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Related Concept Videos

Skin Cancer01:30

Skin Cancer

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.
Basal Cell Carcinoma (BCC): BCC is the most common type of skin cancer, accounting for about 80% of cases. It typically develops in...
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...
Pigmentation01:19

Pigmentation

The color of the skin is influenced by a number of pigments, including melanin, carotene, and hemoglobin. Recall that melanin is produced by cells called melanocytes, which are found scattered throughout the stratum basale of the epidermis. The melanin is transferred to the keratinocytes via melanosomes.
Melanin occurs in two primary forms: eumelanin that provides black and brown pigment and pheomelanin that provides red color. Dark-skinned individuals produce more melanin than those with pale...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...

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Related Experiment Video

Updated: Jun 4, 2026

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis
07:41

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

Published on: March 8, 2022

Pathways to melanoma.

Justin M Ko1, Nicole F Velez, Hensin Tsao

  • 1Department of Dermatology, Harvard Medical School, Boston, MA, USA.

Seminars in Cutaneous Medicine and Surgery
|February 1, 2011
PubMed
Summary
This summary is machine-generated.

Genomic advances reveal multiple pathways driving melanoma, moving beyond the old model. Understanding these molecular profiles is key for personalized medicine, guiding patient risk, counseling, and tailored treatments.

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Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
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A 3D Organotypic Melanoma Spheroid Skin Model
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A 3D Organotypic Melanoma Spheroid Skin Model

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Related Experiment Videos

Last Updated: Jun 4, 2026

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis
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A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

Published on: March 8, 2022

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

A 3D Organotypic Melanoma Spheroid Skin Model
08:49

A 3D Organotypic Melanoma Spheroid Skin Model

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Area of Science:

  • Oncology
  • Genetics
  • Dermatology

Background:

  • Melanoma is an aggressive and complex human cancer.
  • Traditional models of melanoma development are insufficient.
  • Genomic research has uncovered diverse oncogenic pathways.

Purpose of the Study:

  • To review divergent pathways in melanoma development.
  • To highlight recently identified mutations.
  • To discuss implications for patient care and personalized medicine.

Main Methods:

  • Review of recent genomic and molecular studies on melanoma.
  • Analysis of divergent oncogenic pathways.
  • Emphasis on novel mutations and their clinical relevance.

Main Results:

  • Melanoma arises through multiple distinct molecular pathways, not a single linear progression.
  • Specific genetic mutations are identified as key drivers in these divergent pathways.
  • Molecular profiling offers insights into melanoma heterogeneity.

Conclusions:

  • Understanding melanoma's molecular complexity is crucial for advancing treatment.
  • Personalized medicine approaches require detailed knowledge of individual melanoma profiles.
  • Genomic insights guide risk stratification, genetic counseling, and customized therapy for melanoma patients.