In the county of Stockholm, between 1970 and 2002, we have previously reported a 3-fold parallel increase in the incidence of tonsillar squamous cell carcinoma (SCC) and the proportion of human papillomavirus (HPV) positive tonsillar SCC. Here, we have followed the above parameters in all patients (n 5 120) diagnosed with tonsillar SCC during [2003][2004][2005][2006][2007] in the same area, and also in correlation to our previous data. Ninety-eight pretreatment biopsies were available and presence of HPV DNA and HPV-16 E6 and E7 RNA were tested by polymerase chain reaction (

Smoking and alcohol are well‐known etiological factors in tonsillar cancer. However, as in cervical cancer, human papillomavirus (HPV) is currently found in a sizable proportion of tonsillar cancer. Recent reports from the U.S. and Finland show an increase in the incidence of tonsillar cancer, without a parallel rise in smoking and alcohol consumption. This study investigates whether the incidence of tonsillar cancer has also changed in Sweden and whether a possible explanation of the increase is a higher proportion of HPV‐positive tonsillar cancer. The incidence of tonsillar cancer between 1970 and 2002 in the Stockholm area was obtained from the Swedish Cancer Registry. In parallel, 203 pretreatment paraffin‐embedded tonsillar cancer biopsies taken during 1970–2002 from patients in the Stockholm area were tested for presence of HPV DNA by PCR. The incidence of tonsillar cancer increased 2.8‐fold (2.6 in men and 3.5 in women) from 1970 to 2002. During the same period, a significant increase in the proportion of HPV‐positive tonsillar cancer cases was observed, as it increased 2.9‐fold (p < 0.001). The distribution of HPV‐positive cases was 7/30 (23.3%) in the 1970s, 12/42 (29%) in the 1980s, 48/84 (57%) in the 1990s and 32/47 (68%) during 2000–2002. We have demonstrated a highly significant and parallel increase both in the incidence of tonsillar cancer and the proportion of HPV‐positive tumors. Hence, HPV may play an important role for the increased incidence of tonsillar cancer. This should definitely influence future preventive strategies as well as treatment for this type of cancer. © 2006 Wiley‐Liss, Inc.

Cylindrical APE performed in the prone position for low rectal cancer removes more tissue around the tumor that leads to a reduction in CRM involvement and intraoperative perforations, which should reduce local disease recurrence. The cylindrical technique has the potential to improve patient outcomes substantially if appropriate surgical education programs are developed.

The aim of our study was to investigate the physical state and the viral load of HPV-16 in tonsillar cancer and to correlate these findings with clinical outcome. To distinguish between integrated and episomal forms of HPV, 22 freshfrozen tonsillar cancer samples were analysed by a method based on restriction enzyme cleavage, ligation and PCR (rliPCR). HPV-16 was detected in 11/22 and HPV-33 in 1/22 of the cancers, hence 12/22 (55%) of the tumours were HPV positive. Only extrachromosomal forms of HPV-16 were observed. Full-length episomal HPV was detected exclusively in 7/11 of the cancers, whereas both full-length and deleted forms of episomal HPV-16 were found in parallel in 2 other tumours. In 1 tumour only a deleted episomal form of HPV-16 was present. In the remaining HPV-16 positive tumour both full-length episomal as well as an 11 kbp PCR product were detected and if the 11 kbp product contained integrated HPV, or was off-size linearised episomal could not be determined. In 2 cervical cancer controls, HPV-16 was integrated and could be chromosome located. HPV-16 was quantified by real-time PCR and most tonsillar cancers contained between 10 to a few hundred copies of HPV per ␤-actin. Key words: HPV; tonsillar cancer; physical state; viral load; prognosisAccumulating molecular and epidemiological data indicate that the high-risk types of human papillomavirus (HPV) are not only associated with cervical cancer, but may also be associated with certain subtypes of cancer in the head and neck. [1][2][3][4][5] The strongest association has been found for oropharyngeal squamous cell carcinoma, especially tonsillar cancer, where HPV DNA is present in 45-70% of the cases. [1][2][3][5][6][7][8][9] In a nested case-control study it was found that patients who were sero-positive for HPV-16 had a 14.4 excess risk of developing oropharyngeal cancer later in life, and in another study patients with a history of HPV-related anogenital cancer had a 4.3 higher risk of developing tonsillar cancer. 4,10 Furthermore, patients with HPV positive tonsillar cancer seem less likely to be heavy smokers and drinkers, and to have a better prognosis than patients with HPV negative tonsillar cancer. 3,7,8 Similar to cervical cancer, the oncogenes of HPV-16, E6 and E7, are generally expressed in HPV positive tonsillar cancer. 1,9,11,12 The viral protein E6 promotes degradation of p53, whereas E7 inactivates pRb. 13,14 P53 mutations have been reported to be less frequent in HPV positive tonsillar cancer as compared to HPV negative tonsillar cancer, although when assayed by immunohistochemistry the proportion of elevated p53 levels are similar in both HPV positive and negative tumours. 3,12,15 In addition, HPV positive tonsillar cancers seem to have a decrease of pRb, possibly due to E7 activity. 2,9 In cervical cancer the HPV genome is mainly integrated in the host genome. 16,17 Integration leads to disruption and deletion of the viral genes E1 or E2 open reading frame (ORF), which are of importance for viral replication and viral transc...