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Novel concept of antisurvival factor (ASF) therapy produces an objective clinical response in four patients with hormone‐refractory prostate cancer: Case report
Author(s) -
Koutsilieris Michael,
Tzanela Marinella,
Dimopoulos Theodoros
Publication year - 1999
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19990301)38:4<313::aid-pros7>3.0.co;2-8
Subject(s) - medicine , prostate cancer , prostate , oncology , hormone therapy , combination therapy , hormonal therapy , endocrinology , insulin like growth factor , cancer , growth factor , urology , breast cancer , receptor
BACKGROUND Osteoblasts and osteoblast‐derived survival growth factors, such as insulin‐like growth factor I (IGF I), inhibit chemotherapy apoptosis of prostate cancer cells, thereby producing cytotoxic drug‐resistant tumor growth, in vitro. METHODS We tested a novel therapeutic approach, referred to as antisurvival factor (AFS) therapy, that aimed at reduction of osteoblast‐derived IGFs, using dexamethasone (4 mg per os, qD) and growth hormone (GH)‐dependent liver‐derived IGFs, using a somatostatin‐analog (lanreotide, 30 mg, intramuscularly (IM), ql4D) in combination with triptorelin (3.75 mg, intramuscularly, q28D) to produce a clinical response in 4 patients with progressing hormone‐refractory prostate cancer. RESULTS The patients given ASF therapy exhibited an excellent improvement of clinical performance and a decline of prostate‐specific antigen (PSA) within 2 months of ASF therapy. One of them experienced excellent clinical response (normalization of PSA), two experienced good clinical response (decline of PSA of more than 50%), and one experienced stabilization (decline of PSA of less than 50%). CONCLUSIONS We conclude that this novel concept of combination therapy, using ASF with hormone ablation, is a promising salvage therapy that should be further assessed with a randomized clinical trial. Prostate 38:313–316, 1999. © 1999 Wiley‐Liss, Inc.