Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: CHENG
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Tytuł oryginału: Expression of mutant thyroid hormone nuclear receptors is associated with human renal clear cell carcinoma.
Autorzy: Kamiya Yuji, Puzianowska-Kuźnicka Monika, McPhie Peter, Nauman Janusz, Cheng Sheue-yann, Nauman Alicja
Źródło: Carcinogenesis 2002: 23 (1) s.25-33, il., tab., bibliogr. 59 poz.
Sygnatura GBL: 312,779

Hasła klasyfikacyjne GBL:
  • nefrologia
  • onkologia

    Typ dokumentu:
  • praca kliniczna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie

    Streszczenie angielskie: Thyroid hormone (T3) regulates proliferation and differentiation of cells, via its nuclear receptors (TRs). These processes have been shown to be abnormally regulated during carcinogenesis. We have previously found aberrant expression of TRŕ and TRá mRNAs in renal clear cell carcinoma (RCCC), suggesting possible involvement of TRs in the carcinogenesis of RCCC. To understand the molecular actions of TRs in RCCC, cDNAs for TRá1 and TRŕ1 were cloned from 22 RCCC tissues and 20 surrounding normal tissues. Mutations were found in seven TRá1 and three TRŕ1 cDNAs. Two TRá1 cDNAs had a single mutation, while five TRá1 and three TRŕ1 had two or three mutations. Most of the mutations were localized in the hormone-binding domain. Using the TRs prepared by in vitro transcription/translation, we found that these mutations led to a loss of T3 binding activity and/or impairment in binding to thyroid hormone response elements (TREs). Furthermore, nuclear extracts from RCCC tissues also exhibited impairment in binding to TREs. These results indicate that the normal functions of TRs in RCCC tissues were impaired. Together with the aberrant expression patterns, these mutated TRs could contribute to the carcinogenesis of RCCC.


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    Tytuł oryginału: Functionally impaired TR mutants are present in thyroid papillary cancer.
    Autorzy: Puzianowska-Kuźnicka Monika, Krystyniak Agnieszka, Madej Agnieszka, Cheng Sheue-Yann, Nauman Janusz
    Źródło: J. Clin. Endocrinol. Metab. 2002: 87 (3) s.1120-1128, il., tab., bibliogr. 52 poz.
    Sygnatura GBL: 310,620

    Hasła klasyfikacyjne GBL:
  • genetyka
  • endokrynologia
  • onkologia

    Typ dokumentu:
  • praca kliniczna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie

    Streszczenie angielskie: TRs are transcription factors that regulate cell proliferation, differentiation, and apoptosis. They are cellular homologs of the transcriptionally inactive viral oncogene v-erbA. We tested the hypothesis that the functions of TRs could be impaired in cancer tissues as a result of aberrant expression and/or somatic mutations. As a model system, we selected human thyroid papillary cancer, in which the most common abnormalities, RET/papillary thyroid cancer rearrangements (fusion of RET kinase domain to the activating domains of other genes), were found in 40-45 p.c. of cases. We found that the mean expression levels of TRá mRNA and TRŕ mRNA were significantly lower, whereas the protein levels of TRá1 and TRŕ1 were in cancer tissues than in healthy thyroid. Sequencing of TRá1 and TRŕ1 cDNAs, cloned from 16 papillary cancers, revealed that mutations affected receptor amino acid sequences in 93.75 p.c. and 62.5 p.c. of cases, respectively. In contrast, no mutations were found in healthy thyroid controls, and only 11.11 p.c. and 22.22 p.c. of thyroid adenomas had such TRá1 or TRŕ1 mutations, respectively. The majority of the mutated TRs lost their trans-activation function and exhibited dominant negative activity. These findings suggest a possible role for mutated thyroid hormone receptors in the tumorigenesis of human papillary thyroid carcinoma.


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    Tytuł oryginału: Vascular effects of COX inhibition and AT1 receptor blockade in transgenic rats harboring mouse renin-2 gene.
    Autorzy: Cheng Z. J., Tikkanen I., Vapaatalo H., Mervaala E. M. A.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4 p. 1) s.597-613, il., bibliogr. 50 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • szczury

    Streszczenie angielskie: Ang II-induced endothelial dysfunction is associated with perivascular inflammation and increased superoxide production in the vascular wall. The present study examined the role of cyclo-oxygenase (COX)-synthetized eicosanoids in the pathogenesis of Ang II induced endothelial dysfunction in transgenic rats harboring mouse renin-2 gene (mREN2 rats). Five-to-six-week-old, heterozygous mREN2 rats received the following drug regimens for 8 weeks: 1) vehicle, 2) cyclo-oxgenase-2 (COX-2) inhibitor (MF-tricyclic [3-(3,4-difluorophenyl)-4-(4-(methylsulfonyl) phenyl)-2(5H)-furanone], 14 mg/kg p.o.), COX-1/COX-2 inhibitor (sulindac, 14 mg/kg p.o.), 4) angiotensin II receptor antagonist (losartan 40 mg/kg p.o.). Normotensive Sprague Dawley (SD) rats served as controls. In vitro vascular responses of the descending aorta and renal artery were studied using organ bath system. mREN2 rats developed pronounced hypertension which was associated with impaired endothelium-dependent and endothelium-independent vascular relaxations in the aorta. In contrast, the relaxation responses of the renal arteries remained largely unchanged in mREN2 rats. Urinary NOx excretion, a marker of total body NO generation, was also decreased in mREN2 rats. Neither non-selective COX inhibitor sulindac nor COX-2 selective MF-tricyclic were capable of preventing Ang II-induced hypertension or endothelial dysfunction in mREN2 rats, whereas ATireceptor antagonist losartan comletely normalized blood pressure, vascular relaxation responses ...

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