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Related Concept Videos

Embryonic Stem Cells00:58

Embryonic Stem Cells

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Embryonic stem (ES) cells are undifferentiated pluripotent cells, meaning they can produce any cell type in the body. This gives them tremendous potential in science and medicine since they can generate specific cell types for use in research or to replace body cells lost due to damage or disease.
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Embryonic Stem Cells00:57

Embryonic Stem Cells

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Embryonic stem (ES) cells were first discovered in mice in 1981 by Martin Evans. In 1998, James Thomson identified a method to isolate embryonic stem cells from humans. Human embryonic stem cells (hESCs) are obtained from 3-5 day old embryos that remain unused after an in vitro fertilization procedure.
ES cells are grown in a culture medium where they can divide indefinitely, creating ES cell lines. Under certain conditions, ES cells can differentiate, either spontaneously into a variety of...
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Induced Pluripotent Stem Cells01:13

Induced Pluripotent Stem Cells

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Stem cells are undifferentiated cells that divide and produce different types of cells. Ordinarily, cells that have differentiated into a specific cell type are post-mitotic—that is, they no longer divide. However, scientists have found a way to reprogram these mature cells so that they “de-differentiate” and return to an unspecialized, proliferative state. These cells are also pluripotent like embryonic stem cells—able to produce all cell types—and are therefore...
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Adult Stem Cells01:33

Adult Stem Cells

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Stem cells are undifferentiated cells that divide and produce more stem cells or progenitor cells that differentiate into mature, specialized cell types. All the cells in the body are generated from stem cells in the early embryo, but small populations of stem cells are also present in many adult tissues including the bone marrow, brain, skin, and gut. These adult stem cells typically produce the various cell types found in that tissue—to replace cells that are damaged or to continuously...
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DNA Damage Can Stall the Cell Cycle02:36

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Related Experiment Video

Updated: Jan 27, 2026

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C UV-C Damage
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Stem cell damage after chemotherapy- can we do better?

Joy Tang1, Nan Zhu2, Sridhar Rao1

  • 1The Medical College of Wisconsin, Department of Internal Medicine, Division of Hematology and Oncology, Milwaukee, WI, 53226, USA; The Blood Research Institute, Versiti, Milwaukee, WI, 53226, USA.

Best Practice & Research. Clinical Haematology
|April 1, 2019
PubMed
Summary

Therapy-related myeloid neoplasms (t-MNs) arise from chemotherapy and radiation, causing unwanted genetic mutations in hematopoietic stem cells. Research explores mechanisms of injury and potential prevention strategies for these treatment complications.

Keywords:
ChemotherapyHematopoietic nicheHematopoietic stem cellLeukemiaMyelodysplastic syndromeRadiation

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Derivation of Hematopoietic Stem Cells from Murine Embryonic Stem Cells
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Derivation of Hematopoietic Stem Cells from Murine Embryonic Stem Cells

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Area of Science:

  • Oncology
  • Hematology
  • Molecular Biology

Background:

  • Therapy-related myeloid neoplasms (t-MNs) are serious adverse events following cytotoxic chemotherapy and radiation therapy.
  • Unlike other toxin-induced cancers, the inciting agents are necessary for treating a primary life-threatening malignancy.
  • Understanding the mechanisms of t-MN development is crucial for mitigating treatment risks.

Purpose of the Study:

  • To review the biochemical mechanisms underlying therapy-induced myeloid malignancies.
  • To discuss how chemotherapy and radiation induce genetic mutations and clonal expansion.
  • To explore damage to the hematopoietic stem and progenitor microenvironment and potential prevention strategies.

Main Methods:

  • Literature review focusing on biochemical pathways and genetic alterations.
  • Analysis of mechanisms causing DNA damage and promoting malignant clone evolution.
  • Examination of effects on the hematopoietic stem cell niche.

Main Results:

  • Cytotoxic agents induce genetic mutations, facilitating the development and expansion of malignant hematopoietic clones.
  • Chemotherapy and radiation can injure the hematopoietic stem and progenitor microenvironment.
  • Active basic research is investigating strategies to prevent stem cell injury post-therapy.

Conclusions:

  • Therapy-related myeloid neoplasms result from complex biochemical mechanisms initiated by genotoxic cancer treatments.
  • Damage to the hematopoietic stem cell microenvironment contributes to malignancy development.
  • Further research into prevention strategies is essential to improve patient outcomes and reduce treatment-related risks.