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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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 daughter...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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...

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Related Experiment Video

Updated: Jun 23, 2026

Real Time Detection of In Vitro Tumor Cell Apoptosis Induced by CD8+ T Cells to Study Immune Suppressive Functions of Tumor-infiltrating Myeloid Cells
09:57

Real Time Detection of In Vitro Tumor Cell Apoptosis Induced by CD8+ T Cells to Study Immune Suppressive Functions of Tumor-infiltrating Myeloid Cells

Published on: January 29, 2019

Intrinsic tumour suppression.

Scott W Lowe1, Enrique Cepero, Gerard Evan

  • 1Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA. lowe@cshl.edu

Nature
|November 19, 2004
PubMed
Summary
This summary is machine-generated.

Cancer arises from uncontrolled cell division, but cells have built-in tumor suppressors that trigger cell death or arrest. These systems can be therapeutically targeted, even when mutated in cancer.

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Tumor Transplantation for Assessing the Dynamics of Tumor-Infiltrating CD8+ T Cells in Mice

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Last Updated: Jun 23, 2026

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Published on: January 29, 2019

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
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Area of Science:

  • Cellular biology
  • Cancer research
  • Molecular oncology

Background:

  • Uncontrolled cell-cycle progression is a hallmark of cancer.
  • Mammalian cells possess innate tumor-suppressive mechanisms, including apoptosis and senescence, to prevent aberrant proliferation.
  • These mechanisms involve complex networks of sensors and transducers.

Purpose of the Study:

  • To explore the role of tumor-suppressive mechanisms in mammalian cell proliferation.
  • To understand how mutations affecting these networks impact tumor evolution.
  • To identify therapeutic potential in latent tumor-suppressive functions.

Main Methods:

  • Review of existing literature on cell-cycle control and tumorigenesis.
  • Analysis of molecular pathways involved in apoptosis and senescence.
  • Examination of the effects of oncogenic mutations on tumor-suppressive networks.

Main Results:

  • Aberrant cell proliferation is a critical step in cancer development.
  • Innate cellular mechanisms like apoptosis and senescence act as safeguards against uncontrolled growth.
  • Mutations disabling these networks can profoundly influence tumor progression.
  • Latent tumor-suppressive potential may remain even in the presence of oncogenic mutations.

Conclusions:

  • Tumor-suppressive networks are crucial for preventing cancer.
  • Understanding these networks offers opportunities for novel cancer therapies.
  • Targeting residual tumor-suppressive functions presents a promising therapeutic avenue.