Premium
Multiple primary malignancies in patients with sporadic pancreatic endocrine tumors
Author(s) -
Fendrich Volker,
Waldmann Jens,
Bartsch Detlef K.,
Schlosser Katja,
Rothmund Matthias,
Gerdes Berthold
Publication year - 2008
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21044
Subject(s) - medicine , gastrinoma , etiology , multiple endocrine neoplasia , primary tumor , endocrine system , population , metastasis , gastroenterology , cancer , oncology , hormone , biochemistry , chemistry , environmental health , secretion , gastrin , gene
Background To investigate the appearance of multiple primary malignancies in patients with sporadic neuroendocrine pancreatic tumors (NEPTs). Methods One hundred forty‐five patients with NEPTs were treated at the Department of Surgery, Philipps‐University Marburg. Multiple primary malignancies included tumors that were not considered to be a metastasis, invasion, or recurrence of NEPTs. Data on sex, age at diagnosis of cancer, follow‐up time after diagnosis, and death rate were collected. Results Of 115 patients with sporadic NEPTs, 15 (13.0%) patients were identified with at least one malignant tumor, other than a NEPT. The median age at diagnosis of the associated tumor(s) was 57 years (range, 10–72 years). Two of the 15 patients had insulinomas, 5 had gastrinomas and 8 had non‐functioning NEPTs, respectively. The risk of developing multiple cancers was the highest for patients with gastrinoma (21.7%), followed by patients with non‐functioning NFPTs (20.5%). Conclusions In patients with NEPTs multiple primary malignancies are found more frequently than in the general population. The etiology of the increased risk of other primaries is not clearly defined, but it may be the result of accumulated growth stimulation by the secreted hormones or a genetic alteration that leads to tumorogenesis in these patients. J. Surg. Oncol. 2008;97:592–595. © 2008 Wiley‐Liss, Inc.