Aggressive variants of castration-resistant prostate cancer
Himisha Beltran1, Scott Tomlins2, Ana Aparicio2
1Authors' Affiliations: Division of Hematology and Medical Oncology; Institute for Precision Medicine, New York Presbyterian; Department of Pathology and Laboratory Medicine, Weill Cornell Medical College; Department of Oncology, Memorial Sloan Kettering, New York, New York; Department of Pathology, University of Michigan, Ann Arbor, Michigan; Department of Oncology, The University of Texas MD Anderson Cancer Center; Department of Pathology and Laboratory Medicine, The University of Texas Health Science Center, Houston, Texas; Department of Pathology and Laboratory Medicine, University of California, Los Angeles (UCLA), Los Angeles; Prostate Cancer Foundation, Santa Monica, California; Department of Pathology, University of Washington, Seattle, Washington; and Vancouver Prostate Centre, Vancouver, British Columbia, CanadaAuthors' Affiliations: Division of Hematology and Medical Oncology; Institute for Precision Medicine, New York Presbyterian; Department of Pathology and Laboratory Medicine, Weill Cornell Medical College; Department of Oncology, Memorial Sloan Kettering, New York, New York; Department of Pathology, University of Michigan, Ann Arbor, Michigan; Department of Oncology, The University of Texas MD Anderson Cancer Center; Department of Pathology and Laboratory Medicine, The University of Texas Health Science Center, Houston, Texas; Department of Pathology and Laboratory Medicine, University of California, Los Angeles (UCLA), Los Angeles; Prostate Cancer Foundation, Santa Monica, California; Department of Pathology, University of Washington, Seattle, Washington; and Vancouver Prostate Centre, Vancouver, British Columbia, Canada hip9004@med.cornell.edu.
Abstract:
A subset of patients with advanced castration-resistant prostate cancer may eventually evolve into an androgen receptor (AR)-independent phenotype, with a clinical picture associated with the development of rapidly progressive disease involving visceral sites and hormone refractoriness, often in the setting of a low or modestly rising serum prostate-specific antigen level. Biopsies performed in such patients may vary, ranging from poorly differentiated carcinomas to mixed adenocarcinoma-small cell carcinomas to pure small cell carcinomas. These aggressive tumors often demonstrate low or absent AR protein expression and, in some cases, express markers of neuroendocrine differentiation. Because tumor morphology is not always predicted by clinical behavior, the terms "anaplastic prostate cancer" or "neuroendocrine prostate cancer" have been used descriptively to describe these rapidly growing clinical features. Patients meeting clinical criteria of anaplastic prostate cancer have been shown to predict for poor prognosis, and these patients may be considered for platinum-based chemotherapy treatment regimens. Therefore, understanding variants within the spectrum of advanced prostate cancer has important diagnostic and treatment implications.
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