Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cellular proliferation and differentiation of the mammalian mammary gland requires a medley of hormones including the anterior pituitary hormone, PRL. Recent evidence extends the role of PRL as a mammalian mitogen to cells in several physiological systems not directly involved in reproductive functions, such as liver and lymphocytes. PRL administration induces biochemical markers expressed during the G1 phase of cell cycle and activates DNA synthesis in rat liver. Chronic PRL treatment causes hepatomegaly, reflecting its stimulation of the proliferative process. In vitro, a lactogen-dependent cell line, the Nb2 rat node lymphoma cell, serves as a useful paradigm to study PRL action on mitogenesis. These cells, when cultured in the presence of lactogens, proliferate in a dose-dependent manner. The effects of various pharmacological agents on discrete phases of the cell cycle may be readily assessed in these cells since PRL-stimulated entry into cycle is signalled by an elevation of ODC activity at 6 hr and entry into S-phase at 6-12 hr. The parallel effects of phorbol ester tumor promoters and PRL on cell cycle progression in Nb2 lymphoma cells and in hepatic proliferation suggest that PRL may likewise mediate proliferation in aberrant growth conditions such as neoplasia. The data presented support the hypothesis that PRL is capable of promoting hepatocarcinogenesis. Its chronic administration after a hepatic initiating agent stimulated the development of histochemical and biochemical markers characteristic of preneoplasia. Further, the effect of PRL was comparable to that of the hepatocarcinogen when either was administered alone. Thus, hyperprolactinemia may serve to promote the development of hepatic tumors. Phorbol esters are thought to promote tumorigenesis by directly activating PKC. In the Nb2 lymphoma cell model, tumor promoting phorbol esters mimic the effects of PRL. Similarly, PRL-stimulated enzyme induction in liver is mirrored by phorbol ester treatment, and inhibitors of PKC block PRL-stimulated mitogenesis in Nb2 cells. Further, PRL or TPA administration to rats causes translocation of PKC activity from the hepatic cytosol to the membrane fraction, reflecting kinase activation. Therefore, PRL activation of PKC appears to be a physiological phenomenon of general significance, occurring as the result of lactogen receptor stimulation and serving to transmit intracellular signals linked to the regulation of mitogenesis. Further study is required to more fully define the scope of PRL-mediated mitogenic actions as well as its effects on the expression of differentiated products in tissues and cells.
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PMID:Prolactin as a mammalian mitogen and tumor promoter. 325 Feb 31

We present the clinical and immunological features of a rare case of chronic lymphoid leukaemia with lymphoplasmacytoid morphology. The patient was first admitted suffering from weakness, pallor, dyspnoea, marked splenomegaly, hepatomegaly and systemic lymphadenopathy and panhypogammaglobulinaemia. White blood cell count revealed important leukocytosis (220 x 10(9) WBC/l) with 2% neutrophils and 98% lymphoid cells showing lymphoplasmacytoid features, while lymphoid cells of identical morphology severely infiltrated the bone marrow and lymph nodes. The disease, initially controlled by non aggressive chemotherapy over a period of 30 months, later evolved to a clinical and haematological picture suggestive of Richter's syndrome. Immunophenotyping of the leukaemic cells demonstrated a monoclonal expansion of B-cells bearing surface markers of typical CLL (CD5, CD19, CD20, CD21, CD22, CD23, CD24, CD40 and low density IgM+IgD/kappa) and also the CD11c and CD38 antigens. A proportion of these cells expressed activation markers (CD25, CD69 and CD71). Following in vitro activation with TPA or PWM, the cells responded by weak incorporation of 3H-TdR but failed to secrete immunoglobulins. These findings confirm the broad morphological, phenotypical and clinical spectrum of chronic lymphoid leukaemias.
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PMID:Monoclonal expansion of immunoglobulin not-secreting CD5+ CD11c+ CD38+ B-cells in a rare case of chronic lymphoplasmacytoid leukaemia. 797 Dec 44