Search PubMed⌕ Search

Biomedical subjects

A Fusco

Publications and source records attributed to A Fusco.

At least 253 records · Page 14Linked to original sources
PubMed1985

A mos oncogene-containing retrovirus, myeloproliferative sarcoma virus, transforms rat thyroid epithelial cells and irreversibly blocks their differentiation pattern.

Differentiated, cloned rat thyroid epithelial cells (424 cells) were infected with a wild-type and a temperature-sensitive strain of the myeloproliferative variant of the Moloney murine sarcoma virus. The thyroid cells were productively infected and transformed by both virus strains and displayed some of the typical properties of malignant cells, such as morphological changes, growth in soft agar, and in vivo tumorigenicity. The acquisition of the transformed phenotype by the virus-infected cells was accompanied by a loss of the typical differentiated features of the thyroid epithelium, such as thyroglobulin (TG) secretion, iodide uptake, and dependence for growth on six factors including thyrotropin, the physiological thyroid stimulator. TG mRNA could not be demonstrated in cells transformed by both viral strains, suggesting a block at the level of the TG gene transcription. While the transformed state of the cell clones infected with the temperature-sensitive strain could be reverted by shifting the cultures to the temperature nonpermissive for transformation (39 degrees C), no reversion of the differentiated functions took place after such a shift, showing that the v-mos oncogene irreversibly shuts off the differentiation of thyroid epithelial cells in vitro. These results demonstrate, for the first time, an oncogenic potential of the v-mos oncogene family towards differentiated epithelial cells in vitro.

Animals↗
PubMed1985

Changes in nuclear proteins on transformation of rat epithelial thyroid cells by a murine sarcoma retrovirus.

Two-dimensional electrophoresis has been used to document changes in nuclear proteins following viral transformation of an epithelial cell line exhibiting differentiation markers. After transformation, these markers are lost, and the cells become tumorigenic and capable of growth in soft agar. A sharp rise in the phosphorylation of histones H1, H2A, and ubiquitinated H2A is seen on transformation, together with the appearance of three phosphorylated proteins that are extractable by perchloric acid and appear related to high mobility group Protein 14, a constituent of active chromatin. Since comparison is made between normal and transformed cells that are each grown to confluence and since there is little difference between their observed growth rates, the changes seen represent intrinsic differences between the cell lines and are thus a direct reflection of the process of transformation.

Animals↗
PubMed1984

[Paraneoplastic porphyria cutanea tarda in a case of small cell bronchogenic carcinoma].

A case of diffuse hepatic metastasis of small cell bronchial carcinoma is presented. The first symptoms were specific PCT lesions and excessive excretion of urinary porphyrins. The patient was subjected to various instrumental examinations. Selective arteriography, CAT and hepatic echography showed liver to be of enormous size and completely homogeneous, suggesting a diagnosis of Budd-Chiari syndrome. Only hepatic scintigraphy showed multiple take-up lacunae and complete organ substitution. The rarity of the case and the possible pathogenesis of paraneoplastic PCT are discussed.

Carcinoma, Bronchogenic↗
PubMed1984

Continuous suppression of globin gene expression and differentiation of Friend erythroleukemia cells by phorbol 12-myristate 13-acetate (PMA) despite the loss of PMA binding sites by down regulation.

The tumor promoter phorbol 12-myristate 13-acetate (PMA) reversibly inhibits hexamethylene bisacetamide-induced terminal differentiation of Friend erythroleukemia cells (FELC). We were successful in continuously inhibiting FELC differentiation by PMA up to 125 weeks (about 240 serial passages of cells in the presence of PMA). During that period, FELC can be induced to differentiate and enter terminal cell division upon removal of PMA. PMA-mediated suppression of FELC differentiation was associated with only a low level of globin mRNA accumulation. However, a rapid accumulation of globin mRNA in the cytoplasm followed by hemoglobin accumulation occurred upon removal of PMA. A specific, saturable, high-affinity receptor for phorbol esters is present in FELC, as was shown by binding studies with [3H]phorbol 12,13-dibutyrate. A significant (80%) loss in the number of phorbol ester receptors of FELC was observed after a continuous inhibition of differentiation by PMA for as much as 125 weeks. Despite such a down regulation of phorbol ester receptors, these cells respond to PMA with a dose-response similar to that of their parent cells, which have the normal number of phorbol ester receptors. Thus, PMA can suppress reversibly the accumulation of globin-specific mRNA and terminal differentiation of FELC during prolonged periods, despite loss of receptor sites, and our results suggest that only few phorbol ester receptors may be necessary for complete inhibition of FELC differentiation by PMA.

Acetamides↗
PubMed1984

Expression of the onc gene of the Kirsten murine sarcoma virus in differentiated rat thyroid epithelial cell lines.

A systematic study has been performed using a series of differentiated rat thyroid epithelial cell lines either uninfected or infected with Kirsten murine sarcoma virus (KiMSV), to determine the levels of the p21 product of the v-ras-Ki oncogene in transformed and normal cell lines. The p21 levels have been assayed by SDS-polyacrylamide gel electrophoresis of immunoprecipitates of 35S-labelled cell extracts and by a GDP binding assay. All cell lines analysed showed a significant increase in the levels of p21 after transformation with KiMSV compared to the p21 levels of uninfected and untransformed differentiated thyroid cells. The results reported here confirm the potential ability of the v-ras-Ki oncogene product to transform epithelial cells. They show, furthermore, that not only is p21 present in some epithelial cells transformed by KiMSV, but also that it is functionally active, as has been shown for fibroblasts transformed by the same virus, and that its functioning is maintained after passaging in vivo of the transformed cells.

Animals↗
PubMed1984

5-Aza-2'-deoxycytidine induces terminal differentiation of leukemic blasts from patients with acute myeloid leukemias.

In this study, the effects of 5-aza-2'-deoxycytidine on differentiation of human leukemic cells in primary suspension culture are reported for the first time. Morphological and functional differentiation was induced in cells from two acute monoblastic leukemias and two of three acute myeloid leukemias following repeated exposures to 1 mumol/L 5-aza-2'-deoxycytidine. The observation that nontoxic concentrations of the drug are able to induce the in vitro differentiation of both monoblastic and myeloblastic leukemic cells into mature elements may encourage the exploitation of the differentiating properties of 5-aza-2'-deoxycytidine in chemotherapy protocols for acute non-lymphoblastic leukemias.

Azacitidine↗
PubMed1983

[Different shell development in Mytilus galloprovincialis in 2 different populations from the Gulf of Naples].

The size frequency distribution, the shell weight, the semilogarythmic growth, the carbonic anhydrase activity has been investigated between two populations of mussels from different sampling zones. Significative differences were found in the parameters investigated between the two populations. The authors conclude that the reason of this morphological and biochemical differences may arise from different natural hydrobiological factors and/or from different pollution of their habitat.

Animals↗
PubMed1983

Dissociation between transformed and differentiated phenotype in rat thyroid epithelial cells after transformation with a temperature-sensitive mutant of the Kirsten murine sarcoma virus.

Differentiated rat thyroid epithelial cells, infected in vitro with a temperature-sensitive mutant of the Kirsten murine sarcoma virus, expressed at the permissive temperature (33 degrees C) some phenotypic properties typical of transformed cells, including morphological features, colony formation in agar, and induction of tumors in newborn animals. Specific functional markers of these differentiated cells, i.e., synthesis/secretion of thyroglobulin, synthesis of thyroglobulin mRNA and iodide uptake, were blocked during growth at 33 degrees C. Normal morphology, failure to grow in agar, and the requirement of hormones for optimal growth were all restored after shifting to the temperature nonpermissive for transformation (39 degrees C), though the typical differentiated functions remained blocked. Infection with a leukemia helper virus clone (Moloney or Kirsten murine leukemia virus) did not lead to the loss of the differentiated phenotype of rat epithelial thyroid cells, thus demonstrating that the loss of the differentiated phenotype is caused by the sarcoma virus component. These results indicate that the expression of some of the phenotypic properties of transformed differentiated rat thyroid epithelial cells is under the direct control of the p21 thermosensitive activity, whereas the block in the expression of two typical differentiation markers of thyroid epithelial cells is irreversible and probably controlled by different mechanisms.

Animals↗
PubMed1983

Expression of Friend leukemia virus and spleen focus-forming virus-specific sequences in erythroid bursts and granulocyte-macrophage colonies from spleen and marrow of mice infected with Friend leukemia virus.

A large number of studies have been carried out to identify the Friend leukemia virus (FV) target cell(s). In FV-infected mice, the kinetics of "primitive" erythroid burst-forming units (P-BFU-E) is perturbed, and their proliferative rate is enhanced. These results indirectly suggest, but do not prove, that cycling P-BFU-E may serve as FV target. In vitro infection studies showed that normal erythroid colony forming units (CFU-E) and "mature" erythroid burst-forming units (M-BFU-E) are targets for FV, while the largely out-of-cycle normal P-BFU-E are not. In an attempt to shed light on these aspects, we have evaluated the expression of viral cytoplasmic RNA sequences in pools of colonies generated by P-BFU-E and granulocyte-macrophage colony forming units (CFU-GM) from spleen and marrow of polycythemic Friend virus (FVP)-infected mice, as measured by liquid hybridization with FVP- or spleen focus-forming polycythemic virus (SFFVp)-specific DNA probes. Moreover, similar assays were performed on RNAs derived from whole spleen or bone marrow from mice treated with FVP or the anemic strain of Friend virus (FVA). Control studies were performed on corresponding colonies and whole tissues from normal animals. FVP- and SFFVp-specific sequences are more abundant in RNA extracted from infected spleen as compared to marrow by a 10-fold factor. On the other hand, FVP and SFFVp-specific sequences are expressed at a comparable level in both P-BFU-E- and CFU-GM-derived colonies from spleen or marrow of FVP-treated mice. Since in vitro spread of FVP infection was excluded by control studies with addition in culture of antibody to the viral glycoprotein with a molecular weight of 70,000 (gp70) these results indicate that P-BFU-E and CFU-GM are infected in vivo by FVP.

Animals↗
PubMed1983

Role of telethermography and arthrography in rheumatoid wrist.

After briefly reviewing some of the problems relating to an early identification of synovial pathology, the authors have pointed out the actual role of telethermography and arthrography, resulting from their diagnostic experience. The two techniques were applied to a group of 40 patients affected with rheumatoid arthritis and were found to be particularly helpful: (i) either providing quite early information (telethermography); or (ii) allowing an exact topographic definition of synovial and tendinous sheath involvement (opaque arthrography), or eventually (iii) supplying a manageable means to follow their development with.

Arthritis, Rheumatoid↗
PubMed1982

Block in the expression of differentiation markers of rat thyroid epithelial cells by transformation with Kirsten murine sarcoma virus.

Well-differentiated epithelial cells, derived from primary cultures of normal rat thyroid glands (T-79 cells), as well as a cloned cell line also derived from normal rat thyroid glands (FRT-L cells) were infected with Kirsten murine sarcoma virus carrying outer coat of the helper Kirsten murine leukemia virus. Infected T-79 and FRT-L cells changed morphologically and began to proliferate rapidly, suggesting malignant transformation by the virus. Both cell lines can support the replication of both transformation-competent and transformation-incompetent viruses such as murine or rat leukemia viruses. Infected T-79 and FRT-L cells had a high colony-forming efficiency (68 and 64%, respectively) when grown in agar and formed tumors when transplanted s.c. into syngeneic rats. These tumors morphologically resemble undifferentiated adenocarcinomas, thus showing that Kirsten sarcoma virus carrying the outer coat of the helper Kirsten murine leukemia virus is able to transform differentiated epithelial cells. Transformed T-79 and FRT-L cells, in contrast to uninfected cells, neither secrete thyroglobulin concentrate iodide, two biochemical markers of differentiated thyroid function. Thus, expression of the differentiated phenotype is blocked as a consequence of cell transformation. The system described may be useful in studying epithelial cell carcinogenesis in terms of regulated expression of differentiated functions.

Animals↗
PubMed1981

Transformation of rat thyroid epithelial cells by Kirsten murine sarcoma virus.

Fischer rat thyroid epithelial cella (FRT) growing continuously in culture were infected with the Kirsten murine sarcoma virus KiMSV(KiMuLV) and found to produce this virus constitutively. Although the morphology of the FRT cells did not change appreciably, the cells became malignant after infection with KiMSV(KiMuLV) as shown by the growth of infected cels in semi-solid media (uninfected FRT cells did not grow) and by the tumorigenicity of infected when injected into syngeneic animals (uninfected FRT cells or FRT cells infected with non-transforming retro-viruses were not tumorigenic). The induced tumors morphologically resembled moderately differentiated carcinomas. Two markers of thyroid epithelial differentiation were absent in the original FRT clone and remained unexpressed after transformation. Fully differentiated rat thyroid epithelial cells (FRT-L cells) infected with another strain of the Kirsten murine sarcoma virus, the KiMSV(MolMuLV), were also transformed as demonstrated by the ability also of these cells to grow as carcinomas (after in vitro transformation) in syngeneic animals. Our results clearly demonstrate that the Kirsten murine sarcoma virus can transform in vitro cells of epithelial as well as of fibroblastic origin.

Animals↗