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Table 2 Detection of HPV and Helicobacter pylori by type of specimen in esophageal and gastroesophageal cancer cases and matched healthy controls

From: Prevalence of human papillomavirus and Helicobacter pylori in esophageal and gastroesophageal junction cancer biopsies from a case–control study in Ethiopia

Bio-Specimens human papillomavirus Helicobacter pylori
Participant Diagnosis at enrolment, specimen collection Specimen type Specimen source Processing Number specimens available Number Beta-globin positive Number HPV DNA positive Number HPV-16 positive Prevalence 95% CI Prevalence HPV-16 95% CI Other HPV type identified Number H. pylori ureA positive Number H. pylori 16 s positive Number H. pylori ureA/16 s positive Prevalence 95% CI Number cagA + H. pylori in ureA/16 s positive specimens Prevalence cagA+ in ureA/16 s positive specimens 95%
CASES 2012 Tissue, fresh Endoscopy DNA/RNA later, frozen at − 80 °C 62 62 1 1 2% (0–9%) 2% (0–9%)   30 30 34 55% (42–68%) 20* 59% (41–75%)
   Buccal cells, fixed Oral wash saline & gargling Ethanol fixed 61 61 7 1 11% (5–22%) 2% (0–9%) HPV-18, HPV-31, HPV-35, HPV-51, HPV-56, HPV-66 8 3 8 13% (6–24%) 2 25% (3–65%)
CONTROLS 2012–2013 Buccal cells, fixed Oral wash saline & gargling Ethanol fixed 57 56 4 1 7% (2–17%) 2% (0–10%) HPV-18, HPV-35, HPV-39, HPV-53, HPV-66 4 3 4 7% (2–17%) 2 50% (7–93%)
  1. *Two tissue specimens tested positive with PCR amplification of the cagA gene only, with readings of 2 and 27 respectively, while testing negative for the amplification of the ureA and 16S genes. These specimens are included among the 62 used as the denominator to determine the positivity of H. pylori according to ureA and 16S but are excluded from the calculation of the proportion cagA+ among ureA/16S positive specimens