2005 Gilliam Fellows
IMRAN BABAR
As a child, Imran Babar saw science unfolding every day on his family’s Minnesota farm as he grew vegetables and raised sheep. When he wasn’t working on the farm, he fashioned spare machine parts into toys. In school, that penchant for hands-on tinkering led Babar into the biology labs, where he found his calling.

article online:
http://www.hhmi.org/news/babar.html
Imran Babar
Yale University
New Haven, Connecticut
Research Field: Developmental Biology
Photo: Amenah Babar
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"The more I learned, the more I wanted to know," says Babar, 23, the son of a Pakistani father and a Native American mother. As an undergraduate at Carleton College in Northfield, Minnesota, he found himself especially fascinated by basic cell and molecular biology. A devout Christian, Babar also led a nondenominational Bible study group and played in a campus “praise band.”
During his junior year, Babar won a spot in HHMI’s Exceptional Research Opportunities Program (EXROP), which offers summer research experiences for disadvantaged and minority undergraduates in the labs of HHMI investigators or HHMI professors. He spent his EXROP summer doing research in the lab of HHMI investigator Tyler Jacks, a geneticist at the Massachusetts Institute of Technology (MIT) who studies cancer development.
Babar worked on a project to unravel the role of stem cells in tumor formation. He helped isolate a cell type found in the lung tissue of mice that may be an adult lung stem cell. The research has been accepted for publication in the journal Cell.
“I learned so much through EXROP — how to approach scientific questions, organize projects, collaborate, and more,” says Babar. Perhaps most important, he learned to feel more self-confident. “One of the greatest lessons was that I can be successful in science even in the highest-caliber settings,” Babar remarks. Indeed, Jacks notes that Babar is comfortable not only at the lab bench, but also before a crowd, explaining his experiments and results in formal presentations.
It’s a skill that will serve him well this fall, as he enters Ph.D. studies in the Department of Molecular, Cellular and Developmental Biology at Yale University. Babar says he chose the program for its 30 faculty members’ broad range of research. He also likes the environment at Yale. “The people are friendly and personable, intense and excited,” he says. “I can see myself fitting right in.”
IMRAN's cell article (work at MIT)
Identification of Bronchioalveolar Stem Cells in Normal Lung and Lung Cancer
Carla F. Bender Kim1, Erica L. Jackson1, 3, Amber E. Woolfenden1, 2, Sharon Lawrence1, Imran Babar2, Sinae Vogel1, Denise Crowley1, Roderick T. Bronson4 and Tyler Jacks1, 2, ,
1Center for Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139
2Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139
Received 30 June 2004; revised 22 December 2004; accepted 31 March 2005. Published: June 16, 2005. Available online 16 June 2005.
Summary
Injury models have suggested that the lung contains anatomically and functionally distinct epithelial stem cell populations. We have isolated such a regional pulmonary stem cell population, termed bronchioalveolar stem cells (BASCs). Identified at the bronchioalveolar duct junction, BASCs were resistant to bronchiolar and alveolar damage and proliferated during epithelial cell renewal in vivo. BASCs exhibited self-renewal and were multipotent in clonal assays, highlighting their stem cell properties. Furthermore, BASCs expanded in response to oncogenic K-ras in culture and in precursors of lung tumors in vivo. These data support the hypothesis that BASCs are a stem cell population that maintains the bronchiolar Clara cells and alveolar cells of the distal lung and that their transformed counterparts give rise to adenocarcinoma. Although bronchiolar cells and alveolar cells are proposed to be the precursor cells of adenocarcinoma, this work points to BASCs as the putative cells of origin for this subtype of lung cancer.
Imran's PNAS article abstract:
MICROBIOLOGY
Longitudinal analysis of the group A Streptococcus transcriptome in experimental pharyngitis in cynomolgus macaques
Kimmo Virtaneva * , Stephen F. Porcella * , Morag R. Graham * , Robin M. Ireland *, Claire A. Johnson *, Stacy M. Ricklefs *, IMRAN BABAR!!!*, Larye D. Parkins *, Romina A. Romero * , G. Judson Corn *, Don J. Gardner ¶, John R. Bailey ¶, Michael J. Parnell ¶ and James M. Musser *, ||, **
*Laboratory of Human Bacterial Pathogenesis and ¶Veterinary Branch, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840; and ||Center for Human Bacterial Pathogenesis Research, Department of Pathology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030
Communicated by Richard M. Krause, National Institutes of Health, Bethesda, MD, May 10, 2005 (received for review March 3, 2005)
Identification of the genetic events that contribute to host–pathogen interactions is important for understanding the natural history of infectious diseases and developing therapeutics. Transcriptome studies conducted on pathogens have been central to this goal in recent years. However, most of these investigations have focused on specific end points or disease phases, rather than analysis of the entire time course of infection. To gain a more complete understanding of how bacterial gene expression changes over time in a primate host, the transcriptome of group A Streptococcus (GAS) was analyzed during an 86-day infection protocol in 20 cynomolgus macaques with experimental pharyngitis. The study used 260 custom Affymetrix (Santa Clara, CA) chips, and data were confirmed by TaqMan analysis. Colonization, acute, and asymptomatic phases of disease were identified. Successful colonization and severe inflammation were significantly correlated with an early onset of superantigen gene expression. The differential expression of two-component regulators covR and spy0680 (M1_spy0874) was significantly associated with GAS colony-forming units, inflammation, and phases of disease. Prophage virulence gene expression and prophage induction occurred predominantly during high pathogen cell densities and acute inflammation. We discovered that temporal changes in the GAS transcriptome were integrally linked to the phase of clinical disease and host-defense response. Knowledge of the gene expression patterns characterizing each phase of pathogen–host interaction provides avenues for targeted investigation of proven and putative virulence factors and genes of unknown function and will assist vaccine research.