The effect of tamoxifen and estrogen receptor status on survival in gastric carcinoma

Harrison, John W.; Dl, Morris; Ellis, Ian O.; Jones, J. A.; Jackson, I.

doi:10.1002/1097-0142(19890901)64:5<1007::aid-cncr2820640506>3.0.co;2-u

Cited by 62 publications

(34 citation statements)

References 11 publications

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“…A pooled analysis of three studies in Scandinavia found a nonsignificantly, but nearly three-fold increased risk of gastric cancer (Rutqvist et al, 1995), and correspondingly elevated risks have been found also in other studies (Andersson et al, 1991;Curtis et al, 1996;Matsuyama et al, 2000). Finally, a trend of decreased survival among patients with gastric cancer who had been treated with tamoxifen and in whom the gastric cancer was positive for oestrogen receptors was observed in a randomised trial (Harrison et al, 1989). Although, taken together, all these previous studies suggest that tamoxifen might play a role in the aetiology of gastric adenocarcinoma, the association has not been established.…”

Section: Discussionmentioning

confidence: 79%

Tamoxifen exposure and risk of oesophageal and gastric adenocarcinoma: a population-based cohort study of breast cancer patients in Sweden

et al. 2006

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In a population-based cohort study of all women aged over 50 years with breast cancer in the Swedish Cancer Register in 1961 -2003, those diagnosed before 31 December 1987 were regarded as unexposed to tamoxifen, whereas those diagnosed after that date were considered potentially exposed. Crosslinkages within the Cancer Register and the Registers of Death and Emigration enabled follow-up. Standardised incidence ratios (SIRs) of oesophageal and gastric cancer represented relative risks. Among 138 885 cohort members contributing with 1 075 724 person-years of follow-up, we found a nonsignificantly increased risk of oesophageal adenocarcinoma during the potential tamoxifen exposure period (SIR 1.60, 95% confidence interval (CI) 0.83 -3.08), but the risk estimates decreased with increasing latency interval. No association was observed during the unexposed period. No increased risk of cardia adenocarcinoma was identified in either period. The risk of non-cardia gastric adenocarcinoma was increased in the potential tamoxifen period (SIR 1.27, 1.03 -1.57), and almost doubled (SIR 1.86, 95% CI 1.10 -3.14) in the period of longest latency (10 -14 years). The corresponding overall SIR was increased in the unexposed group also, but here SIR did not increase with longer latency intervals. An increased risk of tobacco-related tumours, that is, oesophageal squamous-cell carcinoma and lung cancer, was limited to the unexposed cohort, indicating that confounding by smoking might explain the increased SIR during the unexposed period. We concluded that there might be a link between tamoxifen and risk of non-cardia gastric adenocarcinoma.

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Section: Discussionmentioning

confidence: 79%

Tamoxifen exposure and risk of oesophageal and gastric adenocarcinoma: a population-based cohort study of breast cancer patients in Sweden

et al. 2006

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“…52 Further evidence was provided in a randomised control trial that ER positivity conferred a worse prognosis but disappointingly the administration of tamoxifen at therapeutic concentrations did not prolong survival. 53 Conversely, more recent evidence suggests that patients treated with tamoxifen may have an overall increased risk of development of gastric carcinoma and a shorter latency period between the diagnosis of breast and gastric cancer. 54 A Chinese group 55 hypothesised that, since the amplification of c-erbB-2 oncogene 56 and its overexpression had been implicated in the advancement of gastric carcinoma, and estrogen was known to inhibit its expression in breast cancer cell lines, perhaps estrogen itself could be administered as a reasonable therapeutic option for the treatment of gastric cancer.…”

Section: Estrogen and Gastric Cancermentioning

confidence: 99%

Estrogen and gastrointestinal malignancy

Hogan¹,

Collins²,

Baird³

et al. 2009

Molecular and Cellular Endocrinology

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Summary:The concept that E2 exerts an effect on the gastrointestinal tract is not new and its actions on intestinal mucosa have been investigated for at least three decades. An attempt to consolidate results of these investigations generates more questions than answers, thus suggesting that many unexplored avenues remain and that the full capabilities of this steroid hormone are far from understood. Evidence of its role in esophageal, gastric and gallbladder cancers is confusing and often equivocal. The most compelling evidence regards the protective role conferred by estrogen (or perhaps ERβ) against the development and proliferation of colon cancer. Not only has the effect been described but many mechanisms of action have been explored. It is likely that, along with surgery, chemotherapy and radiotherapy, hormonal manipulation will play an integral role in colon cancer management in the very near future.Introduction:

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“…The prognostic significance of receptor expression is the subject of conflicting reports and remains unclear (Tokunaga et al, 1986;Yozozaki et al, 1988;Harrison et al, 1991). Clinical studies of the efficacy of adjuvant endocrine therapy, mainly involving the administration of tamoxifen, have also been inconclusive, and many studies too small and poorly controlled (Kitaoka, 1983;Kojima and Takahashi, 1986;Harrison et al, 1989b). Nevertheless, determination of sex hormone receptor expression in gastric cancer may play an important role in the understanding of the biochemical and pathophysiological behaviour of this disease.…”

mentioning

confidence: 99%

Expression of oestrogen and progesterone receptors in gastric cancer: a flow cytometric study

et al. 1999

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Summary Increased expression of oestrogen (ER) and progesterone (PR) receptors have been reported in gastric adenocarcinoma, although results have been variable. Immunohistochemical staining methodologies, in particular in the detection of ER, have been inconsistent with many tumours being classified ER-negative. In this study we have used flow cytometry to quantify expression of ER and PR in gastric adenocarcinoma and examine their relationships with established prognostic indicators. Cytokeratin-positive cells obtained from tumour biopsies of 50 patients with gastric cancer and ten control patients were labelled with biotinylated ER or PR antibodies followed by streptavidin PE. Flow cytometry was seen to increase the detection of ER levels in gastric cancer with more receptor-positive patients in this study than in results published to date. We believe this is related to the sensitivity of the flow cytometric assay with the detection of small shifts in ER level detected using cytokeratin gating. On analysis, the data showed no significant correlations with tumour stage and grade, and no differences were seen between normal mucosa and gastric cancer samples.

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The effect of tamoxifen and estrogen receptor status on survival in gastric carcinoma

Cited by 62 publications

References 11 publications

Tamoxifen exposure and risk of oesophageal and gastric adenocarcinoma: a population-based cohort study of breast cancer patients in Sweden

Tamoxifen exposure and risk of oesophageal and gastric adenocarcinoma: a population-based cohort study of breast cancer patients in Sweden

Estrogen and gastrointestinal malignancy

Expression of oestrogen and progesterone receptors in gastric cancer: a flow cytometric study

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