Editorial Comment to Systemic treatment for coexisting mucinous urethral adenocarcinoma and prostate adenocarcinoma

pies. Evidence for this is a part of the carcinosarcoma that showed AE1/3 positivity on immunostaining and that it had the same immunostaining characteristics as mucinous adenocarcinoma (Fig. 3e). In addition, AE1/3-positive adenocarcinoma was found in many lymphatic vessels near the carcinosarcoma of the primary and metastatic sites (Fig. 3f). Autopsy also revealed that carcinosarcomas predominated over mucinous urethral adenocarcinoma at most metastatic sites. Chemotherapies appear to have been successful for mucinous adenocarcinoma but not for carcinosarcoma. We have considered other treatment modalities aside from chemotherapy. In this case, negative results for microsatellite instability were obtained, and immune checkpoint inhibitors were not indicated. In addition, immune checkpoint inhibitors may be ineffective in urethral adenocarcinoma because bladder adenocarcinoma has a low frequency of gene mutations and a low level of PD-L1 expression. By contrast, EGFR inhibitors may be effective for mucinous urethral adenocarcinoma. Bryce et al. reported a case in which multiple-gene panel testing revealed strong amplification and immunostaining of EGFR, contributing to successful treatment with erlotinib. In this case as well, EGFR immunostaining was strongly positive for mucinous urethral adenocarcinoma (Fig. 3c). We recommended multiple-gene panel testing for the administration of erlotinib; however, the patient refused testing because of financial and locationrelated issues.

metastasis and invasion and became resistant to chemotherapies. Evidence for this is a part of the carcinosarcoma that showed AE1/3 positivity on immunostaining and that it had the same immunostaining characteristics as mucinous adenocarcinoma (Fig. 3e). In addition, AE1/3-positive adenocarcinoma was found in many lymphatic vessels near the carcinosarcoma of the primary and metastatic sites (Fig. 3f). Autopsy also revealed that carcinosarcomas predominated over mucinous urethral adenocarcinoma at most metastatic sites. Chemotherapies appear to have been successful for mucinous adenocarcinoma but not for carcinosarcoma.
We have considered other treatment modalities aside from chemotherapy. In this case, negative results for microsatellite instability were obtained, and immune checkpoint inhibitors were not indicated. In addition, immune checkpoint inhibitors may be ineffective in urethral adenocarcinoma because bladder adenocarcinoma has a low frequency of gene mutations and a low level of PD-L1 expression. 11 By contrast, EGFR inhibitors may be effective for mucinous urethral adenocarcinoma. Bryce et al. 4 reported a case in which multiple-gene panel testing revealed strong amplification and immunostaining of EGFR, contributing to successful treatment with erlotinib. In this case as well, EGFR immunostaining was strongly positive for mucinous urethral adenocarcinoma (Fig. 3c). We recommended multiple-gene panel testing for the administration of erlotinib; however, the patient refused testing because of financial and locationrelated issues.

Conclusion
It is important to distinguish mucinous urethral adenocarcinoma from other adenocarcinomas, such as prostate adenocarcinoma, mucinous prostate adenocarcinoma, and secondary cancer. In our rare case of coexisting mucinous urethral and prostate adenocarcinomas, difficulties in diagnosis and treatment arose from histopathological similarities. Thus, when there is a lesion adjacent to the urethra, pathologists should consider immunostaining for PSA, CEA, CK7, CK20, and CDX2 to detect prostate cancer, which is rare. 1 Liaison between the pathologist and the clinician could ensure early diagnosis in such cases. Finally, because no definitive conclu-sions can be drawn from this single case report, further studies based on case accumulation are warranted.

Editorial Comment Editorial Comment to Systemic treatment for coexisting mucinous urethral adenocarcinoma and prostate adenocarcinoma
The coexistence of mucinous urethral and prostate adenocarcinoma is challenging to diagnose because of its rarity. Nezu et al. reported a case of coexisting mucinous urethral and prostate adenocarcinoma managed with systemic treatment. 1 They initially diagnosed a patient with prostate adenocarcinoma. However, hormone therapy and standard chemotherapy for prostate adenocarcinoma were ineffective. Re-biopsy showed mucinous adenocarcinoma, and they changed the hormone drug to a colon cancer regimen, followed by a bladder cancer regimen. Despite their best efforts, the patient died 14 months after clinical presentation. Autopsy implied that epithelial-mesenchymal transition had occurred in the metastatic lesions of the urethral adenocarcinoma.
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Mucinous urethral adenocarcinoma has no standard treatment approach. The authors suggested that erlotinib might be effective because epidermal growth factor receptor (EGFR) immunostaining was strongly positive in this case. Bryce et al. reported a case of mucinous urethral adenocarcinoma in which targetable EGFR amplification led to successful treatment with erlotinib. 2 Before erlotinib, the patient received both traditional bladder cancer and colon cancer regimens. However, the bladder cancer regimen led to only a brief response with severe side effects, and the colon cancer regimen had similar toxicity. Targeted therapy of erlotinib was effective for a full year and provided the highest quality of life for the patient. Genomic tumor analysis would offer a tool to provide precise data to guide the appropriate treatment of these rare cases. EGFR can be tested for in future mucinous urethral adenocarcinoma cases to inform treatment decisions.