Biomedical subjects

Karin Schürfeld

Publications and source records attributed to Karin Schürfeld.

5 recordsLinked to original sources

PubMed2004

CDK9/CYCLIN T1 expression during normal lymphoid differentiation and malignant transformation.

CDK9 is a member of the CDC2-like family of kinases. Its cyclin partners are members of the CYCLIN T family (T1, T2a, and T2b) and CYCLIN K. The CDK9/CYCLIN T1 complex is very important in the differentiation programme of several cell types, controlling specific differentiation pathways. Limited data are available regarding the expression of CDK9/CYCLIN T1 in haematopoietic and lymphoid tissues. The aim of this study was to analyse the expression of the CDK9/CYCLIN T1 complex in lymphoid tissue, in order to assess its role in B- and T-cell differentiation and lymphomagenesis. CDK9/CYCLIN T1 expression was found by immunohistochemistry in precursor B and T cells. In peripheral lymphoid tissues, germinal centre cells and scattered B- and T-cell blasts in interfollicular areas expressed CDK9/CYCLIN T1, while mantle cells, plasma cells, and small resting T-lymphocytes displayed no expression of either molecule. CDK9/CYCLIN T1 expression therefore appears to be related to particular stages of lymphoid differentiation/activation. CDK9 and CYCLIN T1 were highly expressed in lymphomas derived from precursor B and T cells, from germinal centre cells, such as follicular lymphomas, and from activated T cells (ie anaplastic large cell lymphomas). Hodgkin and Reed-Sternberg cells of classical Hodgkin's lymphoma also showed strong nuclear staining. Diffuse large B-cell, Burkitt's lymphomas, and peripheral T-cell lymphomas, among T-cell lymphoproliferative disorders, showed a wide range of values. No expression of CDK9 or CYCLIN T1 was detected in mantle cell and marginal zone lymphomas. However, at the mRNA level, an imbalance in the CDK9/CYCLIN T1 ratio was found in follicular lymphoma and diffuse large B-cell lymphomas with germinal centre phenotype, and in the cell lines of classical Hodgkin's lymphomas, Burkitt's lymphomas, and anaplastic large cell lymphoma, in comparison with reactive lymph nodes. These results suggest that the CDK9/CYCLIN T1 complex may affect the activation and differentiation programme of lymphoid cells. The molecular mechanism through which the CDK9/CYCLIN T1 complex is altered in malignant transformation needs to be elucidated.

Blotting, Western↗

PubMed2002

Orbital solitary fibrous tumor with aggressive behaviorThree cases and review of the literature.

BACKGROUND: Solitary fibrous tumor (SFT) is a rare spindle cell tumor that arises most often in the visceral pleura; however, a review of the literature shows at least 31 cases occurring in the orbit. METHODS: A retrospective case series of three patients with orbital SFT: a 50-year-old man, observed in 1997, with an angioma-like lesion in the upper half of the orbit causing osteolysis of the orbital roof; a 24-year-old man, observed in 1992, with a superotemporal mass in the right orbit occupying the lacrimal gland region, firstly diagnosed as schwannoma, recurring 4 years after dacryoadenectomy; a 70-year-old man, with a retrobulbar mass diagnosed on a biopsy as hemangiopericytoma, recurring and infiltrating the orbital roof 4 years after surgery. RESULTS: A review of the literature and presentation of three cases of SFT which showed infiltration of the orbital roof and/or recurrence. CONCLUSIONS: Our cases provide evidence of how orbital SFT can behave aggressively and mimic other orbital tumors, thus making mandatory the consideration of this relatively new entity in common clinical practice as well as careful follow-up. Their aggressive growth is unusual, described in only 6 of the 31 cases so far reported in the literature. Immunohistochemistry is of importance for the diagnosis, since CD34 immunoreactivity is peculiar to SFT.

Adult↗

PubMed2002

CD-34 stromal expression pattern in normal and altered human corneas.

OBJECTIVE: To test CD-34 immunoreactivity in stromal cornea cells in normal and pathologic samples obtained from penetrating keratoplasty. DESIGN: Prospective, consecutive histopathologic human tissue study. PARTICIPANTS AND CONTROLS: One hundred two cornea buttons from patients with different diseases, submitted for cornea transplant, were examined. Controls were expired corneas from healthy donor patients who died (n = 4), and globes enucleated for primitive intraocular neoplasias, that is, retinoblastomas (n = 8), and malignant choroidal melanomas (n = 2). METHODS: The expression of CD-34 in stromal cornea cells was examined by immunohistochemistry analysis. Other immunohistochemical stains included an endothelial cell marker (CD-31), common leukocyte antigen, and alpha-smooth muscle actin. MAIN OUTCOME MEASURES: Different diseases that may cause blindness and require penetrating keratoplasty have been tested for CD-34 immunoreactivity. RESULTS: In control corneas, keratocytes present strong and consistent CD-34 immunoreactivity. Diseases leading to the loss of transparency and penetrating keratoplasty, such as keratoconus, herpes keratitis, trauma, and heredofamilial dystrophies, are associated with focal or diffuse loss of CD-34 expression, whereas pseudophakic bullous keratopathy and Fuchs' endothelial dystrophy show normal CD-34 immunoreactivity in most cases and patchy unstained stromal areas in a few cases. CONCLUSIONS: Scar tissue formation in the cornea, as in herpes keratitis and trauma, is always associated with loss of CD-34 immunoreactivity, which may otherwise be a primary event in keratoconus and heredofamilial dystrophies. Both in the pseudophakic bullous keratopathy and Fuchs' endothelial dystrophy, CD-34 immunoreactivity may be normal or lost, hence these two diseases may be considered as one and part of the same group with regard to CD-34 expression, as revealed by immunohistochemistry analysis.

Actins↗

PubMed2002

Benign lymphoepithelial lesion associated with squamous cell carcinoma of the skin: an immunohistochemical and molecular genetic study.

BACKGROUND: Benign lymphoepithelial lesions (BLEL) are usually found in salivary glands in autoimmune disorders. Some LEL are recognized to already be, or may progress to become, lymphomas. Skin lesions similar to LEL have been described in lymphomas, and are caused by neoplastic lymphocytes which infiltrate adnexal structures. To date, BLEL have not widely been recognized in the skin. METHODS: We describe skin lesions similar to BLELs, at the periphery of squamous cell carcinomas (SCC) in 8 healthy patients, in one of whom the lesion recurred. Immunocharacterization of both epithelial and lymphocytic components and molecular genetic investigation was performed. Polymerase chain reaction (PCR) analysis was done to detect IgH chain gene, and T-cell receptor beta and gamma gene rearrangements. Association with Epstein-Barr virus (EBV) was also tested by in situ hybridization (ISH) for EBV-encoded RNAs (EBERs). RESULTS: Epithelial cells showed the immunophenotype of eccrine sweat gland ducts. Infiltrating lymphocytes expressed overwhelming B antigens and CD5. Neither clonal B and/or T proliferations nor EBERs signals were demonstrable. CONCLUSIONS: We observed skin lesions similar to BLELs, showing modifications of sweat gland duct and CD5+, B lymphocytic expansion. In our cases there were no associated autoimmune disorders; the local immunoresponse to SCC might have caused BLEL.

Aged↗

PubMedDate not supplied

An ovarian mucinous adenocarcinoma arising from mature cystic teratoma associated with respiratory type tissue: a case report.

Mature cystic teratoma (dermoid cyst) is the most common benign germ cell tumor of the ovary, accounting for approximately 30% of all ovarian tumors. Malignant transformation is rare; the most frequent transformation reported is to squamous-cell carcinoma in 80% of cases, whereas transformation to adenocarcinoma is described in about 7% of cases. We report a case of malignant transformation to mucinous adenocarcinoma arising from respiratory-like epithelium in a mature teratoma of the ovary.

Adenocarcinoma, Mucinous↗