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2012 ibc online -
Louis School of Medicine, St. Alejandro A Gru: ude. Abstract The incidence of invasive breast cancer IBC can be dramatically reduced by improving our abilities to detect and treat ductal carcinoma in situ DCIS. Progress will be based on a detailed understanding of molecular mechanisms responsible for tumor progression. These observations indeed provide hints that FGFR1 is important in this setting, although the issue is very complex and far from resolved.
Invasive breast cancer IBC evolves through a series of increasingly abnormal premalignant stages, over decades in most cases [ 1 , 2 ]. If undetected, at least one-third of cases will progress to IBC [ 4 ]. The incidence of IBC can be dramatically reduced by improving our abilities to detect and successfully treat DCIS, which will be based on a detailed understanding of molecular mechanisms responsible for tumor progression. Although there is much to learn, recent studies have begun to shed light on this important issue [ 5 , 6 ].
Overall, they found reasonable rates of amplification for each oncogene in IBC consistent with many previous studies [ 7 ]. Far fewer studies of DCIS are available for comparison. The main focus of the study was to compare amplification between pure DCIS and IBC, hypothesizing that differences may help identify genes that are important in the transition from in situ to invasive disease. Amplification frequencies in intrinsic molecular subtypes of IBC were also generally consistent with previous studies [ 7 ].
Jang and colleagues also looked at the relationship between amplification and clinical outcome. The twofold elevation of FGFR1 amplification in IBC versus pure DCIS, and the poor prognosis in IBC, led the authors to conclude that activation plays an important role in the progression of breast cancer, including, in particular, the in situ to invasive transition.
This is a reasonable conclusion in the sense that it is also consistent with previous studies showing that FGFR1 activation is oncogenic for breast cancer in transgenic mice [ 9 ], and is associated with increased invasion of breast cancer cell lines in vitro [ 10 ] and poor prognosis in IBC [ 7 , 11 , 12 ], especially in receptor-positive disease [ 11 , 12 ].
Although our understanding of FGFR1 at the molecular level is incomplete, important aspects are known about its function and the consequences of gene amplification [ 13 ]. For example, the gene encodes a tyrosine kinase receptor that is part of a large family of fibroblast growth factors and receptors.
In a normal setting, activation of FGFR1 can lead to transactivation of mitogen-activated protein kinase and AKT, which collectively are essential for breast development, including the growth and differentiation of luminal epithelial cells. However, increased FGFR1 activity, such as occurs through gene amplification, can result in increased luminal cell proliferation and, in transgenic mouse models, this hyperplasia may eventually evolve into in situ and invasive mammary carcinomas.
In humans, the chromosomal region where FGFR1 resides, 8p However, the 8p The study also provides tantalizing hints that FGFR1 may be important in the in situ to invasive transition, which is a critical step in the progression of a nonlethal to potentially lethal disease - and this aspect of the study is entirely novel. Having said this, we need to be cautious about drawing conclusions regarding gene function and malfunction based on correlative studies of this nature alone.
Determining the molecular function, oncogenic potential, and clinical significance of FGFR1 at any stage of breast cancer evolution will require many additional comprehensive laboratory and clinical studies. These studies are particularly worthwhile in the sense that we have effective drugs to inhibit FGFR1 activity [ 13 ]. Jain and Turner have summarized recent interesting data in terms of the functional biology of the fibroblast growth factor receptors and development of inhibitors of these molecules, with emphasis on challenges to successfully target this pathway in breast cancer [ 16 ].
Competing interests The authors declare that they have no competing interests. Notes See related research by Jang et al. FGFR1 is amplified during the progression of in situ to invasive breast carcinoma. Breast Cancer Res. In: Diseases of the Breast. New York: Lippincott Williams and Wilkins; Biological features of human premalignant breast disease and the progression to cancer; pp. Breast Cancer Facts and Figures. J Natl Cancer Inst. Breast cancer: origins and evolution.
J Clin Invest. Differentially expressed genes regulating the progression of ductal carcinoma in situ to invasive breast cancer. Cancer Res. Frequency, prognostic impact, and subtype association of 8p12, 8q24, 11q13, 12p13, 17q12, and 20q13 amplifications in breast cancers. BMC Cancer. Mod Pathol. Inducible dimerization of FGFR1: development of a mouse model to analyze progressive transformation of the mammary gland. J Cell Biol.
Pleiotropic effects of FGFR1 on cell proliferation, survival, and migration in a 3D mammary epithelial cell model. FGFR1 amplification in breast carcinomas: a chromogenic in situ hybridisation analysis. FGFR1 amplification drives endocrine therapy resistance and is a therapeutic target in breast cancer. Fibroblast growth factors in development and cancer: insights from the mammary and prostate glands.
Curr Drug Targets. Comprehensive profiling of 8p amplification in breast cancer. Mol Cancer Res. Amplification of FGFR1 gene and its relationship with gene expression and clinical significance in breast cancer. Modern Pathol. Challenges and opportunities in the targeting of fibroblast growth factor receptors in breast cancer.
: 2012 ibc online
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