Gene Expression 15(3) Abstracts

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Gene Expression, Vol. 15, pp. 105–115, 2011
1052-2166/10 $90.00 + .00
DOI: http://dx.doi.org/10.3727/105221611X13176664479241
E-ISSN 1555-3884
Copyright © 2011 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Gene Expression Profiling: Changing Face of Breast Cancer Classification and Management

Robert Wesolowski and Bhuvaneswari Ramaswamy

Division of Medical Oncology, College of Medicine, The Ohio State University, Columbus, OH, USA

Epithelial breast malignancies are a group of several disease entities that vary in their biology and response to specific therapies. Historically, classification of different molecular types of breast cancer was done through the use of conventional methods such as tumor morphology, grade, and immunophenotyping for estrogen, progesterone, and HER-2/neu receptor expression. Such techniques, although helpful, are not sufficient to accurately predict biologic behavior of breast cancers. Over the last several years, much progress has been made in more precise identification of molecular breast cancer subtypes. Such advances hold a great promise in improving estimation of prognosis and assigning most appropriate therapies. Thanks to use of cDNA microarrays expression echnology and quantitative reverse transcriptase polymerase chain reaction (RT-PCR), tumors with specific gene expression patterns can now be identified. This process is presently reshaping perceptions of how breast cancer should be classified and treated. Categorization of breast cancers by gene expression is only beginning to make its way into the daily clinical practice and likely will complement, but not replace, the conventional methods of classification.

Key words: Breast cancer; Classification; Gene expression profiling; Biologic behavior; Breast cancer subtypes

Address correspondence to Bhuvaneswari Ramaswamy, M.D., Division of Medical Oncology, The Ohio State University, B406 Starling Loving Hall, 320 West 10th Ave., Columbus, OH 43210, USA. Tel: (614) 293-9453; Fax: (614) 293-4372; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Gene Expression, Vol. 15, pp. 117–132, 2011
1052-2166/10 $90.00 + .00
DOI: http://dx.doi.org/10.3727/105221611X13176664479322
E-ISSN 1555-3884
Copyright © 2011 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Role of TGF-b and the Tumor Microenvironment During Mammary Tumorigenesis

Molly A. Taylor, 1Yong-Hun Lee, 1and William P. Schiemann

Case Comprehensive Cancer Center, Division of General Medical Sciences-Oncology, Case Western Reserve University, Cleveland, OH, USA

Transforming growth factor-b (TGF-b) is a multifunctional cytokine that functions to inhibit mammary tumorigenesis by directly inducing mammary epithelial cells (MECs) to undergo cell cycle arrest or apoptosis, and to secrete a variety of cytokines, growth factors, and extracellular matrix proteins that maintain cell and tissue homeostasis. Genetic and epigenetic events that transpire during mammary tumorigenesis typically inactivate the tumor suppressing activities of TGF-b and ultimately confer this cytokine with tumor promoting activities, including the ability to stimulate breast cancer invasion, metastasis, angiogenesis, and evasion from the immune system. This dramatic conversion in TGF-b function is known as the “TGF-b paradox” and reflects a variety of dynamic alterations that occur not only within the developing mammary carcinoma, but also within the cellular and structural composition of its accompanying tumor microenvironment. Recent studies have begun to elucidate the critical importance of mammary tumor microenvironments in manifesting the TGF-b paradox and influencing the response of developing mammary carcinomas to TGF-b. Here we highlight recent findings demonstrating the essential function of tumor microenvironments in regulating the oncogenic activities of TGF-b and its stimulation of metastatic progression during mammary tumorigenesis.

Key words: Mammary tumorigenesis; Metastasis; Microenvironment; Transforming growth factor-b (TGF-b)

1These authors provided equal contribution to this work.
Address correspondence to William P. Schiemann, Case Comprehensive Cancer Center, Case Western Reserve University, Wolstein Research Building, 2103 Cornell Road Cleveland, OH 44106, USA. Tel: 216-844-8797; Fax: 216-844-7832; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Gene Expression, Vol. 15, pp. 133–140, 2011
1052-2166/10 $90.00 + .00
DOI: http://dx.doi.org/10.3727/105221611X13176664479368
E-ISSN 1555-3884
Copyright © 2011 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Role of Epithelial Stem/Progenitor Cells in Mammary Cancer

Robert D. Bruno and Gilbert H. Smith

Mammary Biology and Tumorigenesis Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA

Both mouse and human mammary glands contain stem/progenitor functional hierarchies that are maintained through the entire life span of the animal. Cells with such functional capacities are potential candidates for tumorigenesis as they are long lived, multipotent, and self-renewing. Using the mouse as a model, this review will discuss what is known about the mammary stem/progenitor hierarchy, the evidence that particular progenitor functions are susceptible to tumorigenic stimuli, how these findings in mice are relevant to the disease in humans, and the role of the local microenvironment in controlling tumorigenesis.

Key words: Breast cancer; Mammary biology; Stem cells; Progenitor cells; Tumorigenesis

Address correspondence to Gilbert H. Smith, National Institutes of Health, Bldg. 37, Room 1112B, 37 Convent Drive, Bethesda, MD 20892, USA. Tel: 301-496-2385; Fax: 301-480-1790; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Gene Expression, Vol. 15, pp. 141–151, 2011
1052-2166/10 $90.00 + .00
DOI: http://dx.doi.org/10.3727/105221611X13176664479287
E-ISSN 1555-3884
Copyright © 2011 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Emerging Role of MicroRNAs in Drug-Resistant Breast Cancer

Sarmila Majumder and Samson T. Jacob

Department of Molecular and Cellular Biochemistry, College of Medicine, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA

Intrinsic or acquired resistance to commonly used therapeutic agents is a major challenge in treating cancer patients. Decades of research have unraveled several unique and common mechanisms that could contribute to drug resistance in breast cancer. Recent studies unraveled the regulatory role of small noncoding RNA, designated as microRNA (miRNA), that were thought to be “junk” RNA in the past. Practically all aspects of cell physiology under normal and disease conditions were found to be regulated by miRNAs. In this review, we will discuss how miRNA profile is altered upon resistance development and the critical regulatory role miRNAs play in conferring resistance to commonly used therapeutic agents. It is hoped that further studies will lead to use of these differentially expressed miRNAs as prognostic and predictive markers, as well as novel therapeutic targets to overcome resistance.

Key words: Breast cancer; Drug resistance; MicroRNAs

Address correspondence to Sarmila Majumder, Department of Molecular and Cellular Biochemistry, College of Medicine, Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA. Tel: 614-292-0103; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it