Tiziana Pieramici

Bone marrow histopathological and molecular changes of small B-cell lymphomas after rituximab therapy: comparison with clinical response and patients outcome.

This study correlates bone marrow changes after Rituximab (RTX) treatment with the clinical characteristics and outcome of 26 patients with small B-cell lymphomas. The percentage, phenotypic profile and clonality pattern of bone marrow lymphoid infiltrate were analysed before and after RTX treatment. Clinical, histological and molecular responses to RTX were correlated to the clinical outcome of the patients. Sixteen out of twenty-six patients obtained a complete clinical remission (CR). A favourable histology - follicular lymphoma (FL), hairy cell leukaemia (HCL) and marginal zone lymphoma (MZL) - was associated with a higher frequency of clinical CR and histological remission (HR), in comparison with mantle cell lymphoma (MCL), chronic lymphocytic leukaemia (CLL) and lymphoplasmacytic lymphoma (LPL). Two patterns of bone marrow HR were observed: 1) complete lymphoid cell disappearance (9 patients); or 2) nodular/interstitial T-cell infiltration (10 patients). Three histological persistence (HP) patterns were observed: 1) persistence of CD20+ small lymphoid cells in 1 patient with MCL; 2) loss of CD20 antigen expression in 4 patients with CLL; or 3) persistence only of clusters of monotypic plasma cells in 2 patients with LPL. CR and HR were strongly correlated. The percentage of lymphomatous infiltrate after RTX was higher in patients who subsequently died of the disease. Molecular response showed no correlations with the further clinical course in 12 patients achieving a complete clinical remission. In conclusion, bone marrow morphological and immunohistochemical analysis with a restricted panel of antibodies is useful to avoid 42% false positive and 85% false negative interpretations. Persistence of monoclonality after RTX might have a role in evaluating the molecular pattern of CD20-negative clones that can emerge after RTX as a tumoral escape to therapy.

p63 expression correlates with pathological features and biological behaviour of odontogenic tumours

course. Sinonasal aspergillosis is classically classified as acute fulminant with vascular invasion, chronic invasive with fungal tissue invasion, non-invasive colonization or aspergilloma or fungal ball and allergic with eosinophilia and Charcot-laden crystals. The distinction between invasive and non-invasive forms relies on the evidence of hyphae within the tissue as a sign of invasion, with or without bone erosion. This distinction is important because it determines whether the patient should receive medical treatment or not. The distinction between the two forms may, however, not be clear cut, since observations of non-invasive destructive mycotic sinusitis assigned as ‘semi-invasive’ have been reported. Some authors believe that there is a continuum between these two forms with the possible evolution of mycetoma to invasive disease. The higher incidence of such cases in recent decades may be due to the wider use of CT, endoscopic examination and systematic mycological analysis. The most common clinical manifestations include headache and postnasal discharge, followed by visual changes and cranial nerve palsies or trigeminal pain. In addition to immunosuppressive states, predisposing factors include sea water, maxillofacial trauma, drug sniffing and radiotherapy, none of which was encountered in our case. Diagnosis relies on biopsy and culture: A. fumigatus is the major pathogen found. Treatment consists of surgical debridment in noninvasive forms, combined with triazol agents for fulminant, chronic invasive and ‘semi-invasive’ forms. Corticosteroid therapy is discussed only in allergic forms. In conclusion, chronic invasive fungal sinusitis may mimic a neoplasm and should be kept in mind in the differential diagnosis of pseudoneoplastic sinus lesions.

β- and γ-catenin expression in oral dysplasia

Cell-cell and cell-matrix interactions regulate important cellular functions; they involve a number of specialised molecules and the corresponding receptors, among which a key role is played by cadherins and the associated catenins. Deregulation of these molecules has been associated with tumour progression in many human malignancies. While catenins expression has been extensively studied in many human cancers, including oral carcinoma (OSCC), less is known about their expression in oral epithelial dysplasia. The objective of this study was to evaluate the expression of these proteins in a large group of displastic lesions of the oral mucosa and their relation with subsequent malignant transformation. Expression of beta- and gamma-catenin was investigated by immunohistochemistry using specific monoclonal antibodies in 49 cases of oral epithelial dysplasia and 10 samples of normal oral mucosa. The presence and absence of beta- and gamma-catenin staining was expressed differently in relation to dysplasia grade; while the degree of dysplasia became more severe, we observed a statistically significant loss and/or reduction of catenins expression, the loss of the exclusive membranous expression and a cytoplasmic delocalisation. Progression to OSCC occurred in 10 out of our 49 cases (20.4%); all of them, except one, showed a concurrent and concordantly located beta- and gamma-catenin staining even, if no statistically significant differences were found between cases progressed to invasive OSCC or not. Catenins physiology alterations may be involved in the transformation process; however, the role of catenins expression as possible prognostic markers in precancerous oral lesions seems to be limited. Nonetheless, further studies on larger series of samples are necessary in order to clarify the role of catenins expression in oral carcinogenesis from both a biological and clinical point of view.