The proliferation of keratinocytes in the hair follicle varies from slowly cycling, intermittently proliferating stem cells in the bulge to rapidly proliferating, transient cells in the bulb. To better understand the biological differences between these two compartments, we sought to identify differentially expressed genes using cDNA macroarray analysis. Cyclin D1 was one of 13 genes increased in the bulge compared to the bulb, and its differential expression Hair grows in a regulated cyclical process consisting of three distinct phases: anagen, catagen, and telogen. In human scalp follicles, anagen, the growing phase, lasts several years; catagen, the involution phase, lasts approximately 1 to 3 weeks, and telogen, the resting phase, lasts for approximately 3 months. The cellular mechanisms involved in the maintenance of the phases and the transitions between them are poorly understood. The lack of progress in this area reflects the complicated structure and physiology of the hair follicle. In addition, human hair follicles grow in an asynchronous fashion; the majority (ϳ90%) of hair follicles are in the anagen phase and less than 10% of follicles are in telogen, thus making it difficult to study the hair follicle cycle in humans. However, understanding what controls the proliferation of the follicle could have wide-ranging implications for carcinogenesis and hair disorders.One important aspect of the transition from the telogen phase to the anagen phase is the mechanism which promotes stem cell proliferation. The stem cells of the bulge region are normally quiescent throughout catagen, telogen and most of the anagen phase but proliferate briefly at anagen onset. In contrast, the anagen matrix cells, which are considered "transient amplifying" (TA) cells, proliferate constantly during anagen. In fact, these cells display one of the highest proliferative rates of any mammalian tissue, with a growth fraction of almost 100%, even outranking most malignant tumors. As in many other highly proliferative tissues, such as bone marrow and gastrointestinal epithelium, this may represent a risk for mutagenesis. But malignant tumors derived from matrix keratinocytes are exceedingly rare; although benign tumors, such as pilomatricomas, occasionally arise from hair matrix cells.In mammalian cells, proliferation is under the control of factors that regulate the transitions between different cellcycle stages at two main checkpoints. The better-characterized checkpoint is at the G1-S transition, which initiates DNA replication in S phase. The other checkpoint is at the G2-M transition, which controls mitosis and cell division. The cyclins are a family of key cell-cycle regulators that function by association with and activation of cyclin-dependent kinases (CDKs) at specific points in the cell cycle to phosphorylate various proteins that are im-

In distinction to previous reports, this case reveals that trichilemmal carcinoma can demonstrate significant biological aggression, as reflected by tumor neurotropism and by failure to respond to multiple surgical excisions. The purported outer root sheath differentiation of this neoplasm is confirmed with the use of novel immunohistochemical staining. This immunohistochemical staining may be useful in differentiating trichilemmal carcinoma from other clear cell neoplasms.

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We report an unusual congenital vesiculopustular eruption arising in a neonate as the result of the transient myeloproliferative disorder (TMD) associated with trisomy 21. In this instance, the neonate was phenotypically normal, making the diagnosis more elusive. Initially the lesions were clinically suspicious for herpetic infection. The clinical scenario quickly became highly suggestive of leukemia cutis, given the infant's extremely high white blood cell count. Further examination revealed trisomy 21 in the leukemic cells and disomy 21 in the buccal keratinocytes, and a diagnosis of self-resolving TMD was made. Biopsy specimens of the lesions showed a sparse, perivascular, atypical, mononuclear infiltrate. We suggest that examination for a TMD be undertaken in neonates with a vesiculopustular eruption and leukemic white blood cell counts.