Esophagitis in a population at risk for esophageal carcinoma

Oettle, G J; Paterson, Alan C.; Leiman, Gladwyn; Segal, I

doi:10.1002/1097-0142(19860601)57:11<2222::aid-cncr2820571125>3.0.co;2-3

Cited by 20 publications

(5 citation statements)

References 13 publications

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“…In contrast to reflux esophagitis observed in Western countries, this chronic esophagitis has no association with gastric reflux or erosion (Crespi et al, 1979;Mufioz et al, 1982;Oette et al, 1986). Such esophagitis has been regarded as a precursor lesion of esophageal cancer in high-risk areas includ-ing China, Iran and South Africa (Crespi et al, 1979;Muiioz et al, 1982;Oette et al, 1986). However, clear-cell acanthosis has also been reported to be frequent in low-risk populations in China (Crespi et al, 1984b).…”

Section: Discussionmentioning

confidence: 99%

Human papillomavirus (HPV) DNA in esophageal precancer lesions and squamous cell carcinomas from China

Chang

Syrjänen

Shen³

et al. 1990

Intl Journal of Cancer

115

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A series of 51 biopsies derived from the same number of patients with established invasive squamous-cell carcinoma of the esophagus in Linxian, a high-risk area for esophageal cancer in China, were analyzed histologically and by in situ DNA hybridization to demonstrate human papillomavirus (HPV) infection. Epithelial changes suggesting HPV infection within or adjacent to the carcinoma lesions were found in 25 cases (49.0%). Esophageal lesions with HPV morphology showed both flat (25 cases) and inverted condylomas (2 cases) resembling those found in the genital tract. HPV 6, 11, 16 or 18 DNA sequences were detected in 22/51 (43.1%) of the esophageal specimens. HPV DNA was most frequently localized in epithelium adjacent to carcinomas in areas showing either epithelial hyperplasia (36.1%) or dysplasia (22.2%). Of the lesions with morphological HPV changes, 64% (16/22) were shown to contain HPV DNA. In 2 specimens, HPV DNA was found in frankly malignant cells. High-risk types HPV 16 and/or 18 DNA sequences were found in 16 of the 22 HPV DNA-positive cases (72.7%). Our results confirm previously reported HPV involvement in esophageal squamous-cell lesions, and support the hypothesis of HPV as a possible etiological agent in esophageal carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Human papillomavirus (HPV) DNA in esophageal precancer lesions and squamous cell carcinomas from China

Chang

Syrjänen

Shen³

et al. 1990

Intl Journal of Cancer

115

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“…Therefore, unidentified local factors must play a major role in the development of esophageal cancer in these areas. Common to all high‐incidence areas is the existence of a chronic esophagitis that seems to be the key factor for the locally increased risk of malignant degeneration [1,7–9]. The esophagitis represents the first step of a cascade which progresses via dysplastic changes of the epithelium to cancer [3,9].…”

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confidence: 99%

Detection of a Putative Novel Wolinella Species in Patients with Squamous Cell Carcinoma of the Esophagus

et al. 2003

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“…Long-lasting reflux oesophagitis following oesophageal hiatus hernia is known to be closely related to the occurrence of oesophageal cancer (Kuylenstierna & Munck-Wikland, 1985). Epidemiological studies reveal that a form of chronic oesophagitis, which is thought to result from nutritional deficiencies, is the most frequent lesion found in populations at high risk of oesophageal cancer in such areas as Kashmir in India, southern Africa, northern Iran and Linxian and Huixian in China (Crespi et al, 1979; Munoz et al, 1982;Oettle et al, 1986;Goswami et al, 1987; Guanrei & Songliniang, 1987 Seto et al, 1991; Attwood et al, 1992). Duodenogastric reflux without exposure to carcinongens has been demonstrated to cause gastric carcinoma in rats (Langhans et al, 1981;Kondo et al, 1984;Theuring et al, 1985;Mason, 1986;Miwa et al, 1992 (Figure 1).…”

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Induction of oesophageal and forestomach carcinomas in rats by reflux of duodenal contents

Miwa

Segawa²,

Takano³

et al. 1994

Br J Cancer

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S_mmmmary A study was designed to determine whether oesophageal carcinomas can be induced through reflux of duodenal contents. Male Wistar rats weighing 230 -250 g were divided into three groups according to the surgical procedure performed: (1) the duodenal contents were directed into the forestomach through a stoma (duodeno-forestomach reflux); (2) the duodenal contents were regurgitated into the forestomach through the glandular stomach (duodeno-glandular-forestomach reflux); and (3) a sham operation was performed as a control. Animals were fed standard CRF-1 solid food and tap water that was not exposed to carcinogens and were sacrificed 50 weeks post-operatively. While no neoplasia was observed in any of the 32 control rats, 4/11 (36%) with duodeno-forestomach reflu.x and 3/18 (17%) animals with duodeno-glandular-forestomach reflux developed carcinomas in the lower oesophagus and forestomach. The incidence in each group was significantly higher than in the controls (P<0.01 and P<0.05 respectively). Six of the seven lesions consisted of squamous cell carcinomas, and one was a mucinous adenocarcinoma. Oesophageal columnar epithelial metaplasia was observed in two (18%) of the animals with duodeno-forestomach reflux. Carcinomas were always surrounded by chronic inflammatory changes, including regenerative thickening, basal cell hyperplasia and dysplasia. Additional well-differentiated adenocarcinomas were observed in the prepyloric antrum of 6/18 (33%) animals with duodeno-glandular-forestomach reflux. These findings indicate that chronic reflux of duodenal contents may cause oesophageal carcinoma.Oesophageal adenocarcinoma frequently occurs in the lower oesophagus, in the bed of the columnar-lined epithelium (Barrett's oesophagus) (Naef et al., 1975;McDonald et al., 1977; Witt et al., 1983;Miros et al., 1991). This columnarlined epithelium develops in response to gastro-oesophageal reflux (Mossberg, 1966;Halvorsen & Semp, 1975;Gillen et al., 1988; Seabrook et al., 1992). Thus, the association of adenocarcinoma with gastro-oesophageal reflux is well established. However, there are few data indicating whether squamous cell carcinoma, by far the most frequent type of oesophageal carcinoma, may also occur as a result of reflux. Some clinical evidence supports this assumption. Individuals with a history of gastrectomy occasionally develop squamous cell carcinomas in the lower oesophagus, probably as a consequence of post-surgical reflux oesophagitis (Shearman et al., 1970;Rossi et al., 1984;Maeta et al., 1990;Seto et al., 1991). Long-lasting reflux oesophagitis following oesophageal hiatus hernia is known to be closely related to the occurrence of oesophageal cancer (Kuylenstierna & Munck-Wikland, 1985). Epidemiological studies reveal that a form of chronic oesophagitis, which is thought to result from nutritional deficiencies, is the most frequent lesion found in populations at high risk of oesophageal cancer in such areas as Kashmir in India, southern Africa, northern Iran and Linxian and Huixian in China (Cres...

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Esophagitis in a population at risk for esophageal carcinoma

Cited by 20 publications

References 13 publications

Human papillomavirus (HPV) DNA in esophageal precancer lesions and squamous cell carcinomas from China

Human papillomavirus (HPV) DNA in esophageal precancer lesions and squamous cell carcinomas from China

Detection of a Putative Novel Wolinella Species in Patients with Squamous Cell Carcinoma of the Esophagus

Induction of oesophageal and forestomach carcinomas in rats by reflux of duodenal contents

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