Colleagues: Recently Tenured
AIMÉE KREIMER, PH.D., NCI-DCEG
Senior Investigator, Infections and Immunoepidemiology Branch, National Cancer Institute—Division of Cancer Epidemiology and Genetics
Education: University of Delaware, Newark, Del. (B.S. in animal science, biology; concentration in pre-veterinary medicine); University of Virginia, Charlottesville, Va. (M.S. in health evaluation sciences); Johns Hopkins Bloomberg School of Public Health, Baltimore (Ph.D. in infectious disease epidemiology)
Training: Postdoctoral research at the International Agency for Research on Cancer (Lyon, France) and in the NCI Cancer Prevention Fellowship Program
Came to NIH: First came to NIH in 2004 for postdoctoral training; in 2008 became tenure-track investigator
Selected professional activities: Adjunct associate professor, Otolaryngology, Head and Neck Surgery Department, Johns Hopkins (Baltimore); member of the HPV Vaccine Work Group, which advises the Advisory Committee on Immunization Practices, CDC
Outside interests: Spending time with her family (husband Brad; children Ben, Luca, and Kaya; and her mom and dad) and their two dogs (Peanut and Coco); cooking; dancing; walking and hiking outdoors
Research interests: My research focuses on the etiology and prevention of human papillomavirus (HPV) infection and associated cancers at multiple sites including the cervix, anogenital region, and oropharynx.
HPV is one of the most important human carcinogens, causing some 300,000 cancer deaths per year worldwide. Most of these deaths are due to cervical cancer and occur in low-income countries. The HPV prophylactic vaccines could dramatically reduce the burden of HPV-associated cancers. However, current global vaccination rates are insufficient to meaningfully affect the incidence of these cancers.
I am the co-principal investigator for the NCI Costa Rica HPV Vaccine Trial Long Term Follow-up Study. My colleagues and I have demonstrated that, after four years of follow-up, vaccine efficacy against persistent infection with HPV type 16 or 18 was comparably high among women who received three, two, or even a single dose of vaccine. Other studies are similarly suggesting that one dose of the HPV vaccine may be sufficient.
It would be a huge public-health breakthrough if one dose was enough; one-dose vaccination could dramatically lower the barriers to vaccination in the poorest world regions. My NCI colleagues and I are planning studies to follow up on this important discovery. Our goal is to document the minimum number of doses truly needed to induce durable protection against HPV infections.
In the United States, the HPV vaccine holds great promise for reducing HPV-caused cancers in the generation currently being vaccinated (girls ages 9–26; boys ages 9–21). But we will still experience decades’ worth of these cancers while we wait for vaccinated cohorts to age into the periods when HPV-related cancer is most likely to occur.
We are particularly concerned about the rising rates of oropharyngeal cancer (OPC) linked to HPV; median age at diagnosis is around 55 years. Although effective screening exists for cervical cancer, we have yet to establish an effective approach for the early detection and prevention of OPC. However, my colleagues and I discovered that the E6 antibody marker of HPV type 16 predicts the risk of HPV-driven cancer, especially OPC, years before the cancer develops. I am conducting additional research to determine whether screening for noncervical HPV-driven cancers is feasible and warranted.
KARIN E. PETERSON, PH.D., NIAID
Senior Investigator and Chief, Neuroimmunology Section, Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories (Hamilton, Mont.), National Institute of Allergy and Infectious Diseases
Education: University of Wisconsin–River Falls, River Falls, Wis. (B.S. in biotechnology); University of Missouri–School of Medicine, Columbia, Mo. (Ph.D. in molecular microbiology and immunology)
Training: Postdoctoral training in Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, NIAID
Before coming to NIH: Assistant professor, Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University (LSU; Baton Rouge, La.)
Came to NIH: In 1998 (through 2003) for training; in 2008 as a tenure-track investigator and chief of the Neuroimmunology Section in NIAID’s Rocky Mountain Laboratories
Selected professional activities: Academic editor, PLOS ONE; editorial board, Microbial Pathogenesis; adjunct or affiliate faculty member at LSU School of Veterinary Medicine and at the University of Montana
Outside interests: Bicycling; serving on the board of the Supporters of Abuse Free Environment (SAFE) domestic violence shelter; playing for the Hamilton Wild Things women’s football team; cross-country skiing
Research interests: Viral infection in the central nervous system (CNS) can lead to neuronal damage and the development of neurological diseases. My laboratory examines how the immune and nervous systems respond to virus infection and how these responses affect the development of neurological diseases. We use several animal models to examine viral infections in the CNS.
Our primary studies investigate LaCrosse Virus (LACV), which is the leading cause of arboviral encephalitis in children in the United States. LACV is transmitted by the bite of an infected mosquito, and most cases occur in the upper Midwestern, mid-Atlantic, and southeastern states. Many people infected with LACV show no symptoms or have very mild forms of the disease. However, severe neurological disease can occur after LACV infection, most often in children under the age of 16. Our lab studies how LACV gains access to the brain; how LACV induces damage to neurons in the brain; and the role of the immune response in these processes.
Our lab also studies other viruses that infect the CNS, including retroviruses, herpesvirus, and more recently, Zika virus. Through our work with these viruses, we have identified mechanisms of both neuronal damage and neuronal protection that are mediated by the immune system’s interactions with CNS cells. We are currently examining the regulation of these pathways and mechanisms in order to inhibit viral pathogenesis in the CNS. The ultimate goal of our research is to identify targets for therapeutic treatment of viral-mediated neurological diseases.
HARI SHROFF, PH.D., NIBIB
Senior Investigator and Chief, Section on High Resolution Optical Imaging, National Institute of Biomedical Imaging and Bioengineering
Education: University of Washington, Seattle (B.S.E. in bioengineering); University of California at Berkeley, Berkeley, Calif. (Ph.D. in biophysics)
Training: Postdoctoral research under the mentorship of Eric Betzig (awarded the 2014 Nobel Prize in Chemistry), Howard Hughes Medical Institute's Janelia Farm Research Campus (Ashburn, Va.)
Came to NIH: In 2009
Selected professional activities: Course director, Optical Microscopy in the Biomedical Sciences and taught both neurobiology and physiology courses at the Marine Biological Laboratory (Woods Hole, Mass.); directing the new trans-NIH Advanced Imaging/Microscopy (AIM) facility
Outside interests: Rock climbing; playing board games; hiking; and reading (currently reading an inspiring history of the Wright Brothers)
Research interests: My team develops optical-imaging tools to do real-time studies of three-dimensional (3-D) cellular and developmental processes. We aim to improve the performance of 3-D optical (especially fluorescence) imaging microscopes in resolution, depth, speed, and phototoxicity.
To address resolution and depth, we developed multifocal structured illumination microscopy (MSIM), a version of structured illumination microscopy (SIM). SIM techniques use patterned excitation light and post-processing to double the resolution of a conventional microscope. Unlike other super-resolution techniques, SIM provides resolution enhancement at a relatively low illumination dose. With newer implementations of MSIM, we can image specimens even faster (at hundreds of frames per second) and at even greater depths (more than 200 micrometers from the coverslip surface).
To improve the speed and reduce the phototoxicity associated with live 3-D imaging, we developed an implementation of selective plane illumination microscopy (SPIM). SPIM techniques combine a perpendicular excitation/detection geometry with light-sheet excitation, drastically reducing photobleaching and damage while providing higher signal-to-noise ratio and acquisition rates than confocal microscopy. SPIM has been difficult to use, however, because the geometry is cumbersome, and samples must be prepared in a special way.
So we developed a user-friendly module—inverted selective plane illumination microscopy (iSPIM). The module retains the advantages of SPIM, but can be attached to an epifluorescence microscope, and samples can be conventionally mounted on glass coverslips. More recently, we have improved the resolution of iSPIM by adding a second specimen view (dual-view iSPIM, diSPIM), thereby enabling imaging with isotropic spatial resolution (down to 330 nanometers). Further improvements in spatial resolution are imminent.
We are also working with extramural neuroscientists, scientists, and developmental biologists to understand how a nervous system develops. Using diSPIM to follow all neurons in the developing nematode embryo, we intend to create the first digital atlas of neurodevelopment.
In addition, I am creating a trans-NIH advanced imaging and microscopy (AIM) facility where our precommercial custom-built systems can be made available to the rest of the NIH. Please get in touch with me if you have an imaging challenge or would like to use the facility. We collaborate closely with intra- and extramural researchers (both academic and commercial) to ensure that our microscopes can be both easily and widely used.
LI YANG, PH.D., NCI-CCR
Senior Investigator and Head, Tumor Microenvironment Section, Laboratory of Cancer Biology and Genetics, National Cancer Institute–Center for Cancer Research
Education: Sichuan University, Chengdu, China (B.S. in biology); Wuhan University, Wuhan, China (M.S. in developmental biology and cell biology); Vanderbilt University School of Medicine, Nashville (Ph.D. in cancer biology)
Training: Postdoctoral training at Department of Medicine and Department of Cancer Biology, Vanderbilt University School of Medicine
Before coming to NIH: Research assistant professor, Department of Medicine and Department of Cancer Biology, Vanderbilt University School of Medicine
Came to NIH: In 2009 as principal investigator in Laboratory of Cancer Biology and Genetics, NCI-CCR
Selected professional activities: Ad hoc reviewer for several journals; editorial board, PLOS ONE and International Journal of Biological Sciences; visiting professor, North Sichuan Medical College (Nanchong, China)
Outside interests: Gardening; hiking; traveling
Research interests: Tumor metastases account for most cancer-associated deaths. Unfortunately, there are few effective treatment options. My group uses molecular and genetic approaches in mouse models to study the complex molecular programs that govern the inflammatory tumor microenvironment in the progression of tumor metastases. We mainly focus on two areas of research: the identification of the metastasis-promoting mediator of transforming growth factor–beta (TGF-beta); and inflammation, tumor progression, and metastases.
In our first area of research, we have been tackling a longstanding challenge in cancer biology: understanding how TGF-beta, which is overexpressed in advanced human cancers, switches from a tumor suppressor to a tumor promoter. We discovered that the loss of TGF-beta signaling in epithelial cells induces inflammation and the recruitment of myeloid (bone marrow) cells into the tumor microenvironment. Myeloid TGF-beta signaling is an essential component of the metastasis-promoting activity of TGF-beta.
This observation, however, is in stark contrast to previously reported tumor-suppressing roles of TGF-beta in fibroblasts and epithelial cells. In these types of cells, the deletion of Tgfbr2, the gene for TGF-beta receptor–2—or of genes for the downstream mediators of TGF-beta signaling—accelerates tumor progression. We were the first to discover that tumor suppressors possess a novel anti-inflammatory function. Our findings may contribute to the development of novel treatments for metastasized cancer.
In our second area of research, we demonstrated that cancer-associated inflammation mediates the epigenetic silencing of the kinase inhibitor p21 in tumor progression. We also highlighted the underlying molecular mechanisms of epithelial cancer that are due to alterations in stromal cells. We are now investigating how the inflammation in the tumor microenvironment reprograms metastatic cancer cells through DNA methylation, histone modifications, microRNA expression, and other epigenetic mechanisms. These inflammation-induced epigenetic alterations may enhance genomic instability and genomic heterogeneity and thus allow for the emergence of metastatic malignant cell variants. Our studies will provide insight into the mechanisms of tumor heterogeneity and drug resistance, one of the greatest obstacles in cancer treatment.
This page was last updated on Monday, April 11, 2022