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What is Cancer?02:12

What is Cancer?

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Cells and tissues must meticulously coordinate their activities for the normal functioning of the human body. Therefore, they exhibit socially responsible behavior - resting, growing, dividing, differentiating, or dying - for the organism’s benefit. Cancer arises when cells divide uncontrollably and invade other tissues or organs.
Although people have known about cancer for centuries, it was only in 1761 that Giovanni Morgagni of Padua performed a detailed autopsy of...
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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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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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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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The Tumor Microenvironment02:17

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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...
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Related Experiment Video

Updated: Feb 18, 2026

Monitoring the Cancer-Immunity Cycle and Exploring Tumor Microenvironment Dynamics
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Monitoring the Cancer-Immunity Cycle and Exploring Tumor Microenvironment Dynamics

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Cancer and intercellular cooperation.

Marta Bertolaso1, Anna Maria Dieli2,3

  • 1Departmental Faculty of Engineering and FAST Institute for Philosophy of Scientific and Technological Practice, Università Campus Bio-Medico di Roma, Roma, Italy.

Royal Society Open Science
|November 15, 2017
PubMed
Summary
This summary is machine-generated.

Cancer arises from a breakdown in intercellular cooperation, challenging gene-centric evolutionary models. New frameworks emphasize context and higher-level phenomena, integrating multilevel selection for a comprehensive understanding of cancer evolution.

Keywords:
cancercooperationevolutionary transitionsinclusive fitnessmultilevel selectionnatural selection

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Area of Science:

  • Evolutionary biology
  • Cancer research
  • Developmental biology

Background:

  • Multicellularity relies on intercellular cooperation, shaped by multilevel selection.
  • The Evolutionary Somatic view frames cancer as a loss of this cooperation and multilevel selection balance.
  • Gene-centric Darwinian evolution faces empirical challenges in explaining cancer progression.

Purpose of the Study:

  • To explore the limitations of gene-centric models in cancer research.
  • To propose an integrated framework for understanding cancer through the lens of intercellular cooperation and multilevel selection.
  • To investigate the role of context-dependent factors and higher-level phenomena in cancer development.

Main Methods:

  • Conceptual analysis integrating evolutionary biology and cancer research.
  • Review of empirical challenges in demonstrating somatic cell 'natural selection'.
  • Exploration of recent perspectives on 'fields' and mutation-independent cancer progression.

Main Results:

  • Gene-centric models struggle to empirically validate 'natural selection' of proto-tumoural features.
  • Cancer progression is complex, context-dependent, and not always linked to genetic changes.
  • Higher-level phenomena and 'fields' may play crucial roles in regulating intercellular cooperation and cancer.

Conclusions:

  • The Evolutionary Somatic view offers a unifying framework but requires integration with newer concepts.
  • Understanding cancer necessitates incorporating multilevel selection, context-dependency, and field effects.
  • A comprehensive interpretation of intercellular cooperation and its pathologies demands integrating multiple theoretical frameworks.