Prostate Cancer Treatment May Increase Colorectal Cancer Risk
Researchers observed greater incidences of colorectal cancer among patients who underwent bilateral orchiectomy, surgery, and ADT.
Prostate cancer (PCa) patients who undergo bilateral orchiectomy, radical prostatectomy, or other treatments may be at increased risk of colorectal cancer, a new Swedish study suggests.
A team led by Yunxia Liu, MD, of Karolinska Institutet in Stockholm, used data from 3 national Swedish health registries to calculate the incidence of colorectal adenocarcinoma among 149,743 PCa patients, compared with the general Swedish male population. The investigators divided subjects into 4 groups: group 1, diagnosed between 1961 and 1980, historically received estrogen; whereas groups 2, 3, and 4, diagnosed between 1981 and 2008, underwent bilateral orchiectomy, prostatectomy, and other treatment (mainly gonadotropin-releasing hormone agonists, radiotherapy, or both). Over 601,542 person-years of follow-up, 1,698 patients were diagnosed with colorectal adenocarcinomas.
Compared with the general male population, patients treated with bilateral orchiectomy, prostatectomy, and other non-estrogen treatments had a 30%, 22%, and 37% increased incidence of colorectal cancer, respectively, according to an online report in Cancer Control.
No clear association was found among group 1 patients treated with estrogen. The researchers noted that previous studies in women have linked higher levels of estrogen and progesterone to lower risk of colorectal cancer.
“Treatment for prostate cancer diagnosed after 1980 may be associated with an increased risk of adenocarcinoma, implying a possible connection to ADT, one of the most common treatments in Sweden used after 1980,” the researchers stated. The increased risk among orchiectomy patients could be related to surgical androgen deprivation, they posited, and the risk among non-surgery patients could be due to medically induced androgen deprivation.
Greater risks were observed in cases of adenocarcinoma of the distal colon and rectum than in the proximal colon. The investigators hypothesize that genetic and/or physiological mechanism may explain the differences because the gut originates from different parts of a developing embryo.
The researchers pointed out the strengths of the study, including its nationwide and population-based cohort design identified by from national registries, its large PCa cohort sizes, and long and complete follow-up times. They also acknowledged limitations, such as the absence of detailed information on hormonal treatments such as estrogen or anti-androgen medications.