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相关概念视频

Cancer-Critical Genes I: Proto-oncogenes01:33

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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

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Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
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Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
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相关实验视频

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

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在白血病中的瘤增强剂.

Roger Mulet-Lazaro1,2, Ruud Delwel1,2

  • 1Department of Hematology, Erasmus MC Cancer Institute, Rotterdam, the Netherlands.

Blood cancer discovery
|August 2, 2024
PubMed
概括

增强器功能障碍是白血病发展的关键驱动因素,补充了传统的基因突变研究. 了解这些调节元件的变化是开发白血病新向治疗的关键.

科学领域:

  • 在瘤学瘤学.
  • 遗传学 遗传学 是一个
  • 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

  • 白血病发生研究传统上集中在蛋白质编码基因上.
  • 新出现的证据凸显了增强剂失调在癌症发展中的重要作用.

研究的目的:

  • 审查白血病中瘤增强剂形成的机制.
  • 讨论针对白血病中增强剂元素的治疗策略.

主要方法:

  • 关于白血病发生和增强剂生物学的当前文献的综述.
  • 对影响增强剂的遗传和表观遗传变化的分析.

主要成果:

  • 基因异常,如转位,点突变和副本数变化,可以产生致癌增强剂.
  • 这些失调的增强剂通过改变基因表达来驱动白血病的转变.

结论:

  • 增强器功能障碍是白血病的关键,以前被低估的因素.
  • 针对这些调节因素为精准医学在白血病治疗中提供了有前途的途径.

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