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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