Two Squamomelanocytic Tumors With Dendritic Melanocytes: Thoughts About Origin.

ABSTRACT: Cutaneous malignant squamomelanocytic tumor (SMT) is a rare neoplasm comprising 2 distinct cell populations of squamous cell carcinoma and a second component of either benign or malignant melanocytes. SMT most often presents as a keratotic papule in areas of chronic sun exposure, typically on the head or neck of middle-aged and elderly-aged, White male patient populations. In recent years, there has been an increase in case reports, including a review article published in 2023, identifying a total of 37 cases published in the literature. There are only 3 reported cases in the literature with spindled or dendritic cells in the melanocytic component, as most have been of the epithelioid subtype. Despite the increasing prevalence, the origin and pathophysiology is poorly understood. We report 2 cases of SMT with dendritic melanocytes that are centered around a hair follicle, proposing the theory that these 2 distinct cell types may arise from the hair follicles.

Targeting PTEN but not SOCS3 resists an age-dependent decline in promoting axon sprouting.

Axonal repair is critical for functional recovery after injury of the CNS. We previously reported that neuronal PTEN deletion exhibits an age-dependent decline in promoting axon regeneration from the corticospinal tract (CST). How sprouting of uninjured axons, a naturally occurring form of axonal repair, is impacted by age is unknown. We assessed CST sprouting after unilateral pyramidotomy in PTEN and/or SOCS3-deleted mice at different ages. While PTEN deletion enhances sprouting independently of age, SOCS3 deletion loses its sprouting-promoting effect with age. The synergistic effect of PTEN/SOCS3 co-deletion on CST sprouting is rapidly lost with increased age. Overall, promoting sprouting appears more robust across age than regeneration, yet distinct molecular pathways are differentially impacted by age. Importantly, six-week delayed PTEN deletion promotes CST sprouting across age groups, supporting a clinically relevant time frame for this neural repair strategy independently of age.