MR imaging coupled with contrast material-enhanced dynamic MR imaging is highly accurate in local-regional staging of endometrial carcinoma; more challenging is the assessment of pelvic and lumboaortic lymph nodes.

Summary Accumulating evidence indicates an immunosuppressive role of the thymus‐derived CD4+ T‐cell population constitutively expressing high level of CD25, T regulatory (Treg) cells, in autoimmune diseases. Here we show that the number of Treg cells in the blood is significantly lower in untreated myasthenia gravis patients than in age‐matched healthy subjects, whereas it is normal or elevated in patients on immunosuppressive therapy (prednisone frequently associated with azathioprine). Therapeutic thymectomy (Tx) for either the thymoma or non‐neoplastic thymic alterations that are often associated with myasthenia gravis provided unique material for studying intrathymic Treg cells and correlating them with their peripheral counterparts. We observed that Tx prevents the increase of Treg cells in the circulation that follows immunosuppressive therapy (particularly evident if the thymus is not neoplastic), indicating that the thymus contributes to Treg‐cell normalization. However, thymic Treg cells are not modulated by immunosuppressive therapy and even in thymectomized patients Treg‐cell numbers in the blood eventually recover. The present findings suggest that a deficiency in Treg cells favours the development of myasthenia gravis and that their normalization is an important clinical benefit of immunosuppressive therapy. Treg normalization appears to be largely thymus independent and possibly reflects the reported capacity of corticosteroids to promote Treg‐cell development.

Prolactin (PRL) is a hormone, mainly secreted by lactotroph cells of the anterior pituitary gland. Recent studies have shown it may also be produced by many extrapituitary cells. Its well-recognized PRL plays an important role in lactation during pregnancy, but it is involved in other biological functions such as angiogenesis, immunoregulation and osmoregulation. Hyperprolactinemia is a typical condition producing reproductive dysfunction in both sexes, resulting in hypogonadism, infertility and galactorrhea. It may be also asymptomatic. Lactotroph adenomas (prolactinoma) is one of the most common cause of PRL excess, representing approximately 40% of all pituitary tumors. Several other conditions should be excluded before a clear diagnosis of hyperprolactinemia is made. Hyperprolactinemia may be secondary to pharmacological or pathological interruption of hypothalamic-pituitary dopaminergic pathways or idiopathic. Stress, renal failure or hypothyroidism are other frequent conditions to exclude in patients with hyperprolactinemia. We will review biochemical characteristics and physiological functions of that hormone. Clinical and pharmacological approach to hyperprolactinemia will also be discussed.

We analyzed the expression and amplification of cyclin D1 and CDK4 genes in ovarian carcinomas. Northern blot analysis revealed overexpression of cyclin D1 in 12 of 65 (18%) ovarian carcinomas while CDK4 was overexpressed in 7 of 48 cases (14%). None of the tumors showed amplification of any of the 2 genes. Overexpression of cyclin D1 and CDK4 transcripts was correlated, suggesting a role of both genes in altered growth control of ovarian cancer cells. Elevated levels of cyclin D1 were significantly associated with a wellmoderately differentiated grade (G1-G2) (p F 0.005). No significant association was found between cyclin D1 expression and estrogen receptor, progesterone and epidermal growth factor receptor content. Cyclin D1 expression does not appear to be associated with clinical outcome in human ovarian cancer, although a longer follow-up period and screening of other molecules involved in the same pathway would be necessary to assess this hypothesis. Int. J. Cancer 74:390-395, 1997.r 1997 Wiley-Liss, Inc.The prognostic characterization of patients with ovarian cancer, which is based on clinico-pathological criteria, is largely inadequate. Fifty percent of the patients, after optimal surgical debulking and a pathologically complete response to primary chemotherapy, will develop a recurrence of the tumor and will die within 2 years. Thus, the development of additional prognostic factors, closely related to tumor cell biology, is essential for identification of patients with a particularly poor prognosis.Attention has recently been focused on genetic alterations of several proto-oncogenes and tumor suppressor genes that mediate signal transduction pathways involved in cell proliferation and differentiation as well as cell cycle control. Cyclins are a family of cell cycle control proteins that regulate cell cycle progression by associating with and activating cyclin-dependent kinases (CDKs). Since the major regulatory events leading to mammalian cell proliferation and differentiation occur in the G 0 to G 1 phases and/or in the G 1 to S phase transition during the cell cycle, the deregulated expression of G 1 or G 1 /S phase cyclins or their related CDKs may cause loss of cell cycle control and thereby contribute to neoplastic transformation. Cyclin D1 is known to regulate cell cycle progression at the G 1 -S checkpoint, and its overexpression shortens the G 1 -S transition. To function as a positive regulator of G 1 progression, cyclin D1 needs to bind to its catalytic subunit, CDK4. When activated by cyclin D1, CDK4 phosphorylates the retinoblastoma tumor suppressor protein (pRb), resulting in release of pRbmediated G 1 arrest. Indeed, the unphosphorylated form of pRb is thought to restrain cell cycle progression by binding and inactivating members of the E2F family of transcription factors, the inhibitory effect being abolished by phosphorylation. The cyclin D1/CDK4 complex can be inhibited by various proteins including some members of the p16 family of cell cycle inhibitors. Amplification and/or overexpre...

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We first reported that the most relevant genes involved in gemcitabine metabolism are expressed in ovarian carcinoma, and might be associated with more aggressive histotypes. The assessment of the expression levels of RRM2 as marker of clinical outcome deserves further investigation in a larger series of ovarian cancer patients.

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