39 research outputs found

    Small primary adenocarcinoma in adenomyosis with nodal metastasis: a case report

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    <p>Abstract</p> <p>Background</p> <p>Malignant transformation of adenomyosis is a very rare event. Only about 30 cases of this occurrence have been documented till now.</p> <p>Case presentation</p> <p>The patient was a 57-year-old woman with a slightly enlarged uterus, who underwent total hysterectomy and unilateral adnexectomy. On gross inspection, the uterine wall displayed a single nodule measuring 5 cm and several small gelatinous lesions. Microscopic examination revealed a common leiomyoma and multiple adenomyotic foci. A few of these glands were transformed into a moderately differentiated adenocarcinoma. The endometrium was completely examined and tumor free. The carcinoma was, therefore, considered to be an endometrioid adenocarcinoma arising from adenomyosis. Four months later, an ultrasound scan revealed enlarged pelvic lymph nodes: a cytological diagnosis of metastatic adenocarcinoma was made.</p> <p>Immunohistochemical studies showed an enhanced positivity of the tumor site together with the neighbouring adenomyotic foci for estrogen receptors, aromatase, p53 and COX-2 expression when compared to the distant adenomyotic glands and the endometrium. We therefore postulate that the neoplastic transformation of adenomyosis implies an early carcinogenic event involving p53 and COX-2; further tumor growth is sustained by an autocrine-paracrine loop, based on a modulation of hormone receptors as well as aromatase and COX-2 local expression.</p> <p>Conclusion</p> <p>Adenocarcinoma in adenomyosis may be affected by local hormonal influence and, despite its small size, may metastasize.</p

    Metal backed versus all-polyethylene unicompartmental knee arthroplasty: the effect of implant thickness on proximal tibial strain in an experimentally validated finite element model

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    Objectives Up to 40% of unicompartmental knee arthroplasty (UKA) revisions are performed for unexplained pain which may be caused by elevated proximal tibial bone strain. This study investigates the effect of tibial component metal backing and polyethylene thickness on bone strain in a cemented fixed-bearing medial UKA using a finite element model (FEM) validated experimentally by digital image correlation (DIC) and acoustic emission (AE). Materials and Methods A total of ten composite tibias implanted with all-polyethylene (AP) and metal-backed (MB) tibial components were loaded to 2500 N. Cortical strain was measured using DIC and cancellous microdamage using AE. FEMs were created and validated and polyethylene thickness varied from 6 mm to 10 mm. The volume of cancellous bone exposed to 3000 ”Δ and > 7000 ”Δ maximum principal (tensile) microstrain was computed. Results Experimental AE data and the FEM volume of cancellous bone with compressive strain < -3000 ”Δ correlated strongly: R = 0.947, R2 = 0.847, percentage error 12.5% (p < 0.001). DIC and FEM data correlated: R = 0.838, R2 = 0.702, percentage error 4.5% (p < 0.001). FEM strain patterns included MB lateral edge concentrations; AP concentrations at keel, peg and at the region of load application. Cancellous strains were higher in AP implants at all loads: 2.2- (10 mm) to 3.2-times (6 mm) the volume of cancellous bone compressively strained < -7000 ”Δ. Conclusion AP tibial components display greater volumes of pathologically overstrained cancellous bone than MB implants of the same geometry. Increasing AP thickness does not overcome these pathological forces and comes at the cost of greater bone resection

    Cell cycle regulators and apoptosis-associated proteins in relation to proliferative activity and degree of apoptosis in HNPCC versus sporadic endometrial carcinoma

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    Aims: Mismatch repair gene malfunction occurs early in the carcinogenesis of hereditary non-polyposis colorectal cancers (HNPCCs), leading to an accelerated accumulation of mutations and possibly to change in expression of cell cycle proteins. There is strong evidence that tumorigenesis in HNPCCs differs from sporadic ones. HNPCC-related endometrial cancers are less well studied. Our aim was to compare expression of cell cycle and apoptosis-related proteins in relation to proliferation and apoptosis in HNPCC-related and sporadic endometrial cancers to identify differences in their carcinogenetic pathways. Methods and results: Eighteen HNPCC-related endometrial cancers, each matched by tumour type, stage and grade with two sporadic endometrial cancers, were examined for proliferation, apoptosis and the expression of oestrogen and progesterone receptors, cyclin B1, D3 and E, p21, p27, bcl-2, bax, p53 and COX-2. No differences in proliferation or apoptotic indices were detected between HNPCC-related and sporadic endometrial cancers. Cyclin B1 expression was significantly higher in HNPCC-related cancers than in sporadic endometrial cancers. More HNPCC-related endometrial cancers had total loss of bax expression. Conclusions: Apart from differences in cyclin B1 and bax expression, HNPCC-related and sporadic endometrial cancers are comparable. The subtle differences detected are consistent with the minor clinical diversity between HNPCC-related and sporadic endometrial cancers
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