Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a case of acquired renal cystic disease in a patient with end-stage renal disease (ESRD) secondary to systemic lupus erythematosus who was dialysis dependent for 5 years. Renal hemorrhage and neoplastic transformation of the cyst epithelium are the two major complications of acquired renal cystic disease, and were present in this patient. The full clinical significance of the acquired renal cystic lesion is still unclear, although the possibility of renal tumors and massive renal and retroperitoneal hemorrhage should be considered in the long-term dialysis population.
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PMID:Massive renal and retroperitoneal hemorrhage in a case of acquired renal cystic disease with atypical epithelial cell proliferation. 338 56

Previous work showed that IFN-alpha induced the autoimmune-associated lupus inclusions (LI) in all 16 umbilical cord mononuclear cell samples from healthy mothers. In contrast, IFN-alpha induced LI and the LI-associated protein, p36, in only 2 of 16 human B lymphoblastoid cell lines. Resistance of these 14 cell lines to form LI and p36 may be due to their stage of development or differentiation or their transformed state. We sought to determine whether aging, neoplastic transformation, and HIV infection affected the observed IFN-alpha induction of LI in cord blood mononuclear cells. Expression of LI and p36 was investigated in PBMC on IFN-alpha chemotherapy and on culturing IFN-alpha with PBMC samples prepared from healthy adults and AIDS patients. The IFN-alpha induction of LI (detected by electron microscopy) or p36 (detected by two-dimensional gels) in all of the PBMC samples from these individuals was indistinguishable from the cord blood mononuclear cell response. Furthermore, induction of p36 and LI was not a good indicator of effective IFN-alpha chemotherapy. It may be consequential for autoimmunity induced by IFN-alpha in cancer, AIDS, and systemic lupus erythematosus (SLE). An essential biologic role for p36 and LI is suggested by a highly homologous p36 gene in the invertebrate Caenorhabditis elegans.
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PMID:Interferon-alpha-induced human lupus inclusions and p36 protein in cancer and AIDS. 888 55

A 38-year-old female with systemic lupus erythematosus presented with abdominal pain, diarrhea and iron-deficient anemia. Computed tomogram showed a 2 x 4 cm inhomogeneous lesion of the right adnexa. An unusual mass was identified extending from the appendiceal orifice at colonoscopy, and an 8 cm tubular appendix, apparently prolapsed into the cecum, was identified at celiotomy. An appendectomy with cecectomy was performed. On cut section, mucin was extruded from the lumen of the appendix. A mucinous neoplasm of the appendix with mucinous dissection to the serosal surface was reported at the time of frozen section. No gross ovarian pathology or peritoneal implants were noted. Cystadenoma with associated mucocele formation was verified by permanent histology. Mucocele of the vermiform appendix is a rare condition associated with neoplastic transformation in approximately 75% of all cases. Benign mucinous cystadenoma of the appendix should be differentiated from cystadenocarcinoma by frozen section at the time of celiotomy to ensure appropriate treatment. While systemic lupus erythematosus can lead to cutaneous mucinosis, an association with mucinous cystadenoma of the appendix has not been previously reported. Surveillance for metachronous colonic neoplasms is warranted in patients diagnosed with a mucinous neoplasm of the appendix.
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PMID:Mucinous cystadenoma of the appendix in a patient with systemic lupus erythematosus. 992 68

The role of B-1 cells in the hyperproliferative hematologic disease has been described. Several reports bring evidences that B-1 cells are the main cell population in the chronic lymphatic leukemia. It is also described that these cells have an important involvement in the lupus erythematous systemic. The murine model used to investigate both disease models is NZB/NZW. Data from literature point that mutation in micro-RNA 15a and 16 are the responsible for the B-1 hyperplasia in these mice. Interestingly, it was demonstrated that NZB/NZW B-1 cells are radioresistant, contrariwise to observe in other mouse lineage derived B-1 cells and B-2 cells. However, some reports bring evidences that a small percentage of B-1 cells in healthy mice are also able to survive to irradiation. Herein, we aim to investigate the malignant potential of ionizing-radiation resistant B-1 cells in vitro. Our main goal is to establish a model that mimics the neoplastic transformation originate to a damage exposure of DNA, and not only related to intrinsic mutations. Data shown here demonstrated that radiation-resistant B-1 cells were able to survive long periods in culture. Further, these cells show proliferation index increase in relation to non-irradiated B-1 cells. In addition, radiation resistant B-1 cells showed hyperploid, morphologic alterations, increased induction of apoptosis after anti-IgM stimulation. Based on these results, we could suggest that radiation resistant B-1 cells showed some modifications in that could be related to induction of malignant potential.
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PMID:Radiation-resistant B-1 cells: A possible initiating cells of neoplastic transformation. 2689 18