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Related Concept Videos

Cancers Originate from Somatic Mutations in a Single Cell02:21

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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...
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The endosymbiont theory is the most widely accepted theory of eukaryotic evolution; however, its progression is still somewhat debated. According to the nucleus-first hypothesis, the ancestral prokaryote first evolved a membrane to enclose DNA and form the nucleus. Conversely, the mitochondria-first hypothesis suggests that the nucleus was formed after endosymbiosis of mitochondria.
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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.
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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Related Experiment Video

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Cell Population Analyses During Skin Carcinogenesis
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The reverse evolution from multicellularity to unicellularity during carcinogenesis.

Han Chen1, Fangqin Lin1, Ke Xing2

  • 1Key Laboratory of Gene Engineering of Ministry of Education, Cooperative Innovation Center for High Performance Computing, College of Ecology and Evolution, Sun Yat-sen University, Guangzhou 510275, China.

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|March 10, 2015
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Summary
This summary is machine-generated.

Cancer may be reverse evolution. Metastasis is driven by loss-of-function mutations in genes crucial for multicellularity, reverting cells to a unicellular state.

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Area of Science:

  • Evolutionary biology
  • Cancer biology
  • Genetics

Background:

  • Metazoan multicellularity evolved complex genetic constraints.
  • Cancer's origins and progression remain incompletely understood.
  • Theoretical models link cancer to disruptions in these multicellularity constraints.

Purpose of the Study:

  • To investigate the role of multicellularity genes in cancer metastasis.
  • To characterize the evolutionary trajectory of a xenograft tumor.
  • To explore the relationship between cancer gene evolution and multicellularity.

Main Methods:

  • Whole-life history characterization of a xenograft tumor.
  • Analysis of gene expression patterns.
  • Comparative analysis of cancer gene birth rates and mutation types.

Main Results:

  • Metastasis is driven by positive selection for loss-of-function mutations in multicellularity genes.
  • Downregulation of multicellularity genes and an expression profile shift towards embryonic stem cells were observed.
  • Cancer gene evolution shows an elevated birth rate, with a prevalence of loss-of-function tumor suppressors.

Conclusions:

  • Cancer represents a reverse evolution towards a unicellular state, driven by loss-of-function mutations.
  • This model explains tumor heterogeneity, distant metastases, and has therapeutic implications.
  • Understanding cancer as dedifferentiation provides a new framework for treatment strategies.