The oncologist · 2026
Divergent biology and outcomes of somatic transformations in germ cell tumors.
СтатьяНазвание и аннотация: Перевод в очереди
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Thomas Zachariah, Johns Andrew C, Glover Michael, Crupi Emanuele, Nieto Yago L, Ward John F, Karam Jose A, Hofstetter Wayne L, Desai Monica, Choi Seungtaek L, Shah Amishi Y, Lin John, Moussa Mohammad Jad, Jiang Cindy Y, Alhalabi Omar, Campbell Matthew T
Аннотация
PURPOSE: Somatic-type malignancy (SM) of germ cell tumor (GCT) is rare but demonstrates aggressive behavior. Differences by primary site, time to transformation, and mutational status remain poorly characterized.
PATIENTS AND METHODS: We reviewed all SM patients between June 2016 and May 2025 at a tertiary referral center. Time to somatic transformation (TST) was defined from the initial GCT diagnosis to SM detection. SM were classified based on time of detection- at initial diagnosis (de novo), at consolidative surgery, at relapse within 5 years, and evolved SM at relapse after 5 years. Descriptive statistics, Kaplan-Meier estimates, and Cox regression analyses were used.
RESULTS: 72 patients were identified: 40 (56%) with testicular, 24 (33%) with mediastinal, and 8 (11%) with other primaries. 22/24 (92%) mediastinal tumors with SM had sarcomatous transformation. Sarcoma was seen in 25/42 (60%) of de novo SM while adenocarcinoma was detected as an evolved entity in 5/6 (83.3%) cases. Embryonic type neuroectodermal tumor (ENET) histology carried poor prognosis compared to non-ENET histology (median, OS 1.8 vs 8 years; HR, 1.94; P = 0.1). Genomic data available showed PTEN-AKT-mTOR pathway mutations (33%) and TP53 mutations (33%), enriched in extra-gonadal sarcomatous SM.
CONCLUSIONS: SM exhibits temporal, histologic, and molecular distinctions across primary sites. Response to frontline therapy and survival outcomes are poor. Future direction includes the exploration of underlying predictors of transformation and identification of targetable alterations in the relapsed setting.
PATIENTS AND METHODS: We reviewed all SM patients between June 2016 and May 2025 at a tertiary referral center. Time to somatic transformation (TST) was defined from the initial GCT diagnosis to SM detection. SM were classified based on time of detection- at initial diagnosis (de novo), at consolidative surgery, at relapse within 5 years, and evolved SM at relapse after 5 years. Descriptive statistics, Kaplan-Meier estimates, and Cox regression analyses were used.
RESULTS: 72 patients were identified: 40 (56%) with testicular, 24 (33%) with mediastinal, and 8 (11%) with other primaries. 22/24 (92%) mediastinal tumors with SM had sarcomatous transformation. Sarcoma was seen in 25/42 (60%) of de novo SM while adenocarcinoma was detected as an evolved entity in 5/6 (83.3%) cases. Embryonic type neuroectodermal tumor (ENET) histology carried poor prognosis compared to non-ENET histology (median, OS 1.8 vs 8 years; HR, 1.94; P = 0.1). Genomic data available showed PTEN-AKT-mTOR pathway mutations (33%) and TP53 mutations (33%), enriched in extra-gonadal sarcomatous SM.
CONCLUSIONS: SM exhibits temporal, histologic, and molecular distinctions across primary sites. Response to frontline therapy and survival outcomes are poor. Future direction includes the exploration of underlying predictors of transformation and identification of targetable alterations in the relapsed setting.