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Discovering the causes of cancer and the means of prevention

Aimée R. Kreimer, Ph.D.

Senior Investigator

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Aimée R. Kreimer, Ph.D.

Aimée R. Kreimer, Ph.D.

Organization:National Cancer Institute
Division of Cancer Epidemiology & Genetics, Infections and Immunoepidemiology Branch
Address:NCI Shady Grove
Room 6E104


Dr. Kreimer received a Ph.D. in infectious disease epidemiology from the Johns Hopkins Bloomberg School of Public Health in 2003. She conducted postdoctoral research at the International Agency for Research on Cancer in Lyon, France and the National Cancer Institute, NIH. In 2008, she was appointed to the position of tenure-track investigator within the Infections and Immunoepidemiology Branch. She was awarded scientific tenure by the NIH in 2016. Dr. Kreimer focuses her research on the etiology and prevention of human papillomavirus (HPV) and cancers at multiple sites, including the head and neck and anogenital region. She has particular interests in translational research, cancer etiology related to the natural history of HPV infection at multiple anatomic sites, and cancer prevention.

Research Interests

Dr. Kreimer’s scientific interests lay in the evaluation of:

  • The performance of prophylactic HPV vaccine
  • Understanding the natural history of HPV infections at multiple anatomic sites; and,
  • HPV 16 E6 seropositivity as a possible biomarker for HPV-driven head and neck cancer

HPV type 16 (HPV 16) infection is one of the most important human carcinogens, causing ~300,000 cancer deaths per year worldwide, the majority of which are due to cervical cancer in low-income countries. It is well established that persistent infection with HPV 16, 18, or other carcinogenic HPV genotypes is the necessary, but not sufficient, cause of cervical cancer. Infection with HPV 16 is an established risk factor for some cancers at five additional anatomic sites, including cancers of the anus, oropharynx, vagina, vulva, and penis. Of note, whereas HPV 16 causes about 50% of cervical cancers, at other anatomic sites, it causes upwards of 90% of the non-cervical HPV-driven cancers.

The advent of the HPV prophylactic vaccine has the potential to dramatically reduce the burden of HPV-associated cancers. Despite this success, many important research questions remain. For example, how long will the vaccine protect at the cervix? How many doses are truly needed to provide robust protection? Since the vaccine should confer immunity on all mucosal surfaces where HPV causes cancer, does the HPV vaccine protect against infections at non-cervical anatomic sites where HPV causes cancer?

Dr. Kreimer is co-principal investigator of the Costa Rica HPV Vaccine Trial long-term follow-up study, a study that started as a randomized controlled trial of the bivalent HPV vaccine and has transitioned to an epidemiologic cohort study for the long-term follow-up. Using data from this study, Dr. Kreimer and colleagues demonstrated that that vaccine efficacy against incident persistent HPV 16/18 infection was comparably high among women who received three, two, or even a single dose of vaccine after four years of follow-up. They have also shown that the bivalent vaccine strongly protects against HPV infections at essentially all non-cervical anatomic sites where HPV causes cancer in a woman (i.e., the anus, vulva, and oral region), and that the level of protection was comparably high to that observed at the cervix among the same women. This study will continue to inform the research community as it will follow women for at least 10 years following the initial vaccination. 

Despite the great potential of HPV vaccination, the current birth cohorts (individuals in their 30s, 40s, 50s, etc.) will not experience the protection afforded by prophylactic HPV vaccines. Therefore, screening will remain an important tool in our fight against cancer for decades as these individuals age into cancer-susceptible phases of life. Thus, continued research into possible biomarkers of HPV-driven cancers is necessary. Dr. Kreimer and colleagues discovered that the HPV 16 E6 antibody marker predicts risk of HPV-driven cancer, in particular oropharyngeal cancer, years before cancer development.