Non-melanoma skin cancer represents one-third of all malignancies and its incidence is expected to rise until the year 2040. Cutaneous squamous cell carcinoma (cSCC) represents 20 % of all non-melanoma skin cancer and is a deadly threat owing to its ability to metastasize to any organ in the body. Therefore, a better understanding of cSCC is essential to strengthen preventative measures and curable treatment options. Currently, research demonstrates that cSCC is diagnosed at a rate of 15-35 per 100,000 people and is expected to increase 2-4 % per year. With respect to metastatic cSCC, this disease is more common in men; people over the age of 75 years; and inhabitants of the south and mid-west USA. In 2010, the American Joint Committee on Cancer updated the Cancer Staging Manual's primary tumor designation to now include high-risk factors; however, factors such as immunosuppression and tumor recurrence were not included. Other staging systems such as Brigham and Women's Hospital have allowed for increased stratification of cSCC. High-risk cSCC is defined as a cSCC that is staged as N0, extends beyond basement membrane, and has high-risk features associated with sub-clinical metastasis. High-risk features are depth of invasion (>2 mm), poor histological differentiation, high-risk anatomic location (face, ear, pre/post auricular, genitalia, hands, and feet), perineural involvement, recurrence, multiple cSCC tumors, and immunosuppression. Epidermal growth factor receptor and nuclear active IκB kinase (IKK) expression are also predictive of metastatic capabilities. Clinically, the initial lesions of a cSCC tumor can present as a painless plaque-like or verrucous tumor that can ultimately progress to being large, necrotic, and infected. Tumors can also present with paresthesias or lymphadenopathy depending on the location involved. With respect to prognosis, metastatic cSCC is lethal, with several large studies demonstrating a mortality rate of >70 %. Therefore, treatment of metastatic cSCC is difficult and depends on the location involved and extent of metastasis. Treatment options include surgery, radiation therapy, chemotherapy, and any combination of the above. Surgery alone can be used for metastatic cSCC treatment, but is not as effective as surgery in conjunction with radiation therapy. Radiation therapy has some success as a monotherapy in low-risk or cosmetically sensitive areas such as the external ear, eyelid or nose. According to the 2013 National Comprehensive Cancer Network Guidelines, cisplatin as a single agent or combined with 5-fluorouracil hold the strongest support for the treatment of metastatic cSCC; however, the supporting evidence is inconsistent and a curative chemotherapeutic approach is still lacking. Epidermal growth factor receptor inhibitors are a newer class of agents being used in metastatic cSCC and hold some promise as a therapy for this disease. Other areas of interest in finding curative treatments for metastatic cSCC include p53, hypermethylation of specific genes, chromatin remode...

Myiasis is derived from the Greek word, myia, meaning fly. The term was first introduced by Hope in 1840 and refers to the infestation of live human and vertebrate animals with dipterous (two-winged) larvae (maggots) which, at least for a certain period, feed on the host's dead or living tissue, liquid body-substance, or ingested food. Myiasis is the fourth most common travel-associated skin disease and cutaneous myiasis is the most frequently encountered clinical form. Cutaneous myiasis can be divided into three main clinical manifestations: furuncular, creeping (migratory), and wound (traumatic) myiasis. The flies that produce a furuncular myiasis include Dermatobia hominis, Cordylobia anthropophaga, Wohlfahrtia vigil, and the Cuterebra species. Gasterophilus and Hypoderma are two flies that produce a creeping myiasis. Flies that cause wound myiasis include screwworm flies such as Cochliomyia hominivorax and Chrysomya bezziana, and Wohlfahrtia magnifica. This article reviews current literature, provides general descriptions, and discusses life cycles of each species. It also gives treatment techniques and descriptions of each type of illness that results from interaction/infestation.

Subcorneal pustular dermatosis (SPD), also known as Sneddon-Wilkinson disease, is a rare, benign yet relapsing pustular dermatosis. Its incidence and prevalence have not been well studied. It characteristically presents as hypopyon pustules on the trunk and intertriginous areas of the body. SPD is similar to two other disease entities. Both SPD-type immunoglobulin (Ig)-A pemphigus and annular pustular psoriasis clinically and histologically present similarly to SPD. Immunologic studies separate SPD-type IgA pemphigus from SPD and pustular psoriasis. However, there is still an unclear designation as to whether SPD is its own entity distinct from pustular psoriasis, as the once thought characteristic histologic picture of psoriasis does not hold true for pustular psoriasis. SPD has been reported to occur in association with several neoplastic, immunologic, and inflammatory conditions. Dapsone remains the first-line treatment for SPD, although dapsone-resistant cases have been increasingly reported. Other therapies have been used singly or as adjunctive therapy with success, such as corticosteroids, immunosuppressive agents, tumor necrosis factor inhibitors, and ultraviolet light therapy. This article provides a review of the last 30 years of available literature, with a focus on successful treatment options and a suggestion for reappraisal of the classification of SPD.

Poroma is a benign adnexal neoplasm of the terminal sweat gland duct. Although poromas have traditionally been thought to originate from the eccrine sweat gland, there have been cases of apocrine etiology as well. Eccrine and apocrine poromas typically present as erythematous or flesh-colored nodules on the palms and soles. As these features overlap with a multitude of differential diagnoses, it is imperative to have a firm understanding of the characteristics that make the diagnosis of poroma. In addition, the malignant counterpart to the poroma, the eccrine porocarcinoma, manifests in a similar nonspecific fashion. Case studies and literature reviews have contributed immensely to our present knowledge of poroma and porocarcinoma. Given the rarity of these neoplasms, however, there remains a relative paucity of information on atypical presentations and rates of malignant transformation. In this article, the epidemiology, clinical presentation, diagnosis, and management of poroma and porocarcinoma will be reviewed. This systematic approach may serve as a guide in navigating the diagnostic dilemma of these rare cutaneous lesions.