alexa Bcl-2, an Antiapoptotic Gene Indicator of Good Prognosis in Breast Cancer: The Paradox | Open Access Journals
ISSN: 2157-2518
Journal of Carcinogenesis & Mutagenesis
Like us on:
Make the best use of Scientific Research and information from our 700+ peer reviewed, Open Access Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.
Meet Inspiring Speakers and Experts at our 3000+ Global Conferenceseries Events with over 600+ Conferences, 1200+ Symposiums and 1200+ Workshops on
Medical, Pharma, Engineering, Science, Technology and Business

Bcl-2, an Antiapoptotic Gene Indicator of Good Prognosis in Breast Cancer: The Paradox

Maximino Redondo*

Department of Biochemistry, Hospital Costa del Sol, University of Málaga, REDISSEC, Carretera de Cádiz km 187, 29600, Marbella, Málaga, Spain

*Corresponding Author:
Maximino Redondo
Department of Biochemistry
Hospital Costa del Sol
University of Málaga, REDISSEC
Carretera de Cádiz km 187, 29600
Marbella, Málaga, Spain
E-mail: mailto:[email protected]

Received date: January 21, 2013; Accepted date: January 22, 2013; Published date: February 05, 2013

Citation: Redondo M (2013) Bcl-2, an Antiapoptotic Gene Indicator of Good Prognosis in Breast Cancer: The Paradox. J Carcinogene Mutagene 4:134. doi: 10.4172/2157-2518.1000134

Copyright: © 2013 Redondo M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Journal of Carcinogenesis & Mutagenesis

Breast cancer is the most frequently diagnosed cancer among women. Alterations in different genes are involved in the development of this tumour [1] and alterations in crucial pathways related to proliferation and apoptosis have been used as targets for treatment [2]. Bcl-2 protein is a member of the bcl-2 family that regulates apoptosis. The bcl-2 gene encodes a MR 26000 protein that is mainly localized in the mitochondrial membrane and, to a lesser extent, in the nuclear membrane and the endoplasmic reticulum. Its implication in carcinogenesis and progression makes this gene worthy of investigation. Its tumourigenic potential has been demonstrated: bcl-2 protein blocks apoptosis and cooperates with c-myc in cell transformation [3]. In addition, in the MCF-7 breast cancer cell line the overexpression of bcl-2 enhances both tumourigenicity and metastatic potential [4]. However, in many solid organ tumours, including breast cancer, bcl- 2 expression, paradoxically, is associated with favourable prognostic features and good outcome [5,6]. Interestingly, the expression of bcl- 2 is higher in screen-detected cancers than in symptomatic cancers [7] and, in a recent report, bcl-2 expression was shown to be lower in the stroma of precancerous fibroadenoma lesions than in those of non-cancerous lesions [8]. In their metaanalyses, Dawson et al. [6] supported the prognostic role of bcl-2 in breast cancer, as assessed by immunochemistry, and showed that this effect is independent of other variables.

The mechanisms through which bcl-2 might exert its protective effect in breast cancer are unclear. Thus, it has not been determined whether bcl-2 is involved directly in contributing to this more indolent phenotype or is simply an epiphenomenon that is a marker for another molecular or biologic process. The anti-apoptotic role of bcl-2 is well characterised but its function in cell cycle control has received less attention. Cell line studies have shown that bcl-2 exerts growth inhibitory effects by prolonging G0 and G1 progression [9], and it has been postulated that the dominance of one of these functions over another may depend on the cell type. Therefore, as bcl-2 does not promote cell proliferation, in the absence of additional genetic alteration, bcl-2 positive tumours tend to be relatively non-aggressive. Furthermore, it should be considered that other components of the apoptotic pathway might also play an important role. It is well recognized that apoptosis regulation is very complex and that bcl- 2 is only one member of a family of genes, each with different roles in the regulation of cell death. The mechanisms by which the interactions between the various members of the bcl-2 family finally lead to apoptosis are still unknown. On the other hand, it could be hypothesized that the favourable clinical outcome of patients with high bcl-2 expressing tumours could be better explained by a relationship between bcl-2 expression and differentiation than by the role played by the proto-oncogene in the apoptosis process. In this sense, the presence of bcl-2 immunostaining in normal tissue and its persistence in tumour tissue could indicate a predisposition to differentiation. However, in some series the expression of bcl-2 shows no statistical relationship with differentiation [5,10]. On the other hand, gene-transfer-mediated elevations in bcl-2 protein have been shown to protect tumour cells from cell death induced by radiation and a wide range of anticancer drugs in hematologic malignancies [11]. The down-regulation of bcl-2 during anti-oestrogen treatment would probably produce a favourable response to this therapy. However, significantly longer survival times, irrespective of the type of adjuvant therapy, have been reported [6]. Clearly, therefore, the prognostic power of bcl-2 as a single marker in breast cancer has been demonstrated, but the therapeutic implication of these findings and the question of how bcl-2 might improve the selection of patients for treatment remains to be determined. Accordingly, large-scale studies including clinical trials are needed to confirm its clinical utility.

References

Select your language of interest to view the total content in your interested language
Post your comment

Share This Article

Recommended Conferences

Article Usage

  • Total views: 11800
  • [From(publication date):
    February-2013 - Oct 21, 2017]
  • Breakdown by view type
  • HTML page views : 8026
  • PDF downloads :3774
 

Post your comment

captcha   Reload  Can't read the image? click here to refresh

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri, Food, Aqua and Veterinary Science Journals

Dr. Krish

[email protected]

1-702-714-7001 Extn: 9040

Clinical and Biochemistry Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Business & Management Journals

Ronald

[email protected]

1-702-714-7001Extn: 9042

Chemical Engineering and Chemistry Journals

Gabriel Shaw

[email protected]

1-702-714-7001 Extn: 9040

Earth & Environmental Sciences

Katie Wilson

[email protected]

1-702-714-7001Extn: 9042

Engineering Journals

James Franklin

[email protected]

1-702-714-7001Extn: 9042

General Science and Health care Journals

Andrea Jason

[email protected]

1-702-714-7001Extn: 9043

Genetics and Molecular Biology Journals

Anna Melissa

[email protected]

1-702-714-7001 Extn: 9006

Immunology & Microbiology Journals

David Gorantl

[email protected]

1-702-714-7001Extn: 9014

Informatics Journals

Stephanie Skinner

[email protected]

1-702-714-7001Extn: 9039

Material Sciences Journals

Rachle Green

[email protected]

1-702-714-7001Extn: 9039

Mathematics and Physics Journals

Jim Willison

[email protected]

1-702-714-7001 Extn: 9042

Medical Journals

Nimmi Anna

[email protected]

1-702-714-7001 Extn: 9038

Neuroscience & Psychology Journals

Nathan T

[email protected]

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

John Behannon

[email protected]

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

[email protected]

1-702-714-7001 Extn: 9042

 
© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version
adwords