A Sella1, M Konichezky, D Flex, A Sulkes, J Baniel. 1. Genitourinary Medical Oncology Unit and Department of Oncology, Rabin Medical Center, Beilinson Campus, Petah Tikva, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. avisella@netvision.net.il
Abstract
OBJECTIVES: To describe the clinical parameters of low PSA, progressive metastatic androgen-independent prostate cancer. METHODS: From April 1995 to May 1999, we selected 18 patients with clinically progressive androgen-independent prostate cancer and low PSA (</=10 ng/ml). Patients received cisplatin-based therapy. Specimens from the primary tumor were reviewed and neuroendocrine differentiation was determined with chromogranin-A and neuron-specific enolase immunocytochemical staining. RESULTS: The median initial PSA level was 1.6 ng/ml (0-9.5). Each patient demonstrated elevation of at least one of the following markers: carcinoembryonic antigen, CA 19-9, CA15-3 and CA 125 CA. Metastases involved bone in 11 patients (61.1%) - 5 (27.7%) blastic, 2 (11.1%) lytic, and 4 (22.2%) combined - liver in 10 patients (55.5%), lymph nodes in 8 (44.4%), and lung in 6 (33.3%); solitary sites as orbit, skin and spleen were noted as well. A prostatic pelvic mass was detected in 13 patients (72.2%). Of the 12 patients who consented to chemotherapy, 8 (66.6%) achieved an objective response (95% CI, 34. 8-90%), including 1 patient with complete response. Hematoxylin and eosin evaluation revealed two major groups: neuroendocrine tumors, either pure small cell cancer in 6 patients (37.5%) or combined small cell cancer and adenocarcinoma in 8 (50%), and predominant poorly differentiated prostate cancer in 2 (12.5%). Neuroendocrine immunoreactivity was detected in all the specimens. CONCLUSIONS: Progressive androgen-independent prostate cancer with low serum PSA is characterized by visceral metastases, high proportion of lytic bone disease, sensitivity to cisplatin-based chemotherapy, and histological features of small cell or poorly differentiated prostate cancer. In this subgroup of patients, selection of the therapeutic approach can be based on clinical parameters. The rise of the serum markers may aid in the diagnosis and follow-up of these patients.
OBJECTIVES: To describe the clinical parameters of low PSA, progressive metastatic androgen-independent prostate cancer. METHODS: From April 1995 to May 1999, we selected 18 patients with clinically progressive androgen-independent prostate cancer and low PSA (</=10 ng/ml). Patients received cisplatin-based therapy. Specimens from the primary tumor were reviewed and neuroendocrine differentiation was determined with chromogranin-A and neuron-specific enolase immunocytochemical staining. RESULTS: The median initial PSA level was 1.6 ng/ml (0-9.5). Each patient demonstrated elevation of at least one of the following markers: carcinoembryonic antigen, CA 19-9, CA15-3 and CA 125 CA. Metastases involved bone in 11 patients (61.1%) - 5 (27.7%) blastic, 2 (11.1%) lytic, and 4 (22.2%) combined - liver in 10 patients (55.5%), lymph nodes in 8 (44.4%), and lung in 6 (33.3%); solitary sites as orbit, skin and spleen were noted as well. A prostatic pelvic mass was detected in 13 patients (72.2%). Of the 12 patients who consented to chemotherapy, 8 (66.6%) achieved an objective response (95% CI, 34. 8-90%), including 1 patient with complete response. Hematoxylin and eosin evaluation revealed two major groups: neuroendocrine tumors, either pure small cell cancer in 6 patients (37.5%) or combined small cell cancer and adenocarcinoma in 8 (50%), and predominant poorly differentiated prostate cancer in 2 (12.5%). Neuroendocrine immunoreactivity was detected in all the specimens. CONCLUSIONS: Progressive androgen-independent prostate cancer with low serum PSA is characterized by visceral metastases, high proportion of lytic bone disease, sensitivity to cisplatin-based chemotherapy, and histological features of small cell or poorly differentiated prostate cancer. In this subgroup of patients, selection of the therapeutic approach can be based on clinical parameters. The rise of the serum markers may aid in the diagnosis and follow-up of these patients.
Authors: Sandra M Axiak-Bechtel; Senthil R Kumar; Kristin K Dank; Nicole A Clarkson; Kim A Selting; Jeffrey N Bryan; Thomas J Rosol; Jahna Espinosa; Charles J Decedue Journal: Invest New Drugs Date: 2013-09-13 Impact factor: 3.850
Authors: Jianfei Qi; Koh Nakayama; Robert D Cardiff; Alexander D Borowsky; Karen Kaul; Roy Williams; Stan Krajewski; Dan Mercola; Philip M Carpenter; David Bowtell; Ze'ev A Ronai Journal: Cancer Cell Date: 2010-07-13 Impact factor: 31.743
Authors: Ajalaya Teyateeti; Achiraya Teyateeti; Gregory C Ravizzini; Guofan Xu; Chad Tang; Shi-Ming Tu; Homer A Macapinlac; Yang Lu Journal: Am J Nucl Med Mol Imaging Date: 2021-04-15
Authors: Micsunica Platica; Elena Ivan; James F Holland; Alin Ionescu; Sheryl Chen; John Mandeli; Pamela D Unger; Ovidiu Platica Journal: Proc Natl Acad Sci U S A Date: 2004-01-26 Impact factor: 11.205