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Elena Levantini, PhD

Instructor, Department of Medicine, Harvard Medical School

Research Associate, Hematology-Oncology, Beth Israel Deaconess Medical Center

Contact Info

Elena Levantini
Beth Israel Deaconess Medical Center
CLS 428

Boston, MA, 02115
Phone: 617-735-2233
Fax: 617-735-2222
elevanti@bidmc.harvard.edu

Assistant

Ann Zhang
Administrative Assistant
Hen/Onc
Beth Israel Deaconess Medical Center
CLS 448
3 Blackfan Circle
Boston, MA, 02115
Phone: 617-735-2861
Fax: 617-735-2233
nzhang1@bidmc.harvard.edu

DF/HCC Program Affiliation

Lung Cancer

Research Abstract

Lung cancer is the principal cause of cancer mortality in the world, and its frequency is increasing. Hence, improved therapeutic options are imperative. There is a strong correlation between tobacco exposure and lung carcinogenesis, and the best protection against lung cancer is the avoidance of smoking. Advances in lung cancer therapy require a greater understanding of the molecular pathogenesis of this disease. Previously, we showed that the leucine zipper family transcription factor CCAAT/enhancer binding protein alpha (C/EBPα), a proposed tumor suppressor in acute myeloid leukemia (AML), is down-regulated in non-small cell lung cancer. Furthermore, ectopic expression of C/EBPα in the lung cancer cell lines led to significant growth reduction attributable to proliferation arrest, morphological changes characteristic of differentiation, and apoptosis. Additionally, mice with specific conditional loss of C/EBPα in the lung showed symptoms of respiratory distress accompanied by perinatal death, therefore hinting to potential therapeutical benefits that might be obtained by exploring the C/EBPα pathway in patients with respiratory distress syndrome. Based on these observations, we are exploring the effects of C/EBPα down-regulation in experimental models of lung cancer and tobacco-damaged epithelium, using our inducible models of lung-specific C/EBPα deletion. We are also analyzing the differentiation and self-renewal capabilities of C/EBPα-deleted pulmonary stem cells, in order to gain knowledge on the molecular mechanisms that C/EBPα is orchestrating in lung stem cells.
Characterization of critical regulatory mechanisms governed by the master regulator C/EBPα as well as the aberrant differentiation pathways in C/EBPα-deleted pulmonary stem cells would be of critical relevance for our better understanding the pathogenesis of as well as the identification of novel treatment targets for tobacco-related lung diseases, such as lung cancer and emphysema.

Publications

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