An 80-year-old patient was diagnosed with prostate cancer 7 years ago. The PSA was 43.8 ng/mL. Prostate biopsy was performed by guided transrectal ultrasonography. Histopathological examination of the specimen showed an adenocarcinoma (Gleason score 3+3). We performed magnetic resonance imaging, computed tomography (CT), whole-body bone scan, and chest X-ray (CXR). No meta-static lesions except bladder neck invasion were found (Fig. 1A). The patient underwent EBRT for prostate adenocarcinoma. At 1 year after EBRT, the level of PSA had risen gradually despite the fact that characters of prostate showed no changing on CT (Fig. 1B). Additional ADT had been followed up 3 years. The serum PSA maintained level of the nadir was 0.002 ng/mL. But, the patient did not visit hospital with a private matter during 3 years.

After 3 years, the patient visited Urology Department a complaining with urinary retention and rectal pain with constipation. On the physical examination, huge and hard rectal mass was palpable. The serum PSA was 3.51 ng/mL. CXR showed multiple wide-spread variable-sized nodules in the entire both lung fields. Chest, abdomen and pelvis CT showed an 8-cm-sized rectal mass with poor enhancement and multiple lymph nodes metastasis (Fig. 1C, D). Colonoscopy guided biopsy was done to distinguish recurred prostate cancer and gastrointestinal stromal tumor. The current biopsy contains a minor component of high-grade prostatic aci-nar adenocarcinoma (10%) and a major component of high-grade sarcoma (90%). The high-grade sarcoma components show spindle cells with marked atypia and frequent mitoses and scattered bizarre polygonal large cells are positive for cytokeratin (Fig. 2A). Occasional spindle cells are negative for p63 represented for basal cell marker (Fig. 2B). They are diffusely positive for vimentin (Fig. 2C). The spindle cells and polygonal large cells are focally positive for desmin, smooth muscle actin and myoDl but negative for ALK-1, CD34, CD117, PSA, and cytokeratin AE1/3 (Fig. 2D). The high-grade sarcomatous components show hetero-genous sarcomatous elements consisting of predominantly rhabdomyosarcoma (60%) and leiomyosarcoma (30%). The high-grade acinar adenocarcinoma component is positive for cytokeratin AE1/3 and PSA (immunohistochemical stain, ×200). This patient exhibited the short duration between initial presentation with adenocarcinoma and emergence of carcinosarcoma. The patient was scheduled for CTX as long as possible. Then, he was treated with docetaxel for one cycle. CTX was stopped because of rapid getting worse, and the patient died 5 months later.

The pathogenesis of prostatic carcinosarcoma is not clear and diverse analysis has been proposed for the various elements of carcinosarcoma. The prostatic carcinosarcomas interpreted the heterologous mix of carcinomatous (epithelial) and sarcomatous (mesenchymal) elements, and it could be related to previous RT or to ADT.³ In our case, sarcomatous component was not found at the first biopsy. Carcinosarco-ma was diagnosed with the second biopsy after 3 years of ADT with RT. Some reports content that RT and ADT may lead to transformation of carcinosarcoma.⁴ About half of carcinosarcoma cases, the first biopsies are proven aci-nar-typed adenocarcinoma. It was proposed the period for carcinosarcoma transformation from adenocarcinoma is averagely 3 years as seen in our case.⁵ Carcinosarcomas of prostate often are presented with low levels of serum PSA compared with adenocarcinoma, therefore serum PSA has low effects for the assessment of the sarcomatous element in carcinosarcoma, whereas it may be useful in assessing the progress of the adenocarcinoma component of the tumor. The epithelial component of carcinosarcoma of prostate stains shows positivity for cytokerarin and prostatic acid phosphatase. The sarcoma component of carcinosarco-ma stains show negativity for PSA, epithelial membrane antigen, and keratin.⁶ It is hard to distinguish clearly between carcinosarcoma and other tumors in many diagnostic methods, thus a diagnosis will be confirmed after biopsy. The serum PSA remained low level after RT or ADT, nevertheless, the aggravating disease such as increasing tumor size or spreading metastasis was progress. In that case, it is good to planning for additional biopsy of the prostate. Early diagnosis and treatment may give a chance of improved prognosis in these patients. There is no standard option of treatment. There are various treatment modalities such as aggressive surgical treatments (radical prostatectomy or total pelvic exenteration) or EBRT or ADT or CTX. ADT would be preferred to treat the adenocarcinoma component of the prostatic cancer but would be useless to control the sarcomatoid component of the tumor. Aggressive surgery remains the recommendable therapy method. Early diagnosis and treatment may give a chance of improved prognosis in these patients. The most often use therapeutic modality has been an RT (43%). Other modalities such as surgery (40%), ADT (38%), and CTX (14%) have been used for the patients with prostatic carcinosarcoma in order of precedence.⁷ The sites of metastases were the lung, bone, lymph node, liver, brain, and peritoneum and so on. Most common site is lung.⁷ In cases of advanced disease supportive therapy would be required. Patients with severe obstruction of the rectum would require colostomy as seen in our case. The survival period was extremely disappointing. The mean period was 7 months.⁸ Our patient was treated with CTX, but CTX was stopped because of rapid clinical aggravation, and the patient died 5 months later. Early rebiopsy of prostate in case of progressed disease despite of PSA maintenance after RT or ADT may help diagnose various carcinoma, and early aggressive treatment may help to improve prognosis.