We studied 21 bone marrow specimens from 21 patients with systemic lupus erythematosus (SLE) and peripheral cytopenias: anaemia (Hb < 10 g/dl), and/or leucopenia (white blood cell count < 4 x 10(9)/l), and/or thrombocytopenia (platelets < 150 x 10(9)/l). None of the patients had used immunosuppressive drugs in the 2 months before the study, and 11 (52.4%) had never used these drugs. The global and specific series cellularity, degree of fibrosis and necrosis were evaluated by bone marrow trephine; morphological abnormalities and iron stores were evaluated by cytological smears. The most important abnormalities viewed in bone marrow biopsies were: global hypocellularity (47.6%), increased reticulin proliferation (76.2%) with myelofibrosis in one patient, and necrosis (19.0%). The marrow aspirates were difficult to obtain in four patients, who showed an increased reticulin proliferation on histological analysis. Plasmocytosis was present in 26.7% of cases and in one there was a serum monoclonal component (IgG kappa). Iron stores were normal or increased in 26.7% of specimens and decreased or absent in 73.3%. The most frequent peripheral abnormality was leucopenia in 90.4% (19/21) and granulocytic hypoplasia was observed in 47.3% (9/19) of these patients. We conclude that the bone marrow may be a target organ in SLE with cytopenias.

Mastocytosis are myeloproliferative neoplasms commonly related to gain-of-function mutations involving the tyrosine kinase domain of KIT. We herein report a case of familial systemic mastocytosis with the rare KIT K509I germ line mutation affecting two family members: mother and daughter. In vitro treatment with imatinib, dasatinib and PKC412 reduced cell viability of primary mast cells harboring KIT K509I mutation. However, imatinib was more effective in inducing apoptosis of neoplastic mast cells. Both patients with familial systemic mastocytosis had remarkable hematological and skin improvement after three months of imatinib treatment, suggesting that it may be an effective front line therapy for patients harboring KIT K509I mutation.

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The c-myc protein is known to regulate the cell cycle, and its downregulation can lead to cell death by apoptosis. The role of c-myc protein as an independent prognostic determinant in cervical cancer is controversial. In the present study, a cohort of 220 Brazilian women (mean age 53.4 years) with FIGO stage I, II and III (21, 28 and 51%, respectively) cervical squamous cell carcinomas was analyzed for c-myc protein expression using immunohistochemistry. The diseasefree survival and relapse-rate were analyzed using univariate (KaplanMeier) survival analysis for 116 women who completed the standard FIGO treatment and were followed up for 5 years. Positive c-myc staining was detected in 40% of carcinomas, 29% being grade 1, 9% grade 2, and 2% grade 3. The distribution of positive c-myc according to FIGO stage was 19% (17 women) in stage I, 33% (29) in stage II, and 48% (43) in stage III of disease. During the 60-month follow-up, disease-free survival in univariate (Kaplan-Meier) survival analysis (116 women) was lower for women with c-myc-positive tumors, i.e., 60.5, 47.5 and 36.6% at 12, 36, and 60 months, respectively (not significant). The present data suggest that immunohistochemical demonstration of c-myc does not possess any prognostic value independent of FIGO stage, and as such is unlikely to be a useful prognostic marker in cervical squamous cell carcinoma. Correspondence

Abstract.Postmenopausal women who use tamoxifen present with an increased incidence of endometrial alterations, such as polyps and hyperplasia, in addition to a higher risk of malignant endometrial neoplasms. Among these endometrial changes, polyps are the most common, with a pathogenesis associated with hormonal influence. The objective of this study was to compare the expression of estrogen receptors (ERs) and progesterone receptors (PRs) in endometrial polyps from tamoxifen users with that in endometrial polyps and the atrophic endometrium of postmenopausal tamoxifen non-users. Among women undergoing surgical hysteroscopy, 84 tamoxifen users with benign endometrial polyps were selected. This group was compared to 84 samples of atrophic endometrium and to 252 benign polyps from postmenopausal women who were not treated with tamoxifen. The expression of ER̸PR was assessed by immunohistochemical analysis, according to the percentage of stained cells, intensity of nuclear staining and final score. The polyps from tamoxifen users exhibited a higher expression of ER and PR in the glandular epithelium and stroma compared to the atrophic endometrium (P<0.0001). Compared to the polyps from women not treated with tamoxifen, tamoxifen users exhibited a higher PR expression in the epithelium (P=0.0014) and stroma (P=0.0056), with no difference in the expression of ER. In conclusion, endometrial polyps frequently exhibit an increase in ER expression, regardless of tamoxifen use. High levels of PR expression appear to be consistent with the estrogen agonist effects of tamoxifen.