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Related Concept Videos

Cancer02:18

Cancer

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Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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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.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
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Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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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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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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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.
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Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
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Generation of Heterogeneous Drug Gradients Across Cancer Populations on a Microfluidic Evolution Accelerator for Real-Time Observation
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Generation of Heterogeneous Drug Gradients Across Cancer Populations on a Microfluidic Evolution Accelerator for Real-Time Observation

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Constraints in cancer evolution.

Subramanian Venkatesan1,2, Nicolai J Birkbak1,2, Charles Swanton3,2

  • 1UCL Cancer Institute, CRUK Lung Cancer Centre of Excellence, Paul O'Gorman Building, Huntley St., London WC1E 6DD, U.K.

Biochemical Society Transactions
|February 17, 2017
PubMed
Summary
This summary is machine-generated.

Cancer evolution, driven by intratumour heterogeneity, fuels therapy resistance. However, constraints like parallel and convergent evolution suggest cancer evolution may be exploitable for new diagnostics and therapies.

Keywords:
cancerconvergent cancer evolutionintratumour heterogeneityparallel cancer evolutiontumour evolution

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Area of Science:

  • Oncology
  • Genomics
  • Evolutionary Biology

Background:

  • Intratumour heterogeneity (ITH) and natural selection drive resistance to cancer therapies.
  • Deep genome sequencing enables quantitative analysis of tumour heterogeneity and cancer evolution patterns.
  • Emerging evidence suggests cancer evolution may operate under specific constraints.

Purpose of the Study:

  • To review the origins of intratumour heterogeneity.
  • To focus on the constraints that shape cancer evolution.
  • To explore the potential exploitability of these evolutionary constraints for clinical applications.

Main Methods:

  • Review of current literature on cancer evolution and intratumour heterogeneity.
  • Analysis of evidence for evolutionary constraints, including parallel and convergent evolution.
  • Discussion of the biological impact of mutation order in cancer development.

Main Results:

  • Intratumour heterogeneity arises from various factors and contributes significantly to therapeutic resistance.
  • Cancer evolution is not entirely random and exhibits constraints such as parallel and convergent evolution.
  • The order in which mutations are acquired has a biological impact and suggests predictability.

Conclusions:

  • Understanding cancer evolutionary constraints, or 'rule books', is crucial for developing novel diagnostic and therapeutic strategies.
  • Exploiting these constraints could lead to improved treatment outcomes and patient survival.
  • Further research into cancer evolutionary dynamics can inform precision medicine approaches.