Idiopathic guttate hypomelanosis: an electron microscopy study.

BACKGROUND: Few published data, concerning the electron microscopy findings of idiopathic guttate hypomelanosis have been published so far. OBJECTIVES: To reveal the electron microscopic findings of idiopathic guttate hypomelanosis and their aetiopathogenetic associations. METHODS: Punch biopsy specimens from four patients with idiopathic guttate hypomelanosis, after being properly processed, were observed under the electron microscope. RESULTS: In the epidermis, melanocytes and melanosomes were normal in structure. In some areas, there was a reduced uptake of melanosomes by the keratinocytes. In the dermis, fibroblasts were structurally normal. Also, most elastic and collagen fibres were normal, but there were focal elastotic changes. CONCLUSIONS: No significant structural abnormality of the melanocytes was observed, but rather a functional defect in the transfer of melanosomes from the melanocytes to the keratinocytes.

Update of the cancer-associated molecular mechanisms in oral lichen planus, a disease with possible premalignant nature.

Oral lichen planus (OLP) is a relatively common inflammatory disease. Several reports of oral squamous cell carcinomas (OSCC) developing in the ground of previous OLP lesions exist in the current medical literature. Hence, there is a debate concerning the possible premalignant nature of OLP. The studies that examined the malignant potential of OLP for many years were mainly observational and were seeking to detect the percentage of OLP patients that developed OSCC. The results of these studies varied significantly with reported percents of malignant transformation of OLP ranging from 0 to 12.5%. In recent years the number of OLP studies that investigate molecular biomarkers identified in cancer is on the rise. This article is an update of the molecular pathways identified in OLP that could be suggestive of a malignant potential of this condition.

E2F-1 overexpression correlates with decreased proliferation and better prognosis in adenocarcinomas of Barrett oesophagus.

BACKGROUND: E2F-1 expression is positively associated with tumour growth in oesophageal squamous-cell carcinomas (OSCC), while it exhibits oncosuppressive features in colonic adenocarcinomas (AC). To date there are no data regarding E2F-1 expression and its relationship with tumour kinetics (proliferation, apoptosis) in adenocarcinomas that develop on Barrett oesophagus. AIM: As oesophageal adenocarcinomas occur almost exclusively in the metaplastic Barrett epithelium and the opposing E2F-1 behaviour seems to be cell and tissue-type dependent, we examined the manner in which E2F-1 acts in ACs of Barrett oesophagus. METHODS: We estimated the immunohistochemical expression of E2F-1, Ki-67, caspase-3 and p53 immunohistochemical status in 35 Barrett oesophagus ACs. RESULTS: E2F-1 immunopositivity correlated inversely with Ki-67, by semi-serial section and statistical analysis (p = 0.023, Spearman correlation). Semi-serial section analysis revealed a direct association between E2F-1 and caspase-3 staining. No correlation was found with p53 status. Cases with higher E2F-1 immunoexpression exhibited longer survival (p = 0.047, Cox-regression). CONCLUSIONS: E2F-1 expression was negatively related to tumour proliferation in ACs of Barrett oesophagus. Additionally, E2F-1 immunohistochemical status correlated positively with patient survival. These findings are opposite from those seen in OSCCs, suggesting that the tumour-suppressing E2F-1 behaviour in oesophageal adenocarcinomas is possibly due to the intestinal-type nature of the metaplastic Barrett mucosa.

A new rare allele at the CGG repeat polymorphism in the first intron of human c-H-ras gene.

We have examined a region in the first intron of the human c-H-ras gene containing a CGG repeat. This region was previously shown to be variable in length. The length variation was attributed to the presence of the CGG repeat after estimation of its electrophoretic mobility. In the present report we have characterized in detail this region by PCR-RFLP and automated sequencing, in a total of 102 histologically normal tissues from unrelated individuals affected by lung and breast cancer. Four alleles were detected and analysis of their internal sequence showed that the length alterations of this region were due to the presence of 5, 6, 8 and 9 CGG triplets respectively. The last three occur most often (44.1%, 34.8%, 20.6% respectively) and coincide with three previously reported alleles (Riggins et al, Hum Mol Genet 9: 775, 1992). The fourth allele consisting of 5 repeats is a rare one (0.5%), whilst alleles with 7, and a previously reported one suggested to comprise 11 repeats (1%) were not present in our cohort. This polymorphism coincides in position with an element that was previously shown to possess regulatory activity.

Experimental echinococcus infection in the mouse model: pericystic cellular immunity reaction and effects on the lymphoid organs of immunocompetent and thymectomized mice.

Echinococcus can infect man as an accidental intermediate host causing hydatid disease. The infection persists and the growth of the cysts advances, while the patient usually remains asymptomatic for years. Experimental Echinococcus infection in mice provides a well described model for the study of the parasite-host relationship that permits the evolution of the disease despite the activation of the host's immune system. The aim of the present study was to assess the immune response to Echinococcus infection in normal and thymectomized mice. For this purpose, a total of 150 mice, divided into three equal groups (A, B and C), were infected by intraperitoneal inoculation of live protoscoleses. The mice of groups B and C underwent thymectomy, two weeks prior and after the infection, respectively. The mice of each group were further divided into three subgroups and were sacrificed at three consecutive time points: 45 days, 3 and 6 months post the infection. The hydatid cysts that subsequently developed by the metacestode-lavral stage, along with the spleen and lymph nodes were excised from each mouse and histologically studied. The results revealed a marked activation of the cell-mediated immunity against the parasite at the early stages of the disease. The initial response of the host abated with time and was minimal six months after the infection suggesting a local immunosuppression state that could account for the advancement of the disease. In addition, the thymectomized mice exhibited a higher susceptibility to the infection, which corresponded to the weak and delayed cellular immunity response observed in these groups. These results suggest that the cell-mediated immunity is crucial for the defense against Echinococcus, especially early in the course of the disease where suppression of larval growth is critical for the final outcome of the infection.

The effect of various types of splenectomy on the development of B-16 melanoma in mice.

260 CB57BL/J6 mice were used in an experimental protocol designed to investigate the effects of 4 different varieties of splenectomy on the growth rate of subcutaneously implanted GB-16 melanoma. In addition, the mean and absolute survival of the mice, the histopathology of the tumour and the effects of the same procedures on the immunological status of the tumour-bearing animals as assessed by serum IgG levels and immunoelectrophoresis were determined. The effects of the timing of the splenectomy and the removal of the primary tumour after splenectomy on the above parameters were also annotated. The following were found: First, splenectomy performed 1 week after B-16 melanoma tumour implantation in mice i.e. in the early period of oncogenesis, lengthened the survival of the grafted experiments, delayed tumour growth, reduced the "activity" of the tumour and caused pseudoencapsulation of the tumour by fibrous tissue. It increased, but not by a statistically significant degree (p > 0.05), the circulating levels of the IgG immunoglobulin. Second, splenectomy performed 4 weeks prior to grafting of the same tumour did not affect the circulating IgG levels, nor did it prolong survival; however, it reduced the rate of tumour growth and pseudoencapsulation of the tumour was observed. Third, splenectomy at the early stages of oncogenesis in combination with surgical removal of the primary tumour increased absolute and mean survival, delayed the tumour growth rate, increased the time to relapse and reduced the "activity" of the pseudocapsulated tumour.