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相关概念视频

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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Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

4.7K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
4.7K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

7.3K
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...
7.3K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.1K
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...
9.1K
Mismatch Repair01:20

Mismatch Repair

4.8K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
4.8K
Mouse Models of Cancer Study02:43

Mouse Models of Cancer Study

5.5K
Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...
5.5K

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相关实验视频

Updated: Jun 12, 2025

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

9.5K

在人类癌症中识别非突变的p53功能缺陷

Qianpeng Li1,2,3, Yang Zhang1,2,3, Sicheng Luo1,2,3

  • 1National Genomics Data Center, China National Center for Bioinformation, Beijing 100101, China.

Genomics, proteomics & bioinformatics
|September 26, 2024
PubMed
概括

许多TP53野生型瘤的p53功能受损,错过了DNA测序. 这些瘤表现出与TP53突变癌症相似的特征,影响患者的治疗结果和治疗敏感性.

关键词:
癌症 癌症 癌症 癌症复合表达式是一种复合表达式.基因突变是一种DNA突变.机器学习 机器学习在p53缺乏症下,

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Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
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Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

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相关实验视频

Last Updated: Jun 12, 2025

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

9.5K
Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

2.1K

科学领域:

  • 在瘤学瘤学.
  • 基因组学就是基因组学.
  • 生物信息学是一种生物信息学.

背景情况:

  • 准确的p53功能状态评估对于癌症基因组医学至关重要.
  • 非突变的p53无活化经常被DNA测序遗漏,导致TP53野生型瘤的错误分类.
  • 这种错误分类会影响癌症预后和下游分析.

研究的目的:

  • 开发和验证机器学习模型,以重新评估TP53野生型瘤中的p53功能状态.
  • 通过测序无法检测到的功能性受损的p53的TP53野生型瘤的识别.

主要方法:

  • 支持矢量机 (SVM) 模型被构建以评估p53的功能状态.
  • 模型经过训练,并根据来自多个队伍的癌症基因组图谱 (TCGA) 数据进行交叉验证.
  • 性能指标包括AUROC,精度和回忆.

主要成果:

  • SVM模型显示出高性能 (AUROC 0.9822,精度 0.9747,回忆 0.9784).
  • 显著比例 (87%-99%) 的TP53野生型瘤表现出功能性损害的p53 (TP53WT-pRF).
  • TP53WT-pRF瘤与TP53突变瘤具有共同的基因组 (不稳定性) 和病理生理学 (缺氧) 特性.

结论:

  • 相当数量的TP53野生型瘤具有功能受损的p53,需要先进的评估方法.
  • 与TP53WT-pRF瘤相比,TP53WT-pRF瘤在临床上是截然不同的,与TP53WT-pN瘤相比,其存活率较低,治疗灵敏度更差.
  • 这些发现对个性化癌症医学和治疗策略有影响.