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Borderline Tumour (borderline + tumour)
Selected AbstractsDifference in subcellular localization of maspin expression in ovarian mucinous borderline tumourHISTOPATHOLOGY, Issue 1 2009Takahiro Tsuji No abstract is available for this article. [source] High-grade serous carcinoma arising in a low-grade serous carcinoma and micropapillary serous borderline tumour of the ovary in a 23-year-old womanHISTOPATHOLOGY, Issue 6 2009M Ruhul Quddus No abstract is available for this article. [source] Clinicopathological features and treatment of intraductal papillary mucinous tumour of the pancreasBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 3 2001Dr M. Falconi Background: The surgical strategy in patients with a pancreatic intraductal papillary mucinous tumour (IPMT) is still controversial. In this study the pathological findings in a series of patients were used to rationalize surgical choice. Methods: Fifty-one patients with IPMT were observed between 1988 and 1998 and treated by pancreatic resection. Factors evaluated included symptoms, tumour site, type of operation, histological findings and resection margins, tumour stage, follow-up and survival. Results: Pancreaticoduodenectomy was the most frequent surgical treatment (33 patients; 65 per cent), followed by left pancreatectomy (ten), total pancreatectomy (five) and middle pancreatectomy (three). Histological assessment revealed the tumour to be an adenoma in 13 patients (25 per cent), a borderline tumour in ten (20 per cent) and a carcinoma in 28 (55 per cent), 19 of which were invasive. Mild to moderate dysplasia was present at the resection margin in 20 specimens (41 per cent), and carcinoma in one. Local recurrence was observed in four patients (8 per cent), all of whom underwent a second resection. The 3-year actuarial survival rate for benign and malignant disease was 94 and 69 per cent respectively (P = 0·03). Conclusion: These results suggest that resection should be the treatment for IPMT. Management of the resection margin could be crucial in avoiding tumour recurrence. © 2001 British Journal of Surgery Society Ltd [source] Glomeruloid peritoneal implants in ovarian serous borderline tumours , distinction between invasive and non-invasive implants and pathogenesisHISTOPATHOLOGY, Issue 5 2009Eung-Seok Lee Aims:, To determine whether or not the glomeruloid implants (GI) composed of papillary cores within clear spaces lined by mesothelial cells or tumour cells located in superficial or deep peritoneal tissue in ovarian serous borderline tumours (SBTs) are invasive. Methods and results:, We examined the differences in incidence, histological and immunohistochemical findings among three groups: 100 GI with mesothelial cells lining clear space (type I), 100 GI with tumour cells lining clear space (type II), and 100 invasive implants with clefts but no lining cells from 30 cases of SBT with peritoneal implants. The type I lesion had characteristics of non-invasive implants with a tendency for smooth contours (100/100), superficial location (71/100), absence of desmoplasia (100/100) and absence of surrounding destructive invasion (100/100), In contrast, type II GI had irregular contours (67/100), deep location (93/100), presence of desmoplastic reaction (100/100) and presence of destructive invasion (12/100). Immunohistological studies suggested intermediate forms between the two types of lesions. Conclusions:, Type I GI are non-invasive implants, whereas type II GI are invasive implants and it is important to evaluate the presence and nature of cells lining the clear space in determining whether implants associated with ovarian SBTs are invasive or not. [source] A comprehensive genetic profile of phyllodes tumours of the breast detects important mutations, intra-tumoral genetic heterogeneity and new genetic changes on recurrence,THE JOURNAL OF PATHOLOGY, Issue 5 2008AM Jones Abstract The aims of this study were to identify genetic changes associated with malignant progression of the fibroepithelial neoplasms, phyllodes tumours of the breast (PTs), and to ascertain whether genetic progression occurs when PTs recur locally. A further aim was to assess whether the genetic data support the classification of these tumours into three subtypes, benign, borderline and malignant. 126 PTs (37 benign, 41 borderline, 48 malignant) were analysed by either array-CGH or the Illumina Goldengate assay. The large-scale genetic changes associated with malignant/borderline phenotypes were + 1q, + 5p, + 7, + 8, , 6, , 9p, , 10p and , 13. Cluster analysis of the array-CGH data supported the division of malignant and borderline PTs into two separate groups, one comprising almost all malignant lesions and the other, benign and borderline tumours. Interstitial deletions of 9p21 that involved the p16INK4a locus were present in many malignant/borderline PTs, and some of these appeared to cause homozygous loss. Loss of expression of p16INK4a was found frequently and this was associated with 9p deletion; we also identified one p16INK4a mutation and evidence of methylation of p16INK4a in malignant PTs. Our evidence shows that inactivation of this gene is important in the development of malignant PTs. In selected PTs, multiple areas of stroma were isolated and analysed separately by array-CGH. We found considerable intra-tumoral genetic heterogeneity. Analysis of paired primary and recurrent tumours showed that recurrent tumours often acquired new genetic changes; in particular, benign tumours tended to acquire changes characteristic of the malignant/borderline phenotype. We believe it likely that unfavourable sub-clones not easily identified by histology account for the unpredictable clinical behaviour of these tumours. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] |