Standard chemotherapeutic agents used for the treatment of pre-cancerous skin lesions and non-melanoma skin cancers are not completely effective. Several studies have suggested that repeated inflammatory sunburn reactions, which include the induction of cyclooxygenase-2 (COX-2) and the subsequent production of prostaglandins, play a role in skin cancer development. COX-2 inhibition has been demonstrated to be a potent means of preventing skin cancer development in mice; however, COX-2 inhibitors alone are not effective as chemotherapeutic agents. Data in a variety of cancer types suggest greater efficacy in treating tumors with combination chemotherapies. Therefore, we hypothesized that a combination of the chemotherapeutic agent 5-fluorouracil (5-FU) and the COX-2 inhibitor and anti-inflammatory drug celecoxib would act synergistically to regress tumors in a murine model of ultraviolet light B- (UVB-) induced carcinogenesis. We found that topical treatment with 5-FU and celecoxib together was up to 70% more effective in reducing the number of UVB-induced skin tumors than 5-FU treatment alone. Our data suggest that more effective chemotherapy regimens can be developed to treat the millions of pre-cancerous and cancerous skin lesions that arise every year, which could ultimately lead to a significant reduction in costs and cosmetic defects (scarring) associated with surgical interventions.
The differential diagnosis of lichenoid and granulomatous dermatitis should also encompass primary cutaneous Mycobacterium infection in addition to the other more characteristic entities associated wtih this distinctive reaction pattern. Infection with Mycobacterium induces a TH1 dominant response which would hence produce an infiltrate.
We present a case of malignant melanoma of nodular subtype, which strongly expressed CD34. The spectrum of abnormal phenotypes in malignant melanoma is reviewed, and a possible explanation for the presence of CD34 is discussed. This case demonstrates the potential of malignant melanoma to express CD34, defining an infrequently recognized aberrant phenotype. Whether or not expression of this marker is associated with a more aggressive clinical course remains to be determined.
Fluoxetine may be associated with pseudolymphomata and marginal zone lymphoma. The inhibitory effects on T-lymphocyte function and more specifically T-suppressor function may lead to excessive antigen-driven B-cell proliferation.
Angiolymphoid hyperplasia with eosinophilia (ALHE) is a benign, uncommon idiopathic condition, characterized by cutaneous papules or nodules, whose etiopathogenesis is still unclear. It has been considered an angioproliferating lesion (epithelioid hemangioma) since histologically it is marked by a proliferation of blood vessels, accompanied by an inflammatory infiltrate, consisting mainly of lymphocytes and eosinophils. We present a case of ALHE assessed immunohistochemically for D2-40-a new marker for lymphatic endothelial cells. A biopsy specimen obtained from the same anatomical area of a healthy individual served as a normal control. The ALHE specimen showed increased number of lymphatic vessels when stained for D2-40, whereas the endothelial cells lining blood vessels were negative. The specificity of D2-40 for lymphatic vessels was further substantiated by studying Factor VIII-related antigen expression in consecutive sections of both ALHE and the control specimen. A reverse pattern was appreciated-blood vessels showed Factor VIII positive labeling, whereas lymphatic endothelial cells remained unlabeled. We therefore assume that apart from the lymphocytic infiltrate in the lesion, the recognized lymphoid component in ALHE is due to lymphatic vessel proliferation as well. Hence, this condition may be considered as possibly derived from lymphatic endothelium.
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