Placental site trophoblastic tumor (PSTT) differs from choriocarcinoma in several key ways. Which characteristic is unique to PSTT?
- A PSTT arises from syncytiotrophoblasts and is highly responsive to EMA-CO chemotherapy
- B PSTT is characterized by markedly elevated beta-hCG levels (>100,000 mIU/mL) at presentation
- C PSTT has the highest cure rate of all gestational trophoblastic neoplasias due to chemosensitivity
- D PSTT is relatively chemoresistant and surgery (hysterectomy) is primary treatment; hPL is more elevated than hCG ✓
Explanation
PSTT arises from intermediate trophoblasts (not syncytiotrophoblasts) and produces predominantly human placental lactogen (hPL) with only modest beta-hCG elevation. Unlike choriocarcinoma, PSTT is relatively resistant to standard EMA-CO chemotherapy (only ~30% response). Surgery (hysterectomy) is therefore the cornerstone of treatment even for non-metastatic disease. For metastatic PSTT, EP/EMA (etoposide-cisplatin alternating with etoposide-MTX-actinomycin) has higher activity than EMA-CO. PSTT generally has a worse prognosis than low-risk GTN but can be cured with appropriate surgery. Epithelioid trophoblastic tumor (ETT) has a similar behavior.
Reference: Williams Obstetrics, 26th ed.
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Written and medically reviewed by the StethoPrep medical team.