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ORIGINAL RESEARCH |
From the 1Department of Obstetrics and Gynecology; 2Division of Epidemiology, Department of Internal Medicine; 3Division of Hematology-Oncology, Cancer Research Treatment Center; 4New Mexico Tumor Registry; and 5Department of Mathematics and Statistics, Department of Pathology, New Mexico Tumor Registry, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.
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ABSTRACT |
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 ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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METHODS: Surveillance, Epidemiology, and End Results data were used to identify malignant germ cell tumors (1973–2002). Overall and 5-year incidence rates, estimated annual percentage change, and survival rates were calculated and compared by age at diagnosis, race, stage, and histology.
RESULTS: Of 1,262 cases, there were 414 (32.8%) dysgerminomas, 449 (35.6%) immature teratomas, 37 (2.9%) mature teratomas with malignant degeneration, and 362 (28.7%) mixed germ cell tumors. The 30-year, age-adjusted incidence rate per 100,000 women-years was 0.338, decreasing by 29.4% for dysgerminomas (P = .18) and by 31.5% for mixed germ cell tumors (P = .22). Other nonwhites had higher rates than whites and blacks, but dysgerminoma rates were higher in whites and other nonwhites than in blacks. Using the registries for expanded races, rates were higher for Asian/Pacific Islanders (P = .059) and Hispanics (P = .07). By age at diagnosis, 15–19 year olds had the highest rates and the only significant change in rates (37.5% increase, P = .008). The 5-year relative survival was 83.9%. Survival rates improved significantly over calendar time and varied by histologic subtype, race, stage of disease, and age at diagnosis.
CONCLUSION: Over the past 30 years, germ cell tumor incidence rates have declined in women and differ from rising trends reported for testicular tumors. Survival rates have improved but were lower for older women and for nondysgerminoma subtypes.
LEVEL OF EVIDENCE: II-3
Over the past 3 decades, survival rates for germ cell tumors have dramatically improved, coincident with more aggressive surgical staging and combination chemotherapy. In Asia4 and Africa,5 where the prevalence of epithelial ovarian carcinoma is lower, germ cell tumors account for a much larger proportion of ovarian neoplasms.6,7 In U.S. males, testicular germ cell tumor incidence rates have increased by 44% over 26 years, from 1973 through 1998, are 5-fold higher among whites than blacks, and have been increasing steadily since the 1940s.7 Similar trends have been reported from Canada,7,8 Europe,9 Australia,10 and New Zealand.11 In contrast, little is known about trends in malignant female germ cell tumors. Therefore, the objective of this study was to analyze trends in incidence and survival rates for malignant ovarian germ cell tumors using the Surveillance, Epidemiology, and End Results (SEER) Program Cancer Incidence Public-Use Database (SEERSTAT 6.1.4 SEER 9 Registries Public-Use, November 2004).12
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MATERIALS AND METHODS |
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ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The principal database used was the Incidence - SEER 9 Regs Public-Use, Nov 2004 Sub (1973–2002), National Cancer Institute, DCCPS, Surveillance Research Program, Cancer Statistics Branch, inclusive of the November 2004 submission, released April 2005. Using the statistical software within the SEER 9, incidence rates by race/ethnicity may be calculated only for whites, blacks, and others (Race Recode A variable). Case listings by other race/ethnicity codes were generated using newer SEER codes. Further categorization by race/ethnicity was performed using 2 additional SEER codes. Rates for Asian and Hispanic populations were calculated using the SEER 13 Regs Public-Use, Nov 2004 Sub for Expanded Races (1992–2002) and the Incidence - SEER 13 Regs excluding AK Public-Use, Nov 2004 Sub for Hispanics (1992–2002), respectively. Stage of disease was defined as localized (confined to the organ of origin), regional (spread to adjacent organs or regional lymph node involvement), distant (discontinuous organ spread, distant lymph nodes), and unstaged.13
Malignant female genital germ cell tumors were identified, selecting for females, malignant disease, and morphology codes (International Classification of Diseases for Oncology [ICD-O])14 specific for germ cell tumors identified by female genital tract topography codes (ICD 510–519, 529–549, 559, 569, 570–574, 577–579). The histology codes used were dysgerminoma/seminoma (9060–9064), teratoma (9080–9085, 9090–9091), embryonal carcinoma (9070), yolk sac tumor (9071), polyembryoma (9072), gonadoblastoma (9073), mixed teratoma and seminoma (9085), and choriocarcinoma (9100, 9101, 1903).15 In keeping with our previous analysis of choriocarcinoma using the SEER program, the 27 ovarian choriocarcinomas were included, but the 80 choriocarcinoma cases identified by other female genital tract codes were excluded as probable gestational choriocarcinomas.16 Teratocarcinomas (mixed embryonal carcinoma and teratoma) (9081, 33 cases) were included in the mixed germ cell tumor group.
Overall, and for each sequential 5-year period, age-adjusted incidence rates standardized to the U.S. 2000 census,17,18 absolute counts, and females at risk (woman-years) were calculated, stratified by one or more of 6 characteristics (histology, stage, race, geographic region, age at diagnosis, and year of diagnosis), and then divided into 5-year time periods between 1973 and 2002. P values for rate comparisons were generated by selecting for rate ratios on the last row variable groupings. The ratio P value is the largest P value at which the ratio would be significant using gamma confidence intervals as a test of hypothesis; P 
.05 is statistically significant.12,19–21 For each variable, except when the rate was zero (the natural log of which is undefined), the estimated annual percent change in incidence rates applied to the 30-year time period was calculated by fitting a least squares regression line to the natural logarithm of the rates using calendar years as a regressor variable and 
2 to test for trends.18,22
Relative survival is a measure of net survival, which is calculated by comparing observed (overall) with expected survival from a comparable set of people who do not have cancer to measure the excess mortality that is associated with a cancer diagnosis. Therefore, relative survival is felt to be a more accurate representation of population-based cancer mortality.12,18 Relative survival (± standard error) overall and for each 5-year interval was calculated by using the SEER statistical software. Differences in 5-year relative survival points were compared by using the z statistic.23 To generate survival curves, the "list option" in SEER was used to abstract case-specific data, including histology, race, age at diagnosis, year of diagnosis, histology, and survival (alive versus dead), which was transferred into SAS 8 (SAS Institute Inc, Cary, NC), and the LIFETEST procedure was used to calculate survival curves. Differences in survival were compared by using the log-rank test.12 This study was reviewed and approved by University of New Mexico Institutional Review Board.
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RESULTS |
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By histologic subtype, the highest age-adjusted incidence rates were higher in teratomas (0.13, 95% confidence interval [CI] 0.12–0.14) than for dysgerminomas (0.11, 95% CI 0.10–0.12, ratio P = .005), but not for mixed germ cell tumors (0.10, 95% CI 0.09–0.11, P = .16). Figure 1 depicts trends in 5-year incidence rates by histologic subtype. For all malignant female germ cell tumors combined, the cumulative 30-year, age-adjusted incidence rate per 100,000 woman-years was 0.338. Overall, there was a 9.7% decrease in the 30-year rate (annual percentage change –0.14 per year, P = .71). Stratified by histologic subtype as defined in Table 1, there was a 29.4% decrease in dysgerminomas (annual percentage change –0.65% per year, P = .18), a 31.5% decrease in mixed germ cell tumors (annual percentage change –0.86% per year, P = .22), and a 61.2% increase in teratomas (annual percentage change +0.71% per year, P = .23), including a 51.0% increase in pure immature teratomas (annual percentage change +0.71% per year, P = .22) and a 207% increase in mature teratomas undergoing malignant degeneration (no annual percentage change or P value calculated), probably reflective of changes in coding. These trends differ from those for testicular germ cell tumors (SEER 1973–1998), which indicated that rates increased by 44%, from 3.35 to 4.84 per 100,000 population over 25 years.3
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There was considerable variability in female germ cell tumor age-adjusted incidence rates by registry. Rates in San Francisco-Oakland (Fig. 2) were significantly higher than for all other registries except Hawaii (P .02 to < .001). Rates for San Francisco-Oakland and Hawaii were comparable (P = .90), as were rates for Connecticut, Iowa, Seattle-Puget Sound, Detroit, and New Mexico (all P > .13), and all of these except Detroit had significantly higher rates than Atlanta and Utah (all P < .02). Dysgerminoma rates were significantly lower in Atlanta (0.066, all P .037) than in Hawaii (0.0143), New Mexico (0.141), Iowa (0.123), San Francisco (0.123), or Seattle (0.116). Teratoma rates were highest in San Francisco (0.17, 95% CI 0.14–0.21), higher than for Iowa (0.11, P = .01), New Mexico (0.10, P = .02), and Utah (0.08, P =.001). There were no differences in rates between registries for mixed germ cell tumors. Of note, registries with the highest incidence rates for all germ cell tumors and dysgerminomas also have a larger proportion of other nonwhite populations (Asian and/or Hispanic).
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For all germ cell tumors stratified by race/ethnicity, other nonwhites (0.41, 95% CI 0.34–0.49) had higher incidence rates than whites (0.33, 95% CI 0.30–0.35, ratio P = .014), but nonwhites and blacks (0.34, 95% CI 0.29–0.40, P = .14) and whites and blacks (P = .64) had comparable rates. Dysgerminoma rates among whites (0.11, 95% CI 0.10–0.13, P < .001) and other nonwhites (0.12, 95% CI 0.09–0.17, P = .003) were 2-fold higher than for blacks (0.05, 95% CI 0.03–0.08), but were no different for other nonwhites and whites (P = .84). Teratoma incidence rates were higher for blacks (0.18, 95% CI 0.14–0.22, P = .005) and other nonwhites (0.17, 95% CI 0.13–0.23, P = .013) than rates for whites (0.12, 95% CI 0.11–0.13). For mixed germ cell tumors, incidence rates did not vary by race (other nonwhites 0.12, 95% CI 0.08–0.17; blacks 0.11, 95% CI 0.08–0.10; whites 0.12, 95% CI 0.08–0.17), all P < .23.
Using the SEER 13 Regs Public-Use, Nov 2004 Sub for Expanded Races (1992–2002) database, 743 cases were identified affecting 548 whites (73.8%), 83 blacks (11.2%), 101 Asian/Pacific Islanders (13.6%), and 7 American Indians/Alaska Natives (0.5%). Compared with whites (0.35, 95% CI 0.32–0.38), all germ cell tumor incidence rates were marginally higher in Asian/Pacific Islanders (0.43, 95% CI 0.35–0.53, P = .059). Asian/Pacific Islanders had higher teratoma rates than whites (Asian/Pacific Islanders 0.22, 95% CI 0.17–0.30; whites 0.14, 95% CI 0.12–0.16, P = .006). Dysgerminoma incidence rates were lower in blacks (whites 0.12, 95% CI 0.10–0.13; Asian/Pacific Islanders 0.10, 95% CI 0.06–0.15; blacks 0.045, 95% CI 0.02–0.08; P = .001). Using the Incidence - SEER 13 Regs excluding AK Public-Use, Nov 2004 Sub for Hispanics (1992–2002) database, 740 cases were identified, affecting 179 (24.2%) Hispanics, 553 (74.7%) non-Hispanics, and 8 (1.1%) of unknown race/ethnicity. Compared with non-Hispanics (0.33, 95% CI 0.31–0.36), rates for all germ cell tumors were slightly higher in Hispanics (0.39, 95% CI 0.34–0.47, P = .07), but not significantly so for dysgerminomas (Hispanics 0.12, 95% CI 0.09–0.17; non-Hispanics 0.10, 95% CI 0.08–0.11; P = .17) or teratomas (Hispanics 0.18, 95% CI 0.14–0.24; non-Hispanics 0.14, 95% CI 0.12–0.16; P = .11). There were no differences in mixed germ cell tumor incidence rates (ratio P = 1.00).
By SEER stage, 56.7% had localized disease, and only 4.4% were classified as unstaged. Localized disease age-adjusted incidence rates increased by 7.3% (annual percentage change +0.62% per year, P = .21), regional disease increased by 104.4% (no annual percentage change or P value calculated), distant disease decreased by 32.5% (annual percentage change –1.52% per year, P = .021), and unstaged disease decreased by 81.7% (no annual percentage change or P value calculated). For all histologic subtypes, distant disease rates decreased (dysgerminomas 67.5%, annual percentage change –2.1% per year, P = .08; teratomas 18.9%, annual percentage change –1.17% per year, P = .23; mixed germ cell tumors 23.2%, annual percentage change –0.79% per year, P = .35). Localized disease rates decreased for dysgerminomas by 33.1% (annual percentage change –0.40%, P = .54) and for mixed germ cell tumors by 7.9% (annual percentage change –0.96%, P = .35) but increased for teratomas by 99.7% (annual percentage change +1.26% per year, P = .12).
Figure 3 illustrates trends in age-specific incidence rates by age at diagnosis and by histology. The only significant change in incidence rates by age at diagnosis was a 37.5% increase in 15–19 year olds (annual percentage change +1.30% per year, P = .008). The highest incidence rates were in females 15–19 years of age, and rates were higher in this age group for all histologic subtypes except teratomas (all P .002). Teratoma rates for 15–19 year olds were comparable to rates in 10–14, 20–24, and 30–34 year olds (all P .06), and were marginally lower than rates in 25–29 year olds (P = .048).
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Selecting for actively followed, histologically confirmed malignant cases, 1,187 were included in the relative survival calculations. Those with no survival time, no race recode A specification, or for whom calculations were determined to be invalid by the SEER program were also excluded. The 30-year cumulative 5-year relative survival was 83.9 ± 1.2%. Relative survival was lowest for mixed germ cell tumors (69.7%) compared with dysgerminomas (92.7%) and teratomas (86.9%) (all z scores 
3.0, P = .003). Relative survival increased by 39.5%, from 68.3% in 1973–1977 to 95.3% in 1998–2002. For the first 2 time periods, 1973–1977 and 1978–1982, there was no significant improvement (68.3% versus 73.9%, z score 1.31, P = .19), but survival was higher in 1983–1987 (88.3%) compared with 1973–1977 (z score 4.68, P < .001) or 1978–1982 (z score 3.59, P = .002). For pure immature teratomas, the cumulative 5-year relative survival was 88.4%. For all subtypes, survival rates improved over calendar time. Comparing 1973–1977 with 1998–2002, survival increased by 12.5% for dysgerminomas (from 83.5% to 96.9%), by 26.3% for teratomas (from 72.2% to 91.2%), by 109% for mixed germ cell tumors (from 43.4% to 90.7%), and by 29.3% (from 71.6% to 92.6%) for immature teratomas. Of the teratoma subtypes, adult mature teratomas with malignant degeneration had the lowest survival rates (53.3 ± 11.5%).
Cause of death within SEER is based upon death certificate data. For all 1,262 cases, 1,021 (80.9%) were coded as alive, and 241 (19.1%) as dead—152 (12.04%) from ovarian cancer. Sometimes it was impossible to determine if the cause of death was related to ovarian cancer, complications of treatment, another malignancy, or an unrelated condition. Therefore, overall survival was calculated using alive or dead as end points. Illustrated in Figure 4A, histologic subtype influenced overall survival (dysgerminoma 89.1%, teratoma 84.0%, mixed germ cell tumor 67.4%, log-rank P < .001). The median follow-up was 126 months (range 1–358 months).
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Stratified by the race/ethnicity, the 5-year relative survival by race (whites 83.5%, blacks 80.1%, and other nonwhites 90.3%) was lower for blacks than for other nonwhites (z score 2.16, P = .031) and lower for whites than for other nonwhites (z score 2.0, P = .045), but not for blacks and whites (z score 0.63, P = .59). Further stratified by histology, the difference in 5-year relative survival for dysgerminomas for whites and blacks was not significant (whites 92.0%, blacks 87.5%, other nonwhites 100.0%, z score 1.62, P = .11), but blacks had lower survival rates than other nonwhites (z score 2.03, P = .041). For mixed germ cell tumors (whites 68.7%, blacks 63.8%, and other nonwhites 80.4%) as well as for teratomas (whites 85.5%, blacks 89.3%, other nonwhites 90.3%), differences by race/ethnicity were not significant. Overall survival by histology (whites 80.1%, blacks 77.6%, other nonwhites 89.9%, P = .031) is depicted in Figure 4B. As for relative survival, there was no difference in survival for blacks and whites (P = .43).
Relative survival was affected by SEER stage (localized 93.7%, regional 80.2%, distant 67.2%, and unstaged 72.7%). Relative survivals were higher for localized disease than for regional (z score 5.28, P < .001), distant (z score 11.62, P < .001), or unstaged (z score 5.17, P < .001) disease. Relative survival for regional disease was higher than for distant (z score 2.68, P = .007), but not for unstaged (z score 0.98, P = .35) disease, whereas distant and unstaged disease had comparable survival rates (z score 0.84, P = .40). Figure 4C illustrates differences in overall survival by SEER stage (localized 90.6%, regional 78.6%, distant 64.3%, and unstaged 69.1%, P < .001). Relative survival for dysgerminoma was higher than for nondysgerminoma for all stages of disease except localized disease (localized 95.0% versus 93.1%, z score 1.90, P = .056; regional 89.9% versus 69.9%, z score 2.91, P = .004; distant 88.1% versus 59.2%, z score 4.87, P < .001; unstaged 94.0% versus 60.7%, z score 2.34, P = .019).
Over 30 years, relative survival for localized disease increased by 15.9%, from 84.9% to 98.4% (z score 2.97, P = .003). Five-year time periods were compared to determine when relative survival began to improve. There are no z score calculations for 1998 to 2002, because the cutoff for survival data was December 2001. For localized disease, survival did not improve until the second 5-year period (1978–1982 versus 1983–1987, z score 2.75, P = .005). Survival was consistently higher for all subsequent periods (all z scores 2.75), but there was no additional significant improvement after 1983–1987. For regional disease, relative survival increased by 26.8%, from 67.2% to 85.2% (z score 1.27, P = .20). Distant disease survival increased by 81.3%, from 51.8% to 93.9% (z score 2.29, P = .025). For women with distant disease, survival did not significantly improve until the 1983–1987 period (1973–1977 versus 1978–1982, z score 1.51, P = .13). Relative survival for 1983–1987 was higher than for 1973–1977 or 1978–1982 (z scores 3.04, P = .002, after which there were no further improvements (all z scores 0.04, P .90). Unstaged relative survival rates increased by 185.7%, from 35% to 100% (z score 2.77, P = .006), and were higher for 1978–1982 compared with 1973–1977 (z score 2.29, P = .028), with no further improvements after 1978–1982, (all z scores 0.95, P .31).
Illustrated in Figure 5, the 5-year relative survival was highest in 0- to 9-year-old females (97.6%). Survival rates were lower in women 40–49 years old or older (all z 2.71, P .006) than in younger females. Women 50–59 years old (relative survival 53.4%) had lower survival rates than all other age groups except 40–49 (all z 2.93, P .003). Women 60–85 years old (relative survival 22.3%) had lower survival rates than all other age groups (all z 2.36, P .018).
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DISCUSSION |
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ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Black and white women have lower survival rates for all germ cell tumors than other nonwhites. Lower survival rates among blacks may reflect reduced access to care.15 Black women may be less likely to be offered surgical intervention, increasing the risk of malignant degeneration of mature teratomas. These tumors have a more ominous prognosis, especially when the stage is higher than stage IA.26 Survival rates were poorest in older women and may reflect differences in treatment strategies, a higher proportion of teratoma with malignant degeneration, other disease processes, or a combination of these factors.
Despite reports that the biological mechanism and incidence rates of germ cell tumors are similar for both sexes,24 there are notable differences. Benign germ cell tumors occur more commonly in females, whereas malignant germ cell tumors occur more commonly in males.25 By age at diagnosis, among females, there has been an increase in malignant germ cell tumors only among 15–19 year olds (37.5%, annual percentage change +1.30% per year, P = .008), and an increase in this age group was also found for all histologic subtypes studied. In males, the highest rate of increase has been among 25–29 year olds, and the highest rates of testicular dysgerminomas and nondysgerminomas are in 30–34 and 25–29 year olds, respectively.7
There has been a dramatic reduction in the number of cases with distant and unstaged disease, which suggests that female germ cell tumors are being diagnosed earlier. Unlike epithelial ovarian malignancies, ovarian germ cell tumors grow rapidly and usually present with symptoms secondary to capsular distension, hemorrhage, or necrosis, which may account for why the majority are diagnosed with stage I disease. The survival rate has significantly improved for all ovarian germ cell tumors and for all histologic subsets, as well as for patients with advanced disease, with the greatest change in 1973–1977 and in 1978–1982. Similar data have been reported for testicular germ cell tumors.27 The population impact occurred approximately 3 years after dissemination of clinical trials testing cisplatin-based combination therapy.28,29 Although clinical trials have been performed for ovarian germ cell tumors,30 population-based trends indicate comparable changes in survival for both male and female germ cell tumors, coinciding with completion of the trials for testicular germ cell tumors.28,31 These data are encouraging and indicate that the prognosis for germ cell tumors, unlike that for epithelial ovarian cancer, is excellent.6,28,32–34 However, over the past 15 years there has been no further improvement in survival, and the risk of secondary neoplasms associated with therapy has become known. Survivors of testicular cancer treated with etoposide/cisplatin have a 1.3- to 3.4-fold increase in risk for leukemia, and after radiation therapy, a 2- to 3-fold increased risk for solid tumors (range 1.3–7.5). Further clarification of the role of adjuvant therapy for both male and female germ cell tumors is needed, especially those with stage IA disease, given the high cure rates with salvage therapy.
There are several limitations to these data. Lack of a centralized pathology review is perhaps the most important. The SEER database does not include data regarding the chemotherapy given or its impact on reproductive function. The 31 cases identified by ICD-O code 9081 (teratocarcinoma), which includes mixed embryonal carcinoma and teratoma, were included within the mixed germ cell tumor group but could have been grouped with teratomas. The 80 cases with choriocarcinoma affecting female genital sites other than ovary were not included in this analysis, but primary choriocarcinoma of other genital sites has been reported.38 The prognosis for ovarian germ cell choriocarcinoma is worse than that for gestational choriocarcinomas.39 However, analyses including these cases (not shown) did not significantly alter rates by race/ethnicity or relative survival trends. A later version of the SEER program with longer follow-up would be needed to calculate z scores for the 1997–2002 period. Nevertheless, this study appears to be the largest population-based study of female germ cell tumors to date, based upon a MEDLINE search (English language only, February 1966 through July 2005, selecting for germ cell tumor± females, population-based studies, epidemiology, and a review of 5, 612 identified abstracts) and indicates that survival rates have improved for female germ cell tumors. Further investigation of race/ethnicity and gender differences in incidence and survival is warranted.
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Footnotes |
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Corresponding author: Harriet O. Smith, MD, Department of Obstetrics and Gynecology, University of New Mexico Health Sciences Center, 2211 Lomas Boulevard NE, Albuquerque, NM 87131-5286; e-mail: Hsmith{at}salud.unm.edu.
doi:10.1097/01.AOG.0000216004.22588.ce
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