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相关概念视频

Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Cellular Adaptation IV: Dysplasia and Metaplasia01:24

Cellular Adaptation IV: Dysplasia and Metaplasia

DysplasiaDysplasia refers to abnormal changes in the size, shape, and organization of mature cells, characterized by pleomorphism, nuclear abnormalities, and increased mitotic activity. It commonly affects epithelial tissues, including the cervix, gastrointestinal tract, respiratory mucosa, and endometrium. Although it may occur alongside hyperplasia, dysplasia is not a true adaptive response but a preneoplastic change with potential to progress to cancer.When confined above the basement...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...

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相关实验视频

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Three-dimensional Cell Culture Model for Measuring the Effects of Interstitial Fluid Flow on Tumor Cell Invasion
07:41

Three-dimensional Cell Culture Model for Measuring the Effects of Interstitial Fluid Flow on Tumor Cell Invasion

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瘤形态和表型进化是由微环境的选择性压力驱动的.

Alexander R A Anderson1, Alissa M Weaver, Peter T Cummings

  • 1Division of Mathematics, University of Dundee, Dundee, DD1 4HN, Scotland, UK. anderson@maths.dundee.ac.uk

Cell
|November 30, 2006
PubMed
概括

恶劣的瘤微环境通过选择攻击性克隆来驱动癌症的入侵. 温和的条件允许攻击性和不那么攻击性癌细胞的共存,防止侵入性传播.

科学领域:

  • 在瘤学瘤学.
  • 数学生物学 数学生物学
  • 癌症研究 癌症研究

背景情况:

  • 癌症侵袭是一个复杂的,危及生命的过程,由多种因素驱动.
  • 在驱动入侵过程中,细胞特征和瘤微环境之间的相互作用仍然不太清楚.

研究的目的:

  • 开发一个综合细胞和微环境因素的多尺度数学模型,以了解癌症的入侵.
  • 为了研究不同瘤微环境条件如何影响癌细胞的克隆进化和入侵.

主要方法:

  • 开发一个模拟癌症入侵的多尺度数学模型.
  • 在模型中包括细胞特性和微环境因素 (低氧,细胞外矩阵异质性).
  • 在不同的微环境条件下模拟瘤生长和克隆动态.

主要成果:

  • 恶劣的微环境 (低氧,异质矩阵) 促进具有指纹边缘的侵入性生长,由侵略性克隆主导.
  • 温和的微环境 (normoxia,同质矩阵) 导致带有光滑边缘的非侵入性瘤,允许攻击性和不那么攻击性克隆的共存.
  • 微环境选择性力量被确定为癌细胞克隆进化和侵入性潜力的关键驱动因素.

结论:

  • 瘤微环境在选择驱动入侵的癌细胞表型方面发挥着至关重要的作用.

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  • 数学建模提供了一个框架,用于定量分析微环境对癌症入侵的选择性压力.
  • 这种方法可以指导制定策略,以准和消除促进入侵的选择性力量.