Jerome S. Brody, MD
Emeritus Professor
Boston University School of Medicine
Dept of Medicine
Pulmonary, Allergy, Sleep & Critical Care Medicine Section

MD, University of Illinois Urbana-Champaign



Research special interests include:
-Genomics of smoking-related lung diseases
-Lung cancer diagnostic/prognostic tools
-Genomics and the pathogenesis of COPD
-Developmental biology of the lung
-Relation of lung cancer to lung development

Cigarette smoking is the major cause of the two most costly and lethal pulmonary diseases, lung cancer and COPD. However, only 10-20% of smokers develop lung cancer; an equal number develop COPD. Thus, the majority of smokers develop neither disease. Our laboratory is using a variety of genomic tools to determine: 1) how the lung protects itself from the toxic effects of cigarette smoke; 2) why some smokers develop COPD and/or lung cancer while others are disease-free; 3) how we can use these new tools to define molecular pathways leading to each disease; 4) develop tests for the early diagnosis of lung cancer and for assessing a smokers’ risk of developing lung cancer; 5) and develop new approaches to therapy.

Our growing knowledge of the human genome and of the mechanisms regulating the transcription and translation of human genes coupled with the statistical and computational sciences that form the basis of bioinformatics provides an opportunity to develop new insights into the biologic and molecular processes associated with cigarette smoke-related lung disease.

Our present studies are based on the premise that smoking affects all of the epithelial cells of the respiratory tract and that measuring expression levels and mechanisms of regulating the levels of most of the genes in the human genome in easily accessible airway epithelial cells will provide new diagnostic and risk- assessment tools for the lung cancer as well as information about pathways leading to disease that might identify new pharmacologic targets for treating and preventing lung cancer and COPD. Most of our studies have utilized airway epithelial cells obtained by brushing a major bronchus during bronchoscopy. However, we are in the process of determining whether the airway field of smoking-induced injury extends to more accessible airway epithelial cells in the mouth or nose.

Our data shows the surprising power of this approach. It shows the relative expression levels of over 600 genes that are affected by smoking (current and past) and by the presence of lung cancer. While smoking affects gene expression in airway epithelial cells, there clearly are genes that signal the presence of lung cancer, independent of the current smoking status of the subject.

Our data demonstrates the potential value of the gene expression class prediction model we have built. Relying on bronchoscopy alone we are able to diagnose about 50% of lung cancers. Our class prediction model correctly diagnoses lung cancer 78% of the time. The combination of bronchoscopy and gene expression correctly diagnoses lung cancer 98% of the time. Class prediction in contrast to bronchoscopy, is particularly accurate (>95%) in diagnosing Stage I and II disease.

Preliminary studies of airway epithelial cell gene expression in smokers with COPD suggest that these cells reflect a different type of injury in smokers with COPD than is the case with lung cancer. In COPD, genes associated with inflammation predominate and genes associated with oxidant stress and NF?B pathways are altered.

Our interest in cancer intersects with a long-standing interest in lung development. This is based on the concept that the very processes that are involved in controlling lung cell proliferation and differentiation during development are deregulated in lung cancer. Thus information about the mechanisms regulating lung development may provide insights into pathogenesis and treatment of lung cancer.

Graduate Faculty (Primary Mentor of Grad Students)
Boston University School of Medicine, Division of Graduate Medical Sciences


Boston Medical Center




Tobacco, Cancer and Epithelial Gene Expression
07/01/2003 - 06/30/2007 (Co-PI)
Doris Duke Charitable Foundation

Metastatic Progression of Breast Cancer by Allelic Loss on Chromosome 18q21
09/01/2001 - 08/31/2005 (Co-PI)
PI: Sam Thiagalingam, PhD
Department of Defense/Army

Genetic Determinants of Epithelial DNA Damage in Smokers
09/30/2001 - 06/30/2005 (Co-PI)
NIH/National Institute of Environmental Health Sciences
1 R01 ES10377 01A2

Airway Epithelial Expression in COPD
09/30/2002 - 08/31/2004 (PI)
NIH/National Heart, Lung, and Blood Institute
5 R01 HL71771 02

Cigarette Smoke and Mouse Models of Human Lung Cancer
09/30/1999 - 03/31/2001 (PI)
Massachusetts Institute of Technology NIH NCI


Microsensor Arrays for Salivary Diagnostics
09/01/2006 - 02/28/2013 (PI)
Tufts University NIH-NIDCR



Yr Title Project-Sub Proj Pubs
2009 Field of Injury Based Biomarkers for Lung Cancer 1R44CA139803-01A1
2003 Airway Epithelial Gene Expression in COPD 5R01HL071771-02 4
2002 Airway Epithelial Gene Expression in COPD 1R01HL071771-01 4
2001 POCKET PROTEIN/E2F REGULATES LUNG CELL DIFFERENTIATION 5P01HL047049-10-4 86
2001 REGULATION OF ALVEOLAR EPITHELIAL CELL DIFFERENTIATION 5P01HL047049-10 86
2000 POCKET PROTEIN/E2F REGULATES LUNG CELL DIFFERENTIATION 5P01HL047049-09-4 86
2000 REGULATION OF ALVEOLAR EPITHELIAL CELL DIFFERENTIATION 5P01HL047049-09 86
2000 BIOLOGY OF THE LUNG: A MULTIDISCIPLINARY PROGRAM 5T32HL007035-25 53
1999 POCKET PROTEIN/E2F REGULATES LUNG CELL DIFFERENTIATION 5P01HL047049-08-4 86
1999 REGULATION OF ALVEOLAR EPITHELIAL CELL DIFFERENTIATION 5P01HL047049-08 86
Showing 10 of 46 results. Show All Results
Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.

  1. Silvestri GA, Vachani A, Whitney D, Elashoff M, Porta Smith K, Ferguson JS, Parsons E, Mitra N, Brody J, Lenburg ME, Spira A. A Bronchial Genomic Classifier for the Diagnostic Evaluation of Lung Cancer. N Engl J Med. 2015 Jul 16; 373(3):243-51.View Related Profiles. PMID: 25981554; DOI: 10.1056/NEJMoa1504601;.
  2. Whitney DH, Elashoff MR, Porta-Smith K, Gower AC, Vachani A, Ferguson JS, Silvestri GA, Brody JS, Lenburg ME, Spira A. Derivation of a bronchial genomic classifier for lung cancer in a prospective study of patients undergoing diagnostic bronchoscopy. BMC Med Genomics. 2015; 8:18.View Related Profiles. PMID: 25944280; PMCID: PMC4434538; DOI: 10.1186/s12920-015-0091-3;.
  3. Kathuria H, Gesthalter Y, Spira A, Brody JS, Steiling K. Updates and controversies in the rapidly evolving field of lung cancer screening, early detection, and chemoprevention. Cancers (Basel). 2014; 6(2):1157-79.View Related Profiles. PMID: 24840047; DOI: 10.3390/cancers6021157;.
  4. Senior RM, Brody JS, Williams MC. The Red journal at 25. A perspective from the founding editors. Am J Respir Cell Mol Biol. 2014 May; 50(5):840-1. PMID: 24783953; DOI: 10.1165/rcmb.2014-0105ED;.
  5. Brody JS. The promise and problems of e-cigarettes. Am J Respir Crit Care Med. 2014 Feb 15; 189(4):379-80. PMID: 24528311; DOI: 10.1164/rccm.201312-2263ED;.
  6. Brody JS. Transcriptome alterations induced by cigarette smoke. Int J Cancer. 2012 Dec 15; 131(12):2754-62. PMID: 22961494; DOI: 10.1002/ijc.27829;.
  7. Brody JS, Steiling K. Interaction of cigarette exposure and airway epithelial cell gene expression. Annu Rev Physiol. 2011; 73:437-56.View Related Profiles. PMID: 21090967; DOI: 10.1146/annurev-physiol-012110-142219;.
  8. Gustafson AM, Soldi R, Anderlind C, Scholand MB, Qian J, Zhang X, Cooper K, Walker D, McWilliams A, Liu G, Szabo E, Brody J, Massion PP, Lenburg ME, Lam S, Bild AH, Spira A. Airway PI3K pathway activation is an early and reversible event in lung cancer development. Sci Transl Med. 2010 Apr 7; 2(26):26ra25.View Related Profiles. PMID: 20375364; PMCID: PMC3694402; DOI: 10.1126/scitranslmed.3000251;.
  9. Steiling K, Kadar AY, Bergerat A, Flanigon J, Sridhar S, Shah V, Ahmad QR, Brody JS, Lenburg ME, Steffen M, Spira A. Comparison of proteomic and transcriptomic profiles in the bronchial airway epithelium of current and never smokers. PLoS One. 2009; 4(4):e5043.View Related Profiles. PMID: 19357784; PMCID: PMC2664466; DOI: 10.1371/journal.pone.0005043;.
  10. Schembri F, Sridhar S, Perdomo C, Gustafson AM, Zhang X, Ergun A, Lu J, Liu G, Zhang X, Bowers J, Vaziri C, Ott K, Sensinger K, Collins JJ, Brody JS, Getts R, Lenburg ME, Spira A. MicroRNAs as modulators of smoking-induced gene expression changes in human airway epithelium. Proc Natl Acad Sci U S A. 2009 Feb 17; 106(7):2319-24.View Related Profiles. PMID: 19168627; PMCID: PMC2650144; DOI: 10.1073/pnas.0806383106;.
Showing 10 of 93 results. Show More

This graph shows the total number of publications by year, by first, middle/unknown, or last author.

Bar chart showing 64 publications over 29 distinct years, with a maximum of 5 publications in 1988 and 1990 and 1995

YearPublications
19811
19821
19841
19852
19872
19885
19894
19905
19923
19941
19955
19963
19971
19981
19992
20011
20021
20034
20044
20051
20061
20073
20082
20092
20101
20111
20121
20143
20152
In addition to these self-described keywords below, a list of MeSH based concepts is available here.

lung development
lung genomics
smoking and lung cancer
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72 E. Concord St Housman (R)
Boston MA 02118
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