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Background: The prognosis of hyperproliferative skin lesions, such as psoriasis, basal cell carcinoma, and non‐melanoma skin cancers, is significantly benefited from the levels of tazarotene‐induced gene‐1 (TIG3) expression and subsequent treatment with tazarotene. Such observations suggest that TIG3 could be used as a biomarker for apoptosis, differentiation, and proliferation. The current study aimed to evaluate the expression of TIG3 in normal oral mucosa (NOM) and oral squamous cell carcinoma (OSCC) compared with normal skin (NS) and skin squamous cell carcinoma (SSCC) using immunohistochemistry. Methods: Seventeen cases each of SSCC, OSCC, NOM, and NS were evaluated. Each section was immunohistochemically stained with a rabbit polyclonal TIG3 antibody. The entire procedure was blinded and evaluated by 5 observers. Statistical analysis was performed using the chi‐square test. Results: There was a significant decrease in TIG3 protein expression in OSCC and SSCC compared with that in NOM and NS (P = 0.008). The progressive loss of expression was observed as the grade of both malignancies increased. However, there was no significant difference in the expression among the normal tissue groups and within SCC groups of similar grades. Conclusion: The present study suggests that the loss of TIG3 is an important event in carcinogenesis. TIG3 acts as a regulator of keratinocyte proliferation and terminal differentiation. Therefore, TIG3 could be a potential biomarker to differentiate aggressive and non‐aggressive neoplasms. [ABSTRACT FROM AUTHOR]

Dear Editor, A 54-year-old woman with skin phototype IV had a slow-growing pigmented lesion over the inner lower quadrant of the left breast since 6 months. In the index case, the CD34 negativity may be due to a different clone (EP88).6 In conclusion, this report describes the clinico-dermoscopic features of pigmented trichilemmoma in a patient with dark skin that mimics other pigmented tumours. A discontinuous or absent basement membrane can be due to low cellular differentiation or inflammatory cells that degrade the basement membrane.4 In our case, the dense lymphocyte infiltration was probably responsible for the absent basement membrane. [Extracted from the article]

1b).1 Histopathology showed a well-circumscribed neoplasm comprising of anastomosing cords and strands of basaloid cells in a scant fibro-myxoid stroma that was at many places attached to cystic spaces lined by follicular infundibular type epithelium. Differential diagnosis of seborrhoeic keratosis (SK), basal cell carcinoma (BCC), pigmented actinic keratosis and Bowen disease was considered. A 70-year-old woman with skin phototype V had a slow-growing asymptomatic pigmented lesion on the face for two years. [Extracted from the article]

Differential diagnosis of malignant melanoma, pigmented Bowen disease / intraepidermal carcinoma and porokeratosis was considered. In India, differentiating pigmented Bowen disease / intraepidermal carcinoma from acral lentiginous melanoma is of utmost importance owing to their different management and therapeutic outcome. There was also a very strong clinical clue to differentiating pigmented Bowen disease / intraepidermal carcinoma from melanoma by the presence of pigmented keratin scales. [Extracted from the article]