Occurrence of Gastric Cancer among Patients with Pernicious Anemia at the Boston City Hospital

Zamchegk, Norman; Grable, Ernest; Ley, Allyn B.; Norman, Leona

doi:10.1056/nejm195506302522601

Cited by 125 publications

(58 citation statements)

References 20 publications

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“…Moreover, patients with pernicious anaemia not only have an increased risk of ECL-cell carcinoids, but also of carcinomas in the oxyntic mucosa (Zamcheck et al 1955). We have previously presented data suggesting that a proportion of the gastric carcinomas actually are malignant ECL-omas (Waldum et al 1991).…”

Section: Hormones and Carcinomasmentioning

confidence: 99%

Hormones and carcinogenesis

Waldum¹

1998

Endocrine Related Cancer

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Hormones are important regulators of growth. By stimulating proliferation, hormones may increase the risk of mutation and at the same time stimulate the replication of the mutated cell. Thus, hormones are complete carcinogens. A direct carcinogenic effect of oestrogen in man is known from the occurrence of vaginal carcinomas in girls born of mothers who were treated with oestrogen during pregnancy. There are also experimental animal studies indicating that even peptide hormones may induce malignant tumours.An excellent example is the so-called enterochromaffin-like cell (ECL-cell) carcinoid of the stomach, which is caused by hypergastrinaemia and where the pathogenesis is diffuse hyperplasia, linear and nodular hyperplasia, dysplasia (with micronodules), intramucosal carcinoid, and invasive carcinoid. This sequence of events can be followed not only histopathologically but also by means of image DNA cytometry of the nuclei of the ECL-cells. As soon as clear-cut neoplasia is present, the cytometric DNA distribution pattern switches from the normal diploid type to an aneuploid one. The Endocrine-Related Cancer (1998) 5 45-48 hyperplastic lesions are all reversible, as soon as the hypergastrinaemia is eliminated. H L Waldum et al.: Hormones and carcinogenesis 46Mutations occur at cell divisions with a certain frequency. Mutagens increase the risk of mutation via a direct effect on the genes. Whether a mutation induced by a mutagen gives rise to a clinically overt tumour depends on the type of mutation and also on the replication of the mutated cell. Hormones may stimulate the growth of cells including mutated cells, and they have, therefore, been thought to be important co-carcinogens. By stimulating mitosis, hormones increase the risk of mutation solely by increasing the number of cell divisions (Ames & Gold 1990). Normally most mutations are corrected by DNA repairing mechanisms (Lindahl 1976). These repairing processes take time, and there is reason to believe that speeding up the rate of cell division may increase the risk of permanent mutations being transferred to daughter cells. Thus, hormones may not only be co-carcinogens, but in reality be among the most important carcinogens by increasing the risk of mutations in their normal target cells and at the same time stimulating the growth of the mutated cells. Hormones and growth controlThe lipid soluble steroid hormones affect the growth of their target cells by interaction with hormone responsive elements in the nucleus, affecting the regulation of gene expression (Reichel & Jacob 1993). Peptide hormones influence cellular growth by interacting with their cell membrane receptor, which, via a cascade reaction, affects gene expression. Among the peptide hormones a growth stimulatory effect has been attributed mainly to the hormones interacting with receptors coupled to the formation of inositol trisphosphate (Berridge & Irvine 1984), and only to a lesser extent to hormones coupled to adenylate cyclase (MacManus & Whitfield 1969). We (Brenna & Waldu...

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Section: Hormones and Carcinomasmentioning

confidence: 99%

Hormones and carcinogenesis

Waldum¹

1998

Endocrine Related Cancer

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“…55 Other studies also reported that the gastric cancer risk in patients with pernicious anaemia was three-to five-fold increased. [56][57][58][59][60][61][62] Several prospective studies focused on the development of gastric cancer in patients with intestinal metaplasia type III or more severe dysplasia. One small study following seven patients with type III metaplasia for 6 years observed development of gastric cancer in one of them.…”

Section: Atrophy Metaplasia and Gastric Cancer: Prospective Studiesmentioning

confidence: 99%

Relationship between Helicobacter pylori, atrophic gastritis and gastric cancer

Kuipers

1998

Aliment Pharmacol Ther

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“…It has been estimated that the risk of stomach cancer is increased 3-to 6-fold in pernicious anaemia patients (Berkson et al, 1956;Elsborg & Mosbech, 1979;Eriksson et al, 1981;Hitchcock et al, 1955;Kaplan & Rigler, 1945;Zamcheck et al, 1955), but such figures derive from autopsy studies or prevalence surveys which may have inherent sources of bias. In one prospective study (Blackburn et al, 1968), deaths due to stomach cancer were elevated 4-fold, with evidence of continued elevations 10 or more years after initial treatment, but comparable information on cancer incidence was unavailable.…”

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confidence: 99%

Cancer risk following pernicious anaemia

Brinton

Gridley²,

Hrubec³

et al. 1989

Br J Cancer

140

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Summary A computer-based file of all Veterans Administration (VA) hospitalisation records for the period 1969-1985 was used to identify and follow for cancer development a cohort of 5,161 white males with pernicious anaemia. A total of 34,915 person-years were accrued, with an average length of follow-up of 6.8 years. A total of 481 cancers were diagnosed, slightly higher than the number expected (SIR= 1.2). Significant excesses were observed for cancers of the buccal cavity and pharynx (1.8) and stomach (3.2), and for melanoma (2

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Occurrence of Gastric Cancer among Patients with Pernicious Anemia at the Boston City Hospital

Cited by 125 publications

References 20 publications

Hormones and carcinogenesis

Hormones and carcinogenesis

Relationship between Helicobacter pylori, atrophic gastritis and gastric cancer

Cancer risk following pernicious anaemia

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