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Related Concept Videos

Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
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...
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...
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...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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...

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Related Experiment Video

Updated: Jun 6, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

Apoptosis promotes early tumorigenesis.

D Tang1, M T Lotze, R Kang

  • 1Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA 15213, USA. tangd2@upmc.edu

Oncogene
|December 15, 2010
PubMed
Summary
This summary is machine-generated.

Cancer cells often resist apoptosis, a programmed cell death process. However, surprisingly, key apoptosis inducers like CD95 and PUMA can paradoxically promote tumor growth, revealing complex roles in cancer development.

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Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia
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Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia

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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Related Experiment Videos

Last Updated: Jun 6, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia
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Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia

Published on: July 25, 2017

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Death Research

Background:

  • Cancer is characterized by resistance to apoptosis.
  • Apoptosis plays a critical role in preventing uncontrolled cell proliferation.
  • The dual role of apoptosis in cancer is an area of active investigation.

Purpose of the Study:

  • To investigate the seemingly paradoxical roles of apoptosis regulators in tumorigenesis.
  • To explore how CD95/Fas/Apo1 and PUMA contribute to cancer promotion.
  • To understand the complex involvement of apoptosis in the multifaceted nature of cancer development.

Main Methods:

  • Review of recent studies on apoptosis regulators in cancer.
  • Analysis of the roles of CD95/Fas/Apo1 in death receptor pathway activation.
  • Examination of p53 upregulated mediator of apoptosis/PUMA in mitochondrial apoptotic pathway induction.

Main Results:

  • CD95/Fas/Apo1, a death receptor pathway inducer, was found to promote tumorigenesis.
  • p53 upregulated mediator of apoptosis/PUMA, a mitochondrial pathway inducer, also demonstrated pro-tumorigenic effects.
  • These findings challenge conventional understanding of apoptosis's role in cancer.

Conclusions:

  • Apoptosis regulators CD95/Fas/Apo1 and PUMA have complex, context-dependent roles in cancer.
  • These proteins can paradoxically promote tumorigenesis, highlighting intricate mechanisms in cancer biology.
  • Further research is needed to fully elucidate the multifaceted roles of apoptosis in cancer development and progression.