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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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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...
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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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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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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.
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Skin Cancer01:30

Skin Cancer

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Skin cancer is a type of cancer that occurs when there is an abnormal growth of skin cells, usually triggered by damage to the DNA within the skin cells. It is primarily caused by exposure to ultraviolet (UV) radiation from the sun or artificial sources like tanning beds. Skin cancer is the most common type of cancer worldwide, and its incidence continues to rise.
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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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...
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Related Experiment Video

Updated: Apr 26, 2026

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
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UV and melanoma: the TP53 link.

Yeon Sook Choi1, David E Fisher1

  • 1Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA.

Cell Research
|July 19, 2014
PubMed
Summary

Ultraviolet radiation (UVR) is a known melanoma risk factor. This study reveals that UVR-induced mutations in the TP53 gene accelerate melanoma development driven by BRAF(V600E).

Area of Science:

  • Oncology
  • Dermatology
  • Molecular Biology

Background:

  • Ultraviolet radiation (UVR) is a primary risk factor for melanoma.
  • The precise mechanisms linking UVR exposure to melanoma development (melanomagenesis) remain incompletely understood.

Purpose of the Study:

  • To elucidate the role of UVR-induced genetic alterations in melanoma.
  • To identify specific genes targeted by UVR that contribute to melanomagenesis.

Main Methods:

  • Analysis of gene expression and mutation profiles in melanoma.
  • Investigating the functional impact of TP53 mutations in the context of BRAF(V600E) oncogene activation.

Main Results:

  • TP53 (also known as Trp53) was identified as a direct UVR-target gene in melanoma.

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  • UVR-induced mutations in TP53 significantly accelerate the progression of melanomagenesis driven by the BRAF(V600E) mutation.

    • Conclusions:

    • TP53 mutations are a key consequence of UVR exposure that promotes melanoma.
    • Targeting UVR-induced TP53 alterations may offer new therapeutic strategies for melanoma.