Exocrine pancreatic cancer is significantly more common in yonger men than
in younger women. The male-to-female sex ratio is, in most countries, betwe
en 1.25 and 1.75 to 1, but decreases with increasing age. Moreover, prior o
ophor-ectomy appeared in one study to be significantly more common in women
with pancreatic cancer than in controls. This has raised interest in sex h
ormones in the development in pancreatic cancer. It has been questioned if
there are estrogen receptors in ductal pancreatic cancer, but there are no
doubt estrogen receptors and estrogen-binding protein in human healthy panc
reas. It is also well proven that it is possible to influence experimental
pancreatic cancer with estrogens. However, in clinical studies tamoxifen ha
s repeatedly been shown to be without significant effects.
On the other hand, there are also androgen receptors in pancreatic cancer a
nd testosterone has been shown to strongly promote growth in experimental p
ancreatic cancers. It is therefore of considerable interest that an antiand
rogen recently was shown to significantly prolong life in patients with unr
esectable pancreatic carcinoma. However, in patients with advanced pancreat
ic carcinoma the S-testosterone is low, far lower than what could be expect
ed due to weight-loss and malnourishment alone.
Pancreatic cancer has etiologically been connected to diet, for example the
intake of fat. Cholecystokinin receptors have been found on human pancreat
ic cancer, possible to stimulate in vitro by cholecystokinin (CCK). Studies
with CCK-receptor binding, hybridization with radiolabeled complementary D
NA (cDNA) probes, or reverse-transcription polymerase chain reaction, have
shown that CCK-A receptors also are present in rat pancreatic putative pren
eoplastic lesions and cancer tissue, rat pancreatic-cancer cell lines, panc
reatic carcinomas in transgenic mice, hamster pancreatic cancer, and human
pancreatic cancer cell lines and tumors. Also, CCK-B receptors have been fo
und in some human pancreatic cancers. There are a vast number of experiment
s done on CCK-stimulation of pancreatic cancer. They indicate that CCK may
have a promotional effect on exocrine pancreatic cancer, but it is not prob
able that hyperstimulation with CCK alone induce pancreatic cancer.
At present, however, despite a lot of evidence for a hormone-dependence of
pancreatic cancer there are no data confirming a role for estrogens, androg
ens, CCK or their antagonists in clinical treatment of exocrine pancreatic
cancer.