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Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV
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Expression of p16 in Hypertrophic Lichen Planus.

Katie R Xu1, Kord Honda1,2, Bethany R Rohr1,2

  • 1Case Western Reserve University School of Medicine, Cleveland, OH; and.

The American Journal of Dermatopathology
|February 6, 2025
PubMed
Summary
This summary is machine-generated.

Cytoplasmic p16 overexpression in hypertrophic lichen planus (HLP) suggests a role in malignant transformation to squamous cell carcinoma (SCC). This study compared p16 expression in HLP, SCC, and normal skin.

Keywords:
cell transformationcyclin-dependent kinase inhibitor p16hypertrophic lichen planusneoplasticprecancerous conditionssquamous cell carcinoma

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Area of Science:

  • Dermatology
  • Oncology
  • Molecular Biology

Background:

  • Cutaneous squamous cell carcinoma (SCC) arising from hypertrophic lichen planus (HLP) is rare but accounts for most malignant transformations.
  • The mechanism of malignant pathogenesis in HLP is unknown, but p16 may play a role, as suggested by similar premalignant conditions.
  • This study is the first to examine p16 expression in HLP versus SCC and normal skin.

Purpose of the Study:

  • To investigate p16 expression in hypertrophic lichen planus (HLP).
  • To compare p16 expression in HLP with cutaneous invasive squamous cell carcinoma (SCC) and normal skin.
  • To explore the implications of p16 expression for malignant transformation of HLP to SCC.

Main Methods:

  • p16 immunohistochemistry was performed on HLP (n=34), well-differentiated SCC (WDSCC), and normal skin.
  • Analysis included the percentage of positive cells, staining intensity (nuclear and cytoplasmic), and distribution patterns.
  • Evaluations were conducted by two Board-certified dermatopathologists.

Main Results:

  • Both HLP and WDSCC showed significantly increased p16-positive cells compared to normal skin (P < 0.001).
  • Cytoplasmic p16 was overexpressed in HLP compared to WDSCC (P < 0.05).
  • HLP and WDSCC exhibited basal and suprabasal keratinocyte staining, with weaker superficial staining. WDSCC showed focal cytoplasmic margination.

Conclusions:

  • Cytoplasmic p16 overexpression in HLP indicates a potential mechanism for p16-mediated cell cycle dysregulation.
  • p16 overexpression is a potential contributor to the malignant transformation of HLP into SCC.
  • Further research into p16's role in HLP progression is warranted.