Marjolin ulcer: an overlooked entity.

Marjolin ulcer is a well-defined, but uncommon malignant ulcer that occurs in chronic wounds and cutaneous scars. Jean-Nicolas Marjolin was credited with describing this phenomenon in 1828. This entity is frequently overlooked and therefore inadequately treated leading to a poor prognosis. The malignant transformation of an ulcer is most commonly associated with burn scars, but has been reported in many other types of chronic, non healing wounds such as traumatic wounds, venous stasis and chronic pressure ulcers, fistulas, lacerations and leprosy ulcers. Development of malignancy tends to be slow with an average time of approximately 25 years. Various theories concerning pathogenesis of Marjolin ulcer have been proposed. Well-differentiated squamous cell carcinoma (SCC) is the most common histological type of Marjolin ulcer. Biopsy with histopathologic interpretation remains the gold standard for the diagnosis, with radical surgical excision being the treatment of choice. A high index of suspicion should be held by any health care provider when evaluating a chronic, non healing wound. This is a case report of a Marjolin ulcer arising on the left buttock of a patient with a long-standing history of a traumatic wound.

Reductions in laminin beta2 mRNA translation are responsible for impaired IGFBP-5-mediated mesangial cell migration in the presence of high glucose.

Insulin-like growth factor binding protein-5 (IGFBP-5) mediates mesangial cell migration through activation of cdc42, and laminin421 binding to alpha(6)beta(1)-integrin (Berfield AK, Hansen KM, Abrass CK. Am J Physiol Cell Physiol 291: C589-C599, 2006). Because glomerular expression of laminin beta(2) is reduced in diabetic rats (Abrass CK, Spicer D, Berfield AK, St. John PL, Abrahamson DR. Am J Pathol 151: 1131-1140, 1997), we directly examined the effect of hyperglycemia on mesangial cell migration and laminin beta2 expression. Migration mediated by IGFBP-5 is impaired in the presence of 25 mM glucose. This reduction in migration was found to result from a loss in mesangial cell synthesis of laminin421, and IGFBP-5-induced migration could be restored by replacing laminin421. Additional studies showed that there was selective reduction in mRNA translation of laminin beta2 in the presence of high glucose. Preserved synthesis of laminin beta1 indicates that not all proteins are reduced by high glucose and confirms prior data showing that laminin411 cannot substitute for laminin421 in IGFBP-5-mediated migration. Given the importance of mesangial migration in the reparative response to diabetes-associated mesangiolysis, these findings provide new insights into abnormalities associated with diabetic nephropathy and the potential importance of differential control of protein translation in determination of alterations of protein expression.