Human papillomavirus (HPV) 16 infection is not detected in rectal carcinoma

Abstract

Introduction: Persistence of human papillomavirus (HPV) infections is associated with squamous cell carcinomas of different human anatomic sites. Several studies have suggested a potential role for HPV infection, particularly HPV16 genotype, in rectal cancer carcinogenesis.. The aim of this study was to assess the frequency of oncogenic HPV 16 viral DNA sequences in rectal carcinomas cases retrieved from the pathology archive of Braga Hospital, North Portuga. Methods: TaqMan-based type-specific real-time PCR for HPV 16 was performed using primers and probe targeting HPV16 E7 region. Results: Most of the rectal cancer patients (88.5%, n = 206 patients), were symptomatic at diagnosis. The majority of the lesions (55.3%, n = 129) presented malignancies of polypoid/vegetant phenotype. 26.8% (n = 63) had synchronic metastasis at diagnosis. 26.2% (n = 61) patients had clinical indication for neoadjuvant therapy. Most patients with rectal cancer were stage IV (19.7% patients), followed by stage IIA (19.3%) and stage I (18.5%). All cases of the present series tested negative for HPV16. Conclusion: The total of negative tests for HPV 16 infection is a robust argument to support the assumption that HPV 16 infection, despite of previous evidences, is not involved in rectal cancer carcinogenesis and progression.

Does human papillomavirus cause human colorectal cancer? Applying Bradford Hill criteria postulates

“…The positivity ratio of HPV detection in CRC samples was varied population wise from 0% [ 11 , 12 , 17 , 23 , 26 , 32 , 41 , 43 , 45 , 46 , 50 , 59 ] to 100% [ 13 , 54 ] in all the 59 studies, whereas the positivity ratio of HPV detection in normal and adjacent/benign samples was varied from 0% [ 21 , 22 , 29 , 30 , 43 , 49 ] to 84% (28) and 0% [ 17 , 22 , 26 , 41 , 42 , 45 , 46 , 50 , 52 , 57 ] to 69.56% [ 54 ], respectively.…”

“…The HPV positivity ratio reported in these studies was varied between 0% [ 11 , 12 , 17 , 23 , 26 , 32 , 41 , 43 , 45 , 46 , 50 , 59 ] and 100% [ 13 , 54 ]. In most of the case–control studies [ 12 , 17 – 27 , 29 – 32 , 35 – 57 ], the positivity ratio for HPV detection was higher in the cancerous samples as compared to the controls, whereas, in some studies [ 28 , 33 , 34 , 58 ], HPV positivity ratio was higher in the controls as compared to the CRC samples. Possible reasons for such population-specific inequalities in HPV detection could be non-modifiable factors such as genetic makeup and socially controllable factors such as health-seeking behaviour and differential access to the health facilities.…”

“…Only a single study [ 32 ] has been carried out in Portugal to date to relate the HPV with human CRC. In total, 144 CRC samples were screened in this study using PCR with primers specific for the E7 region of the viral genome and showed a 0% HPV detection ( Table 1 ).…”

“…Some of the studies that we summarised analysed only the CRC samples [ 8 , 11 , 13 , 59 , 64 , 65 , 67 , 71 , 74 , 75 , 79 , 80 , 84 ] and did not allow us to compare their results with normal or adjacent/benign controls. However, most of the studies also analysed the normal and adjacent/benign tissues along with CRC samples, and the comparison of their results demonstrated that HPV detection positivity ratios in CRC samples were higher in [ 12 , 17 , 27 , 29 – 32 , 35 – 57 ] studies, whereas lower in [ 28 , 33 , 34 , 58 ] studies as compared to the normal and adjacent/benign controls. However, none of the studies has reported the association of HPV with specific CRC subtype and histologic grade.…”

The first comprehensive genomic characterization of rectal squamous cell carcinoma

“…In different series (25), presence of TP53 mutation in aSCC is likely to be associated with HPV-negative tumors and confers poor prognosis as well as tumor relapse. It is licit to now consider HPV as a risk factor for rSCC like it is for aSCC and contrary to rADC [ 33 , 34 ]. This result gives an additional argument for treating rSCC like aSCC.…”