Clinical and pathological features of myeloid leukemia cutis

Abstract: Background: Myeloid leukemia cutis is the terminology used for cutaneous manifestations of myeloid leukemia. Objective: The purpose of this study was to study the clinical, histopathological and immunohistochemical features of myeloid leukemia cutis. Methods: This was a retrospective study of clinical and pathological features of 10 patients with myeloid leukemia cutis. Results: One patient developed skin lesions before the onset of leukemia, seven patients developed skin infiltration within 4-72 months after the onset of leukemia, and two patients developed skin lesions and systemic leukemia simultaneously. Of these patients, five presented with generalized papules or nodules, and five with localized masses. The biopsy of skin lesions showed a large number of tumor cells within the dermis and subcutaneous fat layer. Immunohistochemical analysis showed strong reactivity to myeloperoxidase (MPO), CD15, CD43 and CD45 (LCA) in most cases. NPM1 (nucleophosmin I) and FLT3-ITD (Fms-like tyrosine kinase 3-internal tandem duplication) mutations were identified in one case. Five patients with acute myelogenous leukemia and one patient with chronic myelomonocytic leukemia died within two months to one year after the onset of skin lesions. Study limitations: This was a retrospective and small sample study. Conclusions: In patients with myelogenous leukemia, skin infiltration usually occurs after, but occasionally before, the appearance of hemogram and myelogram abnormalities, and the presence of skin infiltration is often associated with a poor prognosis and short survival time. myeloid leukemia cutis often presents as generalized or localized nodules or masses with characteristic pathological and histochemical findings.

The deubiquitinase USP38 affects cellular functions through interacting with LSD1

BACKGROUND: Deubiquitination is a posttranslational protein modification prevalent in mammalian cells. Deubiquitinases regulate the functions of the target protein by removing its ubiquitin chain. In this study, the effects of the deubiquitinase USP38's functions on the LSD1 protein and on cell physiology were investigated. MATERIALS AND METHODS: Western blotting, real-time quantitative PCR, immunoprecipitation, denaturing immunoprecipitation and luciferase reporter assays were used to analyze the protein stability, protein interactions and changes in the ubiquitin chain. Cell proliferation assays, colony formation assays, drug treatments and western blotting were used to explore the functions of USP38 in cells. RESULTS: The deubiquitinase USP38 stabilizes protein LSD1 in cells by binding LSD1 and cleaving its ubiquitin chain to prevent the degradation of LSD1 by the intracellular proteasome. USP38 enhances the ability of LSD1 to activate signaling pathways and hence promotes cellular abilities of proliferation and colony formation through interacting with LSD1. Furthermore, USP38 enhances the drug tolerance of human colon cancer cells. CONCLUSIONS: USP38 is an LSD1-specific deubiquitinase that affects cellular physiology through interacting with LSD1.

Inducible T-cell co-stimulators regulate the proliferation and invasion of human hepatocellular carcinoma HepG2 cells

Abstract Background This study determined the regulatory effects of inducible T-cell co-stimulators (ICOS) in human hepatocellular carcinoma HepG2 cells using a RNA interference (RNAi) technique. Methods A RNAi technique was used to knockdown the expression of ICOS. ICOS expression after knockdown was detected as mRNA and protein levels by RT-PCR and Western blot, respectively. A MTT colorimetric assay was used to detect cell proliferation, and the Transwell assay was used to detect cell invasion. Western blot was carried out to detect the level of Bcl-2, AKT, and PI3K protein expression in different groups. Results The proliferation of HepG2 cells were significantly decreased after ICOS siRNA transfection (EG group). Similarly, the results of the Transwell experiment showed that invasion of HepG2 cells in the EG group was clearly reduced compared to the negative control (NC) and blank control groups (CON). Western blot analysis showed that knockdown of ICOS expression reduced the levels of Bcl-2 and AKT, and also significantly up-regulated the level of PI3K phosphorylation (P < 0.01). Conclusion Down-regulating ICOS expression in HepG2 cells suppressed cell proliferation and invasion. The underlying mechanism may be related to the expression of the downstream factor, PI3K/AKT.

Expression of autophagy-related proteins PTEN and MAP1LC3 in tongue squamous cell carcinoma / 口腔疾病防治

Objective @#This study ai ms to evaluate the expression of autophagy-related protein cancer phosphatase and tensinhomology deleted on chromosome ten (PTEN) and microtubule-associated protein 1 light chain 3 (MAP1LC3) and investigate its significance in tongue squamous cell carcin oma (TSCC). @*Methods @#About 46 TSCC samples, 13 cases of precancerous lesion and 13 cases of adjacent tissues were enrolled. Immunohistochemistry were performed to examine the expression of PTEN, MAP1LC3. Statistical analyses were carried out to assess the associations among clinic pathologic parameters. @*Results @# The positive expression rate of PTEN (34.78%) in TSCC was significantly lower than that in adjacent tissues (69.23%, χ2 = 4.926, P = 0.026) and precancerous lesions (76.92%, χ2 = 7.302, P = 0.007). The positive expression rate of MAP1LC3 (28.26%) in TSCC was significantly lower than that of adjacent tissues (61.53%, χ2 = 4.896, P = 0.027) and precancerous lesions (69.23%, χ2 = 7.275, P = 0.007), the difference was statistically significant. The expression of PTEN and MAP1LC3 was not correlated with age, sex, smoking, alcohol consumption and cell differentiation (P > 0.05). There was a significant difference in the expression of PTEN and MAP1LC3 in subgroup with different clinical stage and in subgroup with or without lymph node metastasis (P < 0.05). There is a significant difference in the tumor recurrence between PTEN protein expression positive subgroup and PTEN protein expression negative subgroup (χ2 = 4.629,P = 0.039), and there was no significant difference in the tumor recurrence between MAP1LC3 protein expression positive subgroup and MAP1LC3 protein expression negative subgroup (χ2 = 0.343,P = 0.453). There was a positive correlation between PTEN and MAP1LC3. @*Conclusion@#The expression of PTEN and MAP1LC3 suggested that autophagy associated proteins play a pivotal role in the progression, diagnosis and prognosis of TSCC. Down-regulation of PTEN and MAP1LC3 was observed in TSCC.