Table 1 - uploaded by Rommel Burbano
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Twelve breast fibroadenomas were analyzed cytogenetically and only four were found to have clonal alterations. The presence of chromosomal alterations in fibroadenomas must be the consequence of the proliferating process and must not be related to the etiology of this type of lesion. In contrast, the few fibroadenomas that exhibit chromosomal alter...
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... Embora classificado entre as neoplasias benignas, alguns autores o consideram uma lesão hiperplásica ou mesmo mal formativa. Como regra geral, o fibroadenoma apresenta-se como nódulo único, bem delimitado, em pacientes jovens 5 . ...
O presente trabalho estabeleceu a densidade de micronúcleos e a distribuição do colágeno intersticial no tecido tumoral benigno e maligno de mama humana. Foram utilizadas a reação histoquímica de Feulgen e tricrômico de Masson, e a análise digital de imagens. Foram selecionados fragmentos de tecido mamário, diagnosticados como Fibroadenoma (FA), Doença fibrocística (DF) e Carcinoma Ductal Infiltrante (CDI). Para controle, foram utilizadas amostras de plástica mamária com tecido normal. A reação histoquímica foi realizada através da reação de Feulgen, para evidenciação dos micronúcleos, e, para a análise de colágeno intersticial, foi utilizada a coloração tricrômico de Masson. O número médio de micronúcleos exibiu valores semelhantes em amostra de FA (90,8 ± 4,5), DF (80,3 ± 4,0) e tecido normal (83,0 ± 4,1). Entretanto, valores significativamente menores que aqueles foram encontrados no CDI (176,5 ± 88,3). Quanto à distribuição do colágeno intersticial, constatou-se um aumento estatisticamente significante (p< 0,001) nos casos de FA (8101,4 ± 405,07) e DF (7046,78 ± 352,33), quando comparados ao tecido mamário normal (1733,13 ± 86,65) e ao CDI (2165,94 ± 108,29). Pode-se concluir que tanto o método de análise de imagem como a reação de Feulgen mostraram-se eficientes para evidenciar as alterações do núcleo celular e da matriz extracelular de tumores de mama.
... Data from the literature show that clonal alterations involve chromosomes 1, 4, 6, 12, 17 and 20 in structural rearrangements, and chromosomes 5,8,11,12,16,17,18,19,20 and 21 in aneuploidies [3,4,7,8]. Most FAs do not exhibit any detectable cytogenetic abnormalities [4]. ...
... Data from the literature show that clonal alterations involve chromosomes 1, 4, 6, 12, 17 and 20 in structural rearrangements, and chromosomes 5,8,11,12,16,17,18,19,20 and 21 in aneuploidies [3,4,7,8]. Most FAs do not exhibit any detectable cytogenetic abnormalities [4]. ...
... The aim of this study was to investigate numerical alterations of chromosome 21 in breast FAs by FISH. Previously, our laboratory found a high incidence of chromosome 21 monosomy in breast FA [8]. Possible correlations between these findings and histopathological characteristics were also evaluated and may result in prognostic parameters in this neoplasia. ...
Fibroadenoma (FA) is a benign breast tumour that occurs in about 25% of women. Cytogenetic studies suggest that numerical chromosomal aberrations may contribute to tumorigenesis, but chromosomal instability is still poorly characterised in breast cancer. The aim of this study was to investigate numerical alterations of chromosome 21 in 15 breast FAs. All samples were analysed by classical cytogenetics and by fluorescence in situ hybridisation (FISH) for chromosome 21 DNA sequences. Classical cytogenetics analysis showed that all cells were diploidies with modal number varying between 43 and 47 chromosomes, and clonal chromosome alterations in 46.7% of tumours. Clonal numerical alterations involved, preferentially, chromosomes 8, 10, 12, 16 and 21. FISH analysis showed a statistically significant difference for chromosome 21 monosomy between seven samples and control group. This monosomy varied from 24.5% to 43.5% of analysed cells. The presence of chromosomal alterations in FAs may be a consequence of the proliferation process and is probably not related to the aetiology of this type of lesion. The study of benign proliferations and comparison with chromosome alterations in their malignant counterparts should result in an understanding of the genes acting in cell proliferation alone and those that cause these cells to both undergo malignant transformation and become invasive.
... Cavalli et al. (2001) used culture methods that favor the mesenchymal part of the tissue (serum-rich medium). The types of chromosome aberrations in fibroadenomas we found are similar to those found in other studies; monosomies were frequent, including 19, 3, and 18 (Tibiletti et al., 2000; Burbano et al., 2001; Cavalli et al., 2001). The breakpoints 6p21 and 17q25 in case B3 (Table 1) have also been reported in benign and malignant tumors (Pandis et al., 1993; Dietrich et al., 1995; Rohen et al., 1996; Polito et al., 1998). ...
Cytogenetic changes are common in breast cancer and have also been described in fibroadenomas and fibrocystic disease, but not in histologically normal breast tissue. Cytogenetic analysis was performed on nonmalignant breast tissue from benign breast lumps (n = 8), reduction mammoplasties (n = 31), and grossly nontumorous tissue from cancerous breasts (n = 84), using standard techniques and G-banding. All samples were reviewed histologically. Clonal chromosomal changes were found in three of eight benign breast tumors (38%). Of the reduction mammoplasties, 17 samples contained nonproliferative changes, and three of these (18%) showed a clonal deletion of 3p. No pathology was identified in the other 14 samples, of which one (7%) contained two clonal changes, apparently balanced translocations. Of nontumorous tissues from cancerous breasts, 15 (18%) showed clonal chromosomal abnormalities. Five of these samples were histologically normal. Two clones were identical to those found in the corresponding cancer. In 18 additional samples, single cells were detected with the same change as that seen in clones or single cells in the cancer. Only 4 of these 20 samples contained detectable cancer cells. Clonal abnormalities found in two or more samples included trisomies X, 7, and 20 and monosomies 19 and 18. Clonal changes were not significantly more frequent in proliferative than in nonproliferative lesions. The Icelandic BRCA2 founder mutation, 999del5, was detected in four samples, all histologically normal, two of which had clonal chromosomal abnormalities. In conclusion, clonal chromosomal changes are not infrequent in nonmalignant breast tissue and can be detected even in the absence of histological abnormalities.
Open studies suggest that mirtazapine has efficacy in panic disorder treatment. We designed an open study that evaluates changes induced by mirtazapine compared with paroxetine in panic disorder. Methodology Patients 18–65 years old consecutively referred to a psychiatry liaison service with panic disorder (DSM-IV criteria) were offered either mirtazapine or paroxetine treatment. Results There were statistically significant reductions from baseline to week 3 and from week 3 to 8 for mirtazapine and paroxetine groups for: number of panic attacks, Beck Anxiety or Depression Inventory (BAI, BDI) Clinical Global Impresion (CGI) of panic disorder severity and CGI of panic disorder response (these variables were evaluated by the patient, the clinician or a blind evaluator). Responders at week 3 (BAI decrease of 50%) were 83% for the mirtazapine group and 84% for the paroxetine group. Responders at week 8 (number of panic attacks equal to 0) were 77% for the mirtazapine group and 73% for the paroxetine group Statistically significant differences between mirtazapine and paroxetine were found for number of panic attacks at weeks 3 and 8 and BAI at week 3, suggesting a faster response for mirtazapine. Responders at week 8 maintained a no recurrence figure of 95% at follow-up 6 months later. Panic disorder either with or without comorbid depression improved in both groups of treatment. Discussion Our study supports the hypothesis that mirtazapine has efficacy in the treatment of panic disorder either with or without comorbid depression.
The cytogenetic data on fibroadenomas and cystosarcoma phyllodes tumor of the breast, which are both biphasic breast tumors composed of epithelial and stromal components, are quite limited. In this study, we report on clonal chromosomal alterations in three fibroadenomas and one cystosarcoma phyllodes analyzed by GTG banding. The fibroadenomas presented mostly numerical abnormalities involving chromosomes 16, 18, and 21. One case presented a deletion on 17p. The cystosarcoma phyllodes presented numerous numerical abnormalities, mostly chromosome gains, and several marker chromosomes.
