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6 t h A n n u a l E u r o p e a n C o n f e r e n c e o n
Gastroenterology
Journal of Clinical Gastroenterology and Hepatology
ISSN 2575-7733
J u n e 1 9 - 2 0 , 2 0 1 8
P a r i s , F r a n c e
Euro Gastro 2018
Page 19
Helge L. Waldum, J Clin Gastroenterol Hepatol 2018, Volume: 2
DOI: 10.21767/2575-7733-C1-001
The steroid hormones, particularly sex hormones, play an important role in
carcinogenesis.Surgicalordrugtreatmenttoreducetheeffectofsexhormones
on cancers have been used for decades. Peptide hormones, on the other hand,
have not had such a position. Moreover, most experts have claimed that even sex
hormones are not complete carcinogens, only having a growth promoting effect in
cells where an initial hit (mutation) has started the process of malignancy. When
long-term drug inhibition of gastric acidity induced malignant tumors originating
from the gastrin target cell, the ECL cell, in rodents, the question of whether gastrin
was a carcinogen became of utmost importance. Subsequent studies have
shown that every condition with long-term hypergastrinemia in whatever species
develop ECL derived tumors. We started to study the role of gastrin in gastric
carcinogenesis around 1985 after we first had shown that gastrin stimulated
gastric acid secretion solely by releasing histamine from the ECL cell. Parallel to
the stimulation of histamine release, gastrin stimulates ECL cell proliferation by
the same receptor and same concentration dependence. On the background of
problems indistinguishingbetweenadenocarcinomas andneuroendocrine tumors
both in man and rodents, we started to examine human gastric carcinomas with
regard to ECL cell differentiation with the help of the most sensitive and specific
methods available at the time of the study. We detected ECL cell differentiation
in many of the carcinomas, and especially those of the diffuse type according to
Lauren, and among them those belonging to the signet ring subgroup. Recently
we could show expression gastrin receptor on hyperplastic and neoplastic ECL
cells including a proportion of tumors originally classified as adenocarcinomas.
The gastrin antagonist netazepide reduces ECL cell hyperplasia and can eradicate
gastric neuroendocrine tumours (NETs) (carcinoids). Netazepide may also have
an effect on the growth of gastric carcinomas with gastrin receptor as well. The
recent epidemiological studies showing that proton pump inhibitors predispose to
gastric cancer further incriminate gastrin in gastric carcinogenesis.
Biography
Helge L Waldum fulfilled his MD at University of Oslo in 1971
with excellence (reported to the King). He became Specialist
in Internal Medicine and Gastroenterology at the University of
Tromsø in 1980, the same year as he defended his first thesis
on Studies on Group I Pepsinogens and Secretin. Since then he
has worked at the University Hospital of Trondheim, except for
one year where he stayed in Paris at Hospital Bichat where he
in 1993 defended his second thesis on Enterochromaffinelike
cell (ECL) - a key cell in the gastric mucosa with the mention,
Very Honorable with Felicitatons. He has supervised twenty
candidates for PhD and published about 487 papers and
100 scientific letters. He was the Head of Department of
Gastroenterology and Liver Diseases at Trondheim University
Hospital for more than twenty years. In 2011 he was appointed
“Knight of 1stdegree of the order of Saint Olav” by the Norwegian
king for his translational research. He is presently serving as
Editor-in-Chief, Scandinavian Journal of Gastroenterology.
Gastrin is a complete carcinogen for the
oxyntic mucosa
Helge L Waldum
University Hospital, Norway