetic regulation. It is essential to elucidate stress-response pathways and develop therapeutic interventions in hematological malignancies.
We are requesting review articles and original research articles addressing hematological stress which is including but not limited to the following themes:
1. Establishing functional screen system to identify stress-response pathways or gene regulation network in hematopoietic disease pathogenesis, combined with bioinformatics (e.g., gene expression profiling, chromatin accessibility profiling, etc.).
2. Exploring how transcriptional reprogramming might be involved in skewed differentiation and cell-fate determination of stem cells under stress.
3. Pinpointing biomarkers (e.g., gene mutation, gene modification, etc.) that could activate quiescent stem cells and drive pre-leukemic HSCs expansion.
Hematopoietic stem cells (HSCs) remain quiescence or undergo self-renewal toward differentiation to replenish mature blood cells throughout adult life. Under hematopoietic homeostasis, HSCs returns to steady state to minimize exhaustion. However, under condition of stress, including aging, DNA damage, chronic inflammation, radiation, metabolic and oxidative stress, etc., HSCs experience abnormal differentiation and dysregulations in repair mechanisms. Stress-response pathways could offer fitness of HSC and contribute to rapid growth of malignant cells.
Studies have shown that: loss of function of genes (e.g., DDX41, SF3B1, etc.) could result in DNA replication stress and lead to genetic instability and impair cell proliferation; Mutation in transcriptional repressor ETV6 impacts hematopoiesis and promotes leukemogenesis; HSC exhaustion via redox stress could contribute to initial leukemia stem cell transformation. Pharmacological targeting of the hematopoietic stress is highly needed to limit malignant transformation.
The purpose of this research topic is to stimulate research in understanding molecular processes in response of stress in hematopoietic cells, also identifying new therapeutic targets for blood disorders and blood cancer.
Quiescence in pre-leukemic HSCs is crucial for the progression and maintenance of the leukemia clone. However, the underlying molecular mechanisms are not entirely clear. Genetic screening has been done in recent studies, and quiescence-associated genes are indispensable for proliferation and survival of leukemia cells. Studies in markers of inflammation and other stress will help attenuation of disease progression.
In response to stress, cell signaling pathways (e.g., AMPK) are involved in gene transcriptional/epigenetic regulation. It is essential to elucidate stress-response pathways and develop therapeutic interventions in hematological malignancies.
We are requesting review articles and original research articles addressing hematological stress which is including but not limited to the following themes:
1. Establishing functional screen system to identify stress-response pathways or gene regulation network in hematopoietic disease pathogenesis, combined with bioinformatics (e.g., gene expression profiling, chromatin accessibility profiling, etc.).
2. Exploring how transcriptional reprogramming might be involved in skewed differentiation and cell-fate determination of stem cells under stress.
3. Pinpointing biomarkers (e.g., gene mutation, gene modification, etc.) that could activate quiescent stem cells and drive pre-leukemic HSCs expansion.
