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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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Renewal of Skin Epidermal Stem Cells01:12

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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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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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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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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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Cell Population Analyses During Skin Carcinogenesis
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Basal cell carcinoma: pathophysiology.

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    Basal cell carcinoma (BCC), the most common skin cancer, originates from the pilo-sebaceous unit. The patched/hedgehog pathway is crucial for BCC development, and inhibiting smoothened (SMO) shows therapeutic promise.

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    Area of Science:

    • Dermatology
    • Oncology
    • Molecular Biology

    Background:

    • Basal cell carcinoma (BCC) is the most prevalent human skin cancer, characterized by slow growth and local invasiveness.
    • BCC is linked to the pilo-sebaceous unit, potentially arising from pluripotent cells in the basal epidermis or hair follicle.
    • The patched/hedgehog signaling pathway is implicated in both sporadic BCC and Gorlin syndrome.

    Purpose of the Study:

    • To elucidate the role of the patched/hedgehog pathway in basal cell carcinoma development.
    • To highlight the significance of sonic hedgehog, Patched (PTCH), and smoothened (SMO) proteins in BCC pathogenesis.
    • To underscore the therapeutic potential of SMO inhibitors in advanced BCC.

    Main Methods:

    • Review of existing literature on BCC etiology and molecular pathways.
    • Analysis of the role of the patched/hedgehog signaling cascade in cell growth and differentiation.
    • Examination of the mechanism of action for vismodegib, an SMO inhibitor.

    Main Results:

    • The patched/hedgehog pathway is essential for regulating cell growth and differentiation; its dysregulation contributes to BCC.
    • Sonic hedgehog signaling, mediated by PTCH and SMO, drives abnormal cell proliferation in BCC.
    • Vismodegib, an SMO inhibitor, has demonstrated efficacy in treating advanced BCC.
    • UV-induced mutations in TP53 and PTCH genes are associated with BCC development.

    Conclusions:

    • The patched/hedgehog pathway is a critical factor in the pathogenesis of basal cell carcinoma.
    • Targeting the SMO component of this pathway offers a viable therapeutic strategy for advanced BCC.
    • Further research into UV-induced genetic alterations may provide additional insights into BCC prevention and treatment.