ECL cell origin of gastric carcinomas not only in rodents, but also in man

2001 ◽  
Vol 120 (5) ◽  
pp. A251-A252
Author(s):  
Helge L. Waldum ◽  
Gunnar Qvigstad ◽  
Arne K. Sandvik
Keyword(s):  
2018 ◽  
Vol 19 (12) ◽  
pp. 4109 ◽  
Author(s):  
Helge Waldum ◽  
Reidar Fossmark

Gastric cancer has reduced prevalence, but poor prognoses. To improve treatment, better knowledge of carcinogenesis and cells of origin should be sought. Stomach cancers are typically localized to one of the three mucosae; cardial, oxyntic and antral. Moreover, not only the stem cell, but the ECL cell may proliferate and give rise to tumours. According to Laurén, the classification of gastric carcinomas seems to reflect biological important differences and possible different cell of origin since the two subtypes, intestinal and diffuse, do not transform into the other and show different epidemiology. The stem cell probably gives rise to the intestinal type, whereas the ECL cell may be important in the diffuse type. Elevation of gastrin may be the carcinogenic factor for Helicobacter pylori as well as the recently described increased risk of gastric cancer due to proton pump inhibitor treatment. Therefore, it is essential to determine the role of the gastrin target cell, the ECL cell, in gastric carcinogenesis. Clinical trials with gastrin antagonists could improve prognoses in those with gastrin receptor positive tumours. However, further studies on gastric carcinomas applying relative available methods and with the highest sensitivity are warranted to improve our knowledge of gastric carcinogenesis.


2001 ◽  
Vol 120 (5) ◽  
pp. A251-A252
Author(s):  
H WALDUM ◽  
G QVIGSTAD ◽  
A SANDVIK
Keyword(s):  

2020 ◽  
Vol 40 (6) ◽  
pp. 3203-3208 ◽  
Author(s):  
JUNG WOOK YANG ◽  
JEONG-HEE LEE ◽  
JONG SIL LEE ◽  
DONG CHUL KIM ◽  
DAE HYUN SONG ◽  
...  

1993 ◽  
Vol 84 (8) ◽  
pp. 879-884 ◽  
Author(s):  
Yasuhiko Kitadai ◽  
Wataru Yasui ◽  
Hiroshi Yokozaki ◽  
Hiroki Kuniyasu ◽  
Ayse Ayhan ◽  
...  

PLoS ONE ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. e46214 ◽  
Author(s):  
Dun-Fa Peng ◽  
Tian-Ling Hu ◽  
Barbara G. Schneider ◽  
Zheng Chen ◽  
Ze-Kuan Xu ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3159
Author(s):  
Helge Waldum

Malignant tumors are a consequence of genetic changes mainly occurring during cell division, sometimes with a congenital component. Therefore, accelerated cell divisions will necessarily predispose individuals, whether due to conditions of chronic cell destruction or hormonal overstimulation. It has been postulated that two genetic hits are necessary for the development of malignancy (Knudson). The correct view is probably that the number of genetic changes needed depends on the role the mutated genes have in proliferation and growth control. Hormones should accordingly be regarded as complete carcinogens. In this review based upon experience of gastric cancer where gastrin is central in the pathogenesis, it is argued that oxyntic atrophy—and not metaplasia as postulated by Correa—is the central precancer change in gastric mucosa. Moreover, the target cell of gastrin, the enterochromaffin-like (ECL) cell, is central in gastric carcinogenesis and most probably the cell of origin of gastric carcinomas of the diffuse type according to Lauren (a classification probable in accordance with biology). The distinction between adenocarcinomas and neuroendocrine carcinomas based upon a certain percentage of cancer cells with neuroendocrine differentiation is questioned. To make progress in the treatment of cancer, a correct classification system and knowledge of the pathogenesis are necessary.


2003 ◽  
Vol 145 (2) ◽  
pp. 103-107 ◽  
Author(s):  
Mafalda Pinto ◽  
Ying Wu ◽  
Gianpaolo Suriano ◽  
Rob G.J Mensink ◽  
Alex Duval ◽  
...  

Pathobiology ◽  
2001 ◽  
Vol 69 (6) ◽  
pp. 315-320 ◽  
Author(s):  
Kazuhiro Sentani ◽  
Naohide Oue ◽  
Humihiro Kondo ◽  
Kazuya Kuraoka ◽  
Junichi Motoshita ◽  
...  

1993 ◽  
Vol 43 (11) ◽  
pp. 654-661 ◽  
Author(s):  
Teiichi Motoyama ◽  
Kikuo Aizawa ◽  
Hidenobu Watanabe ◽  
Masayuki Fukase ◽  
Kiyoko Saito

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