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Related Concept Videos

Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
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...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...

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Updated: May 21, 2026

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
08:18

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene

Published on: December 31, 2014

MAX and MYC: a heritable breakup.

Alberto Cascón1, Mercedes Robledo

  • 1Hereditary Endocrine Cancer Group, Spanish National Cancer Research Centre, Madrid, Spain. acascon@cnio.es

Cancer Research
|June 19, 2012
PubMed
Summary
This summary is machine-generated.

MYC overexpression disrupts the MYC/MAX/MXD1 network, driving cancer. MAX mutations in hereditary pheochromocytoma highlight MAX

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The MYC/MYC-associated protein X (MAX)/MAX dimerization protein 1 (MXD1) network regulates cell growth and differentiation.
  • MYC overexpression is common in tumors and disrupts this network's balance.
  • Recent findings suggest MYC has functions independent of MAX.

Purpose of the Study:

  • To investigate the role of the MYC/MAX/MXD1 network in cancer development.
  • To explore the significance of MAX mutations in hereditary cancers.
  • To identify MYC as a potential therapeutic target.

Main Methods:

  • Analysis of the MYC/MAX/MXD1 network.
  • Examination of germline MAX mutations in hereditary pheochromocytoma patients.
  • Review of genetic hallmarks in neural tumors.

Main Results:

  • Germline MAX mutations indicate MAX's role as a negative regulator.
  • MYC deregulation is implicated in hereditary cancer predisposition.
  • Impairment of the MYC/MAX/MXD1 axis is crucial for aggressive neural tumors.

Conclusions:

  • MYC plays a significant role in hereditary cancer predisposition.
  • The MYC/MAX/MXD1 axis is critical in aggressive neural tumor development.
  • Targeting MYC may be a viable strategy for metastatic pheochromocytoma treatment.