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      Clinical utility of RASSF1A methylation in human malignancies

      review-article
      Author(s): 1 , 1 , *
      Publication date (Electronic):
      Journal: British Journal of Cancer
      Publisher: Nature Publishing Group
      Keywords: RASSF1A, hippo pathway, gene methylation, cancer, biomaker

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          Abstract

          The high frequency of RASSF1A methylation has been noted in a vast number of patients in a broad spectrum of malignancies, suggesting that RASSF1A inactivation is associated with cancer pathogenesis. However, whether this recurrent incidence of RASSF1A hypermethylation in human malignancies and its association with more aggressive tumour phenotype is a frequent event across different cancer types has not yet been discussed. In this review, we interrogated existing evidence for association of RASSF1A hypermethylation with clinicopathological characteristics that can indicate more invasive lesions.

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          Metastasis: a question of life or death.

          Patrick Mehlen, Alain Puisieux (2006)
          The metastatic process is highly inefficient--very few of the many cells that migrate from the primary tumour successfully colonize distant sites. One proposed mechanism to explain this inefficiency is provided by the cancer stem cell model, which hypothesizes that micrometastases can only be established by tumour stem cells, which are few in number. However, recent in vitro and in vivo observations indicate that apoptosis is an important process regulating metastasis. Here we stress that the inhibition of cell death, apart from its extensively described function in primary tumour development, is a crucial characteristic of metastatic cancer cells.
          Article 0 comments Cited 582 times – based on 0 reviews     Review now
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            Gene expression profiling in breast cancer: classification, prognostication, and prediction.

            Jorge S. Reis-Filho, Lajos Pusztai (2011)
            Microarray-based gene expression profiling has had a major effect on our understanding of breast cancer. Breast cancer is now perceived as a heterogeneous group of different diseases characterised by distinct molecular aberrations, rather than one disease with varying histological features and clinical behaviour. Gene expression profiling studies have shown that oestrogen-receptor (ER)-positive and ER-negative breast cancers are distinct diseases at the transcriptomic level, that additional molecular subtypes might exist within these groups, and that the prognosis of patients with ER-positive disease is largely determined by the expression of proliferation-related genes. On the basis of these principles, a molecular classification system and prognostic multigene classifiers based on microarrays or derivative technologies have been developed and are being tested in randomised clinical trials and incorporated into clinical practice. In this review, we focus on the conceptual effect and potential clinical use of the molecular classification of breast cancer, and discuss prognostic and predictive multigene predictors. Copyright © 2011 Elsevier Ltd. All rights reserved.
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              Epigenetic inactivation of a RAS association domain family protein from the lung tumour suppressor locus 3p21.3.

              R Dammann, C LI, J. Yoon … (2000)
              Allelic loss at the short arm of chromosome 3 is one of the most common and earliest events in the pathogenesis of lung cancer, and is observed in more than 90% of small-cell lung cancers (SCLCs) and in 50-80% of non-small-cell lung cancers (NSCLCs). Frequent and early loss of heterozygosity and the presence of homozygous deletions suggested a critical role of the region 3p21.3 in tumorigenesis and a region of common homozygous deletion in 3p21.3 was narrowed to 120 kb (ref. 5). Several putative tumour-suppressor genes located at 3p21 have been characterized, but none of these genes appear to be altered in lung cancer. Here we describe the cloning and characterization of a human RAS effector homologue (RASSF1) located in the 120-kb region of minimal homozygous deletion. We identified three transcripts, A, B and C, derived from alternative splicing and promoter usage. The major transcripts A and C were expressed in all normal tissues. Transcript A was missing in all SCLC cell lines analysed and in several other cancer cell lines. Loss of expression was correlated with methylation of the CpG-island promoter sequence of RASSF1A. The promoter was highly methylated in 24 of 60 (40%) primary lung tumours, and 4 of 41 tumours analysed carried missense mutations. Re-expression of transcript A in lung carcinoma cells reduced colony formation, suppressed anchorage-independent growth and inhibited tumour formation in nude mice. These characteristics indicate a potential role for RASSF1A as a lung tumour suppressor gene.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Br J Cancer
                Journal ID (iso-abbrev): Br. J. Cancer
                Title: British Journal of Cancer
                Publisher: Nature Publishing Group
                ISSN (Print): 0007-0920
                ISSN (Electronic): 1532-1827
                Publication date (Print): 28 July 2015
                Publication date (Electronic): 09 July 2015
                Volume: 113
                Issue: 3
                Pages: 372-381
                Affiliations
                [1 ]CRUK/MRC Oxford Institute, Department of Oncology, University of Oxford , Oxford, UK
                Author notes
                Article
                Publisher Item ID: bjc2015221
                DOI: 10.1038/bjc.2015.221
                PMC ID: 4522630
                PubMed ID: 26158424
                SO-VID: 4798d25a-8256-40c6-af3a-f6e7a582031b
                Copyright © Copyright © 2015 Cancer Research UK
                License:

                From twelve months after its original publication, this work is licensed under the Creative Commons Attribution-NonCommercial-Share Alike 4.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

                History
                Date received : 19 February 2015
                Date revision received : 11 May 2015
                Date accepted : 13 May 2015
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: rassf1a,hippo pathway,gene methylation,cancer,biomaker
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: rassf1a, hippo pathway, gene methylation, cancer, biomaker

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