ABSTRACT
AIMS: Patients who have undergone prostate radiation are at increased risk for developing urothelial carcinoma. Radiation changes can cause significant cytological atypia in benign prostate glands that may mimic pagetoid spread of urothelial carcinoma. GATA3 is a common marker for differentiating prostatic adenocarcinoma from urothelial carcinoma. The aim of this study was to investigate the expression of GATA3 in the epithelium of irradiated benign and malignant prostate tissue. METHODS AND RESULTS: We performed a retrospective review of prostate cases with radiation atypia. GATA3 staining was performed on benign prostate tissue with and without radiation atypia, as well as on residual/recurrent prostatic adenocarcinoma after radiation therapy. PIN4 immunohistochemical (IHC) staining was performed on prostate tissue with radiation atypia to confirm the presence of both basal and luminal cells. We identified 31 cases with benign prostate glands containing radiation atypia. The average time between treatment with radiation therapy and the surgical procedure was 10 years (range 5-20 years). PIN4 IHC staining confirmed the presence of basal and luminal cells in benign prostate glands with radiation atypia. Thirty-one of 31 (100%) cases of benign prostate tissue with radiation atypia showed staining for GATA3 in both basal and luminal cells. Eight of eight (100%) cases of benign prostate glands without radiation atypia and no inflammatory changes showed GATA3 positivity limited to basal cells. GATA3 was negative in 12/12 (100%) cases of prostatic adenocarcinoma after radiation therapy. CONCLUSION: Benign prostate glands with radiation atypia show diffuse positivity for GATA3. This staining pattern, along with the cytological atypia resulting from radiation, can mimic urothelial carcinoma.
Subject(s)
Biomarkers, Tumor/analysis , GATA3 Transcription Factor/biosynthesis , Neoplasms, Radiation-Induced/diagnosis , Prostate/pathology , Radiation Injuries/diagnosis , Adenocarcinoma/diagnosis , Aged , Carcinoma, Transitional Cell/diagnosis , Diagnosis, Differential , GATA3 Transcription Factor/analysis , Humans , Male , Middle Aged , Prostate/radiation effects , Prostatic Neoplasms/diagnosis , Retrospective StudiesABSTRACT
Many effective therapeutic options are available for patients with chronic myelogenous leukemia (CML). Imatinib, a first-generation tyrosine kinase inhibitor (TKI), is one of several options for patients who present with CML, whether in chronic phase, accelerated phase, or blast crisis. Although CML is very responsive to the selective TKIs, with response rates in chronic phase of greater than 90%, unusual presentations have been documented. Response rates for patients with CML in accelerated phase and blast crisis are notably lower to both first- and second-generation TKIs. This report presents a recent case of a young woman with newly diagnosed CML who presented with an accelerated phase isolated central nervous system (CNS) relapse after standard imatinib therapy, who initially experienced a complete hematologic response. Further treatment options, and monitoring of disease response, are discussed. Aggressive strategies, such as intrathecal chemotherapy, change in tyrosine kinase inhibitor to one with increased CNS penetration, and consideration of allogenic stem cell transplantation, are potential therapeutic modalities. Prophylaxis of the CNS in patients deemed at risk is an area requiring further study.