Subsequent primary malignancies after endometrial carcinoma and ovarian carcinoma.
BACKGROUND
Population-based data on subsequent neoplasms after women are diagnosed with endometrial and ovarian carcinomas are limited, particularly regarding specific histologic tumor types.


METHODS
The nationwide Swedish Family-Cancer Database of 10.2 million individuals, which includes 19,128 invasive endometrial carcinomas and 19,440 ovarian carcinomas, was used to calculate standardized incidence ratios (SIRs) and 95% confidence intervals (95% CIs) for second primary carcinomas. SIRs were calculated for specific follow-up periods. Data on histopathologic types also were used.


RESULTS
An excess of subsequent malignancies after women were diagnosed with endometrial carcinoma was noted at 11 sites. The highest SIRs were recorded for synchronous or metasynchronous ovarian carcinomas (SIR, 55.77; 95% CI, 48.82-63.43) and carcinomas of the small intestines (SIR, 14.71; 95% CI, 4.64-34.59). Primary ovarian carcinoma was followed by an increased risk of developing endometrial carcinoma, and the risks of developing many other malignancies also were increased after women were diagnosed with endometrial carcinoma, including intestinal malignancies, renal cell carcinoma, bladder carcinoma, squamous cell skin carcinoma, connective tissue malignancies, and leukemia. When ovarian endometrioid histology was diagnosed synchronously with primary endometrial carcinoma, the SIR was 140; when endometrial carcinoma was the subsequent neoplasm, the SIR was 87. A small familial component was found in the cooccurrence of endometrial carcinoma and ovarian carcinoma.


CONCLUSIONS
The current data show a strong clustering of endometrial carcinomas and ovarian carcinomas, particularly involving tumors of endometrioid morphology. The patterns of second neoplasms also suggest that hereditary nonpolyposis colorectal carcinoma may contribute to the association between endometrial and ovarian malignancies. Increased risks for connective tissue tumors and leukemia may signal a response to treatment, and an increased risk for squamous cell skin carcinoma may signal a depressed immune function.
Hemminki
Kari
K
Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden. kari.hemminki@cnt.ki.se
Aaltonen
Lauri
L
Li
Xinjun
X
D018269:Carcinoma, Endometrioid / Q000453:epidemiology* / Q000209:etiology / Q000235:genetics / Q000473:pathology; D016889:Endometrial Neoplasms / Q000453:epidemiology* / Q000209:etiology / Q000235:genetics / Q000473:pathology; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008499:Medical Records; D008875:Middle Aged; D009378:Neoplasms, Multiple Primary / Q000453:epidemiology* / Q000209:etiology / Q000235:genetics / Q000473:pathology; D016609:Neoplasms, Second Primary / Q000453:epidemiology* / Q000209:etiology / Q000235:genetics / Q000473:pathology; D010051:Ovarian Neoplasms / Q000453:epidemiology* / Q000209:etiology / Q000235:genetics / Q000473:pathology; D012042:Registries; D012189:Retrospective Studies; D013548:Sweden / Q000453:epidemiology; D044465:White People / Q000235:genetics