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Lutz, S.Z. ; Todenhöfer, T.* ; Wagner, R. ; Hennenlotter, J.* ; Ferchl, J.M.* ; Scharpf, M.O.* ; Martus, P.* ; Staiger, H. ; Fritsche, A. ; Stenzl, A.* ; Häring, H.-U. ; Heni, M.

Higher prevalence of lymph node metastasis in prostate cancer in patients with diabetes.

Endocr. Relat. Cancer 25, L19-L22 (2018)
Verlagsversion DOI PMC
Free by publisher
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Extract: Prostate cancer (PCa) and type 2 diabetes mellitus are under the most frequent diseases in men with a tremendous impact on morbidity and mortality (Giovannucci, et al. 2010). Incidence of many common types of cancer is known to be higher in diabetes (Giovannucci et al. 2010). However, studies reported that incidence of PCa is not increased in men with type 2 diabetes, some studies even found reduced prevalence (Kasper, et al. 2009). In contrast, PCa survival is markedly reduced in patients with coincident type 2 diabetes (Chen, et al. 2017). The underlying molecular mechanisms for shortened survival are still under ongoing debate and not fully understood. They might include altered insulin or IGF-1 signaling and enhanced androgen receptor activity. Of note, diabetes and PCa share numerous risk factors, most importantly the nonmodifiable risk factor age and the modifiable risk factor obesity (Giovannucci et al. 2010). Although PCa incidence is not elevated in obese men, patients with excess bodyweight are reported to display higher cancer-related mortality (Ma, et al. 2008). Carefully adjusted studies for these risk factors investigating the impact of diabetes on PCa outcomes and aggressiveness are sparse. To better understand why PCa related survival is shortened in men with concommittant diabetes, we evaluated the relation of diabetes with TNM-staging and an established PCa risk score (Mohler, et al. 2016), independent of age and body weight ...
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Mellitus; Risk
ISSN (print) / ISBN 1351-0088
e-ISSN 1479-6821
Quellenangaben Band: 25, Heft: 3, Seiten: L19-L22 Artikelnummer: , Supplement: ,
Verlag BioScientifica
Verlagsort Bristol
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed