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Related Concept Videos

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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Cancers Originate from Somatic Mutations in a Single Cell02:21

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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...
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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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A hair follicle or HF is a small part of the skin that produces the hair shaft. Paul Gerson Unna was the first to observe a bulge in the human hair follicle's outer root sheath (ORS). The bulge is present between the sebaceous gland and the arrector pili muscle and is the niche for hair follicle stem cells (HFSCs). The bulge is also a niche for melanocyte stem cells, and their loss results in graying of hair. The HFSCs express Sox9 and Lhx2, which help them maintain stemness and prevent...
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The skin is divided into epidermis, dermis, and hypodermis, the skin's outermost, middle, and inner layers. The human epidermal layer regularly undergoes renewal, where old, dead cells are replaced by new cells. Epidermal stem cells or EpiSCs divide and differentiate to restore the lost cells. For the renewal process, some EpiSCs continuously self-renew. In contrast, few others differentiate into transit-amplifying cells, which later form prickle or spinous cells, followed by granular...
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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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Updated: Jan 11, 2026

Cell Population Analyses During Skin Carcinogenesis
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Does Basal Cell Carcinoma Arise from a Precursor Lesion?

Sunny Y Wong1, Paul W Harms2, Andrzej A Dlugosz1

  • 1Department of Dermatology, University of Michigan, Ann Arbor, Michigan, USA; Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan, USA.

The Journal of Investigative Dermatology
|November 15, 2025
PubMed
Summary

Basal cell carcinoma (BCC) development requires more than just Hedgehog pathway activation. Additional genetic changes are necessary for this common skin cancer to form, suggesting a stepwise progression model.

Keywords:
BCCBFHBasaloid follicular hamartomaHedgehog signalingNonmelanoma skin cancer

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Area of Science:

  • Oncology
  • Dermatology
  • Genetics

Background:

  • Basal cell carcinoma (BCC) is primarily driven by mutations activating the Hedgehog (HH) signaling pathway.
  • Unlike other skin cancers, BCC lacks a clearly identifiable precursor lesion.
  • Genomic studies indicate that BCC formation involves multiple genetic alterations.

Purpose of the Study:

  • To explore the genetic underpinnings of Basal cell carcinoma (BCC) development.
  • To investigate the role of additional genetic changes beyond Hedgehog pathway activation in BCC formation.
  • To propose a stepwise tumor progression model for BCC.

Main Methods:

  • Analysis of genomic data from human and mouse BCC tumors.
  • Review of studies on Gorlin syndrome patients with germline PTCH1 mutations.
  • Integration of convergent evidence from various research findings.

Main Results:

  • BCC development necessitates both Hedgehog pathway activation (via PTCH1 or SMO mutations) and other genetic changes.
  • A stepwise tumor progression model, involving accumulation of multiple mutations, is suggested for BCC.
  • Subclinical precursor lesions, such as basaloid follicular hamartomas, may precede BCC formation in some cases.

Conclusions:

  • Hedgehog pathway activation is a necessary but insufficient driver for Basal cell carcinoma (BCC) development.
  • The findings support a multi-step carcinogenesis model for BCC.
  • This understanding impacts basic research, mouse models, and therapeutic strategies for BCC.