Telomerase expression in sebaceous lesions of the skin Background: Recent studies have demonstrated telomerase expression in ophthalmologic sebaceous carcinoma and have suggested possible diagnostic utility in distinguishing these neoplasms from sebaceous adenomas. The aim of this study was to evaluate telomerase expression via human telomerase reverse transcriptase (hTERT) immunohisto- chemical staining in a spectrum of sebaceous lesions of the skin. Methods: Paraffin-embedded sections from sebaceous hyperplasia (11), nevus sebaceus (22), sebaceous adenoma (19), sebaceoma (11), and sebaceous carcinoma (14) were evaluated for intensity (0 to 3+) and pattern of anti-hTERT staining. Results: Strong (2 to 3+) hTERT staining was observed in nucleoli of germinative cells and immature sebocytes in all sebaceous lesions, whereas mature sebocytes were negative. The distribution pattern paralleled features seen by routine haematoxylin and eosin-stained sections. Conclusions: All hyperplastic and neoplastic sebaceous skin lesions expressed hTERT in this immunohistochemical study. The pattern of staining was predictive of the histologic pattern of the process but does not significantly add to our diagnostic armamentarium of sebaceous lesions. Olsen SH, Su LD, Thomas D, Fullen DR. Telomerase expression in sebaceous lesions of the skin. J Cutan Pathol 2007; 34: 386–391. # Blackwell Munksgaard 2006. Stephen H. Olsen 1 , Lyndon D. Su 1,2 , Dafydd Thomas 1,3 and Douglas R. Fullen 1,2 1 Department of Pathology, 2 Department of Dermatology, and 3 Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA Douglas R. Fullen, MD, M3261, Medical Sciences I, Department of Pathology, University of Michigan Medical Center, 1301 Catherine, Ann Arbor, MI 48109-0602, USA Tel: þ1 734 764 4460 E-mail: dfullen@med.umich.edu Accepted for publication May 15, 2006 Telomeres are tandem nucleotide repeats, (TTAG- GG) n , located at the ends of chromosomes in all vertebrates; they function to protect chromosomes from degradation and aberrant recombination dur- ing replication. 1–5 Telomere length or number of repeats, in turn, is maintained by the ribonucleo- protein DNA polymerase complex, telomerase, although alternate pathways exist. 6,7 This complex is composed of an RNA moiety (hTR) and an RNA- dependant DNA polymerase (hTERT). Telomerase expression is repressed in most human somatic cells, resulting in progressive loss of telomeres and short- ening of chromosomes with successive cell divisions. Eventually, chromosomes reach a critical length at which cell division ceases, senescence begins, and the cells ultimately undergo apoptosis or cell death. 8,9 In addition, telomerase activity has been detected in germline cells, somatic cells during fetal develop- ment, germinal centres of lymph nodes, regenerative epithelium of the gastrointestinal tract, proliferative endometrium, the bulge region of hair follicles, stem cells of the epidermis, sweat glands, and sebaceous glands. 10–17 Immortalized cell lines of a vast array of human cancers, such as breast, colorectal and ovarian cancers, and melanoma, have been shown to over- express telomerase. 18–24 In addition to melanoma, several other cutaneous neoplasms have been shown to express telomerase, including basal cell carcinoma, in situ and invasive squamous cell carcinoma, eccrine carcinoma, poroma and porocarcinoma, trichilem- mal carcinoma, common acquired and Spitz nevi, and seborrheic keratosis. 16,17,25–27 Thus, telomerase is reputed to play a role in the unregulated prolif- eration and ultimate immortality of somatic cells in a variety of benign and malignant tumors. 28–32 Telomerase has been identified in sebaceous car- cinoma of the orbit, but not in sebaceous adenomas, J Cutan Pathol 2007: 34: 386–391 doi: 10.1111/j.1600-0560.2006.00624.x Blackwell Munksgaard. Printed in Singapore Copyright # Blackwell Munksgaard 2006 Journal of Cutaneous Pathology 386