Literature DB >> 23240926

Evidence of a low prevalence of RAS mutations in a large medullary thyroid cancer series.

Raffaele Ciampi1, Caterina Mian, Laura Fugazzola, Barbara Cosci, Cristina Romei, Susi Barollo, Valentina Cirello, Valeria Bottici, Giulia Marconcini, Pelizzo Maria Rosa, Maria Grazia Borrello, Fulvio Basolo, Clara Ugolini, Gabriele Materazzi, Aldo Pinchera, Rossella Elisei.   

Abstract

BACKGROUND: Approximately 60% of sporadic medullary thyroid carcinomas (sMTC) remain orphan of a recognized genetic cause. Recently, a high percentage of RAS point mutations have been described in RET-negative sMTC. The aim of this study was to assess the prevalence of RAS point mutations in a large series of MTC collected in four Italian centers.
METHODS: For this purpose, we studied codons 12, 13, and 61 of H-, K-, and N-RAS genes in 188 MTC samples, either hereditary or sporadic, by direct sequencing. Correlations between the RAS mutational status and the clinical-pathological features of MTC patients as well as a meta-analysis of all published data were performed.
RESULTS: The prevalence of RAS mutations in the present series of MTC was 10.1%, and 17.6% when considering only RET-negative cases. RAS mutations were found in MTC tumoral tissue, but not in peripheral blood indicating their somatic origin. A novel mutation in codon 72 (M72I) was found, but with a low or null transforming potential. No association was found between the presence of RAS mutations and the clinical-pathological features of the patients. Although not statistically significant, a positive association between the presence of RAS mutations and a better outcome was observed. The meta-analysis of all published studies confirmed a prevalence of 8.8% for RAS mutations in MTC.
CONCLUSIONS: The prevalence of RAS mutations in our MTC series was relatively low and consistent with the meta-analysis data. Only somatic RAS mutations were found and only in RET-negative sMTC. Likewise, MTCs that harbor a RAS mutation identify a subgroup of tumors with less aggressive behavior. To our knowledge, this is the largest series of MTCs studied for the presence of mutations in RAS genes and the first meta-analysis on this specific topic.

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Year:  2012        PMID: 23240926     DOI: 10.1089/thy.2012.0207

Source DB:  PubMed          Journal:  Thyroid        ISSN: 1050-7256            Impact factor:   6.568


  58 in total

1.  Overexpression of genes involved in miRNA biogenesis in medullary thyroid carcinomas with RET mutation.

Authors:  Cinzia Puppin; Cosimo Durante; Marialuisa Sponziello; Antonella Verrienti; Valeria Pecce; Elisa Lavarone; Federica Baldan; Antonio Francesco Campese; Amelie Boichard; Ludovic Lacroix; Diego Russo; Sebastiano Filetti; Giuseppe Damante
Journal:  Endocrine       Date:  2014-02-26       Impact factor: 3.633

2.  RET fusion as a novel driver of medullary thyroid carcinoma.

Authors:  Elizabeth G Grubbs; Patrick Kwok-Shing Ng; Jacquelin Bui; Naifa L Busaidy; Ken Chen; Jeffrey E Lee; Xinyan Lu; Hengyu Lu; Funda Meric-Bernstam; Gordon B Mills; Gary Palmer; Nancy D Perrier; Kenneth L Scott; Kenna R Shaw; Steven G Waguespack; Michelle D Williams; Roman Yelensky; Gilbert J Cote
Journal:  J Clin Endocrinol Metab       Date:  2014-12-29       Impact factor: 5.958

Review 3.  Revised American Thyroid Association guidelines for the management of medullary thyroid carcinoma.

Authors:  Samuel A Wells; Sylvia L Asa; Henning Dralle; Rossella Elisei; Douglas B Evans; Robert F Gagel; Nancy Lee; Andreas Machens; Jeffrey F Moley; Furio Pacini; Friedhelm Raue; Karin Frank-Raue; Bruce Robinson; M Sara Rosenthal; Massimo Santoro; Martin Schlumberger; Manisha Shah; Steven G Waguespack
Journal:  Thyroid       Date:  2015-06       Impact factor: 6.568

4.  2012 European thyroid association guidelines for genetic testing and its clinical consequences in medullary thyroid cancer.

Authors:  R Elisei; M Alevizaki; B Conte-Devolx; K Frank-Raue; V Leite; G R Williams
Journal:  Eur Thyroid J       Date:  2012-12-19

Review 5.  Thyroid C-Cell Biology and Oncogenic Transformation.

Authors:  Gilbert J Cote; Elizabeth G Grubbs; Marie-Claude Hofmann
Journal:  Recent Results Cancer Res       Date:  2015

6.  Lack of mutational events of RAS genes in sporadic thyroid cancer but high risk associated with HRAS T81C single nucleotide polymorphism (case-control study).

Authors:  Mosin S Khan; Arshad A Pandith; Mahboob Ul Hussain; Mohammad Iqbal; Nighat P Khan; Khurshid A Wani; Shariq R Masoodi; Syed Mudassar
Journal:  Tumour Biol       Date:  2012-11-13

7.  In vitro and in vivo activity of cabozantinib (XL184), an inhibitor of RET, MET, and VEGFR2, in a model of medullary thyroid cancer.

Authors:  Frauke Bentzien; Marcus Zuzow; Nathan Heald; Anna Gibson; Yongchang Shi; Leanne Goon; Peiwen Yu; Stefan Engst; Wentao Zhang; Donghui Huang; Lora Zhao; Valentina Vysotskaia; Felix Chu; Rajana Bautista; Belinda Cancilla; Peter Lamb; Alison H Joly; F Michael Yakes
Journal:  Thyroid       Date:  2013-09-17       Impact factor: 6.568

Review 8.  Update: the status of clinical trials with kinase inhibitors in thyroid cancer.

Authors:  Samuel A Wells; Massimo Santoro
Journal:  J Clin Endocrinol Metab       Date:  2014-01-13       Impact factor: 5.958

9.  [Medullary thyroid carcinoma].

Authors:  V Tiedje; S Ting; H Dralle; K W Schmid; D Führer
Journal:  Internist (Berl)       Date:  2015-09       Impact factor: 0.743

Review 10.  RAS mutations in thyroid cancer.

Authors:  Gina M Howell; Steven P Hodak; Linwah Yip
Journal:  Oncologist       Date:  2013-07-19
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