February 2009 CEBP Highlights

Cervical cancer is a preventable disease caused in part by persistent infection with human papilloma virus (HPV). Vaccines against HPV represent extremely effective tools in the prevention of cervical cancer. In light of the recent Food and Drug Administration approval of HPV vaccines, Hughes and colleagues re-evaluated HPV awareness and knowledge in caregivers of adolescents living in southeastern North Carolina. Through telephone interviews, Hughes and colleagues determined that most caregivers were indeed aware and knowledgeable of both HPV and the HPV vaccine. However, fewer African American caregivers (68%) had knowledge of the vaccine compared to White caregivers (87%). Most caregivers preferred to learn more about HPV and the HPV vaccine through health care professionals and the internet. These findings indicate that disparities exist in knowledge of HPV vaccines, but that information regarding cervical cancer prevention can be disseminated and absorbed by caregivers. In addition, these studies reinforce the importance of primary care doctors, nurses, and medical web sites for further informing the public about cervical cancer prevention.

Over 25% of stage II colorectal cancer patients develop recurrent cancer and ultimately die of their disease. The identification of biomarkers that could accurately predict disease progression and possibly serve as therapeutic targets would be of great clinical benefit. Kevans and colleagues used immunohistochemical staining to examine the use of clusterin as a biomarker in a cohort of 251 stage II colorectal cancer patients. They found that within the epithelial component of these tumors, cytoplasmic clusterin staining was higher in tumor samples compared with normal tissue. In the stroma, cytoplasmic clusterin staining was lower in tumor compared to normal tissue. Furthermore, Kevans and colleagues report that survival was significantly associated with clusterin staining intensity. These results support the potential utility of clusterin as a prognostic biomarker for stage II colorectal cancer.

Number of nevi are a risk factor of melanoma and the majority of nevi develop during childhood. Many studies have established a positive association between nevi and the number of waterside vacations. However, these studies were conducted on European populations whose sun exposure patterns are likely far different than US residents. Pettijohn and colleagues examined the association between nevi found on Colorado youth born in 1998 and the number of waterside vacations. Similar to the European studies, a positive association between nevi and the number of waterside vacations was identified in Colorado youth. This association was only evident for waterside vacations that occurred more than a year before skin examination, indicating a lag time in the development of new nevi. In addition, the number of days spent at waterside vacations was not related to nevi size, suggesting that children quickly obtain a threshold dose of UV exposure. These studies about potential dangers of sun exposure may be valuable to parents planning waterside vacations with young children.

The p63 transcription factor is underexpressed in prostate adenocarcinomas and this lower expression is associated with the development of lethal prostate cancer. Dhillon and colleagues conducted a prospective study of 298 prostate cancer patients enrolled in the Physicians’ Health Study to further evaluate the use of p63 as a biomarker for advanced prostate cancer. In this study, tissue microarrays were generated from archived prostate cancer tissue and examined for p63 staining, cell proliferation and apoptosis. Dhillon and colleagues found strong cytoplasmic staining of p63 in prostate tumor samples. These results are surprising because p63 is normally weakly expressed in prostate cancer tissue and exhibits a distinct nuclear staining pattern in benign prostate tissue. The strong cytoplasmic p63 staining was associated with increased cell proliferation and prostate cancer mortality up to 20 years after diagnosis. These findings are unexpected and suggest a role for mislocalized cytoplasmic p63 in prostate oncogenesis.