Reduced E-cadherin expression contributes to the loss of p27-mediated mechanism of contact inhibition in thyroid anaplastic carcinomas

نویسندگان

  • Maria Letizia Motti
  • Daniela Califano
  • Gustavo Baldassarre
  • Angela Celetti
  • Francesco Merolla
  • Floriana Forzati
  • Maria Napolitano
  • Barbara Tavernise
  • Alfredo Fusco
  • Giuseppe Viglietto
چکیده

Maria Letizia Motti, Daniela Califano, Gustavo Baldassarre, Angela Celetti, Francesco Merolla, Floriana Forzati, Maria Napolitano, Barbara Tavernise, Alfredo Fusco and Giuseppe Viglietto Dipartimento di Biologia e Patologia Cellulare e Molecolare ‘‘L.Califano’’ Facolt a di Medicina e Chirurgia, Universit a Federico II, via S. Pansini 5, 80131, Napoli, Italy, Istituto Nazionale Tumori, via M. Semmola, 80131, Napoli, Italy, Divisione di Oncologia Sperimentale 2, CRO National Cancer Institute, Via Pedemontana Occidentale 28, 33081 Aviano, Italy, Istituto di Endocrinologia ed Oncologia Sperimentale del CNR c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare ‘‘L.Califano’’ Facolt a di Medicina e Chirurgia, Universit a Federico II, via S. Pansini 5, 80131, Napoli, Italy and Laboratorio Oncologia Molecolare III, Dipartimento di Medicina Sperimentale e Clinica, Facolt a di Medicina e Chirurgia, Universit a ‘‘Magna Graecia’’, Campus Universitario Germaneto, Viale Europa, 88100 Catanzaro, Italy

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Reduced E-cadherin expression contributes to the loss of p27kip1-mediated mechanism of contact inhibition in thyroid anaplastic carcinomas.

In the present study, we have characterized several human thyroid cancer cell lines of different histotypes for their responsiveness to contact inhibition. We found that cells derived from differentiated carcinoma (TPC-1, WRO) arrest in G(1) phase at confluence, whereas cells derived from anaplastic carcinoma (ARO, FRO and FB1) continue to grow after reaching confluence. Furthermore, we provide...

متن کامل

بررسی فراوانی بروز مارکرهای E-Cadherin , Dysadherinدر کارسینوم های پستان

Background and purpose: Breast carcinoma is the most common malignant tumor and the leading cause of death due to cancer among women. Previous studies have shown that increased expression of dysadherin promotes cancer metastasis and reduced expression of E-cadherin was also associated with progression of epithelial tumors. The aim of this study was concurrent assessment of E- cadherin and dysad...

متن کامل

E-Cadherin: A Differentiation Marker in Thyroid Malignancies1

Loss of E-cadherin (uvomorulin), a Ca2*-dependent cell adhesion mole cule required for normal epithelial function, has been attributed a pathogenetic role in tumor invasion. The expression of E-cadherin was studied in normal and neoplastic follicular epithelium of the human thyroid by Northern blot analysis and immunofluorescence on frozen tissue sections. In the normal thyroid (n = 10) and in ...

متن کامل

E-cadherin: a differentiation marker in thyroid malignancies.

Loss of E-cadherin (uvomorulin), a Ca(2+)-dependent cell adhesion molecule required for normal epithelial function, has been attributed a pathogenetic role in tumor invasion. The expression of E-cadherin was studied in normal and neoplastic follicular epithelium of the human thyroid by Northern blot analysis and immunofluorescence on frozen tissue sections. In the normal thyroid (n = 10) and in...

متن کامل

Gene Expression and Promoter Methylation Status of VHL, Runx-3, E-cadherin, P15 and P16 Genes During EPO-Mediated Erythroid Differentiation of CD34+ Hematopoietic Stem Cells

Background: VHL (von Hippel-Lindau), Runx-3 (Runt-related transcription factor 3), E-cadherin (Epithelial cadherin), P15 (INK4a, cyclin dependent kinase inhibitor), and P16 (INK4b) genes are essential in hematopoiesis. The aim of this study was to explore the correlation between gene expression and promoter methylation in CD34+ stem cells before and after differentiation to erythroid lineage. M...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2005